A comprehensive literature search was conducted in MEDLINE, Embase, the Cochrane Database of Systematic Reviews, the Cochrane Central Register of Controlled Trials, and the EU Clinical Trials Register to identify eligible studies published from inception through August 2025. Clinical trials reporting ASDAS-ID or ASDAS-LDA were included. Eligible studies enrolled patients with radiographic or nonradiographic axSpA treated with biologic therapies, including tumor necrosis factor inhibitors (TNFi), interleukin 17 inhibitors (IL17i), or targeted synthetic disease-modifying antirheumatic drugs (tsDMARDs) such as Janus kinase inhibitors (JAKi). Risk of bias (ROB) was assessed using the Cochrane ROB tool, and 2 independent reviewers screened all records, with disagreements resolved by a senior author. A metaanalysis was performed, and data were synthesized using forest plots to calculate pooled odds ratios with 95% CIs. Study heterogeneity was assessed using the I² statistic.

A total of 41 unique studies were included; 19 RCTs were identified with 6171 patients included in the metaanalysis. Additionally, 22 open-label extension (OLE) studies were included. Several OLE publications originated from the same parent RCT and therefore did not represent independent studies. The pooled proportion of patients achieving ID status in the treatment group was 0.24 (95% CI 0.18-0.31) at 12-24 weeks, and in the OLE phases 0.22 (95% CI 0.17-0.28) during weeks 48-52 and 0.35 (95% CI 0.25-0.43) during weeks 96-156. The odds of achieving ID were 0.30 (95% CI 0.17-0.51) compared to LDA in the treatment group.

This study demonstrates that attainment of ASDAS-ID in axSpA clinical trials is consistently low, reflecting the stringency of this remission threshold within trial designs. These findings underscore the importance of interpreting ASDAS-ID alongside ASDAS-LDA, which may represent a more attainable and clinically meaningful disease state when remission is not achieved.

Four separate commensal oral bacteria species were cultured with human neutrophils to induce neutrophil extracellular trap formation (NETosis). The resultant NETs contained neutrophil-derived peptidylarginine deiminase 4 (PAD4), which, within the NET milieu, became activated and mediated citrullination of both bacterial and neutrophil self-proteins. Citrullination was evaluated by adding rabbit anticitrulline antibody followed by Alexa Fluor 647–conjugated antirabbit IgG secondary antibody.

Our data demonstrate that citrullinated oral bacteria induce Toll-like receptor 9 (TLR9)–spleen tyrosine kinase (Syk)-mediated human B cell activation, differentiation, proliferation, and antibody secretion, including the development of plasmablasts secreting anticitrullinated protein antibodies (ACPAs). Some ACPAs bind citrullinated oral bacteria to form immune complexes (ICs) that can activate monocyte-derived macrophages in vitro to differentiate into CD11b⁺CD64⁺ proinflammatory macrophages that secrete tumor necrosis factor and interleukin 6. In contrast, ACPA citrullinated–antigen complexes inhibit differentiation of antiinflammatory MerTK^hiTREM2^hiLYVE1^hi macrophages that clear apoptotic cells and promote tissue repair. These data suggest ICs formed by ACPAs binding citrullinated antigens augment proinflammatory responses and inhibit antiinflammatory response.

Our data support the hypothesis that in RA patients with PD, citrullinated oral bacteria breach damaged periodontal tissue to enter the circulation and induce both innate and adaptive proinflammatory responses that promote synovial tissue destruction.

In this retrospective study, 409 patients with RA undergoing TKA (2000-2021) were age- and sex-matched with OA patients. A validated DL model quantified medial and lateral mJSW from anteroposterior knee radiographs at 2 timepoints: early (> 2 years before TKA) and late (≤ 2 years before TKA). The rate of JSN was calculated in 302 patients with paired radiographs. Mixed-effects models adjusted for BMI and alignment. RA disease activity, serology, and medications were recorded.

RA demonstrated narrower lateral mJSW than OA at the late timepoint (5.6 vs 7.0 mm; P < 0.001), with comparable medial values. RA exhibited uniform bicompartmental JSN, whereas OA showed medial narrowing. RA had a faster mean lateral mJSW (0.11 mm/year; P = 0.01), whereas OA had a faster mean medial mJSW (0.21 mm/year; P < 0.001). Longer RA duration and higher inflammatory markers were negatively associated with lateral mJSW. Seronegative patients showed faster lateral mJSW in the surgical knee than seropositive patients (0.12 vs 0.06 mm/year; P = 0.03).

Patients with RA demonstrated diffuse, symmetric cartilage loss that contrasted with medial-predominant narrowing in patients with OA. Automated DL-based measurement enables scalable, compartment-specific assessment of joint degeneration patterns.

This cross-sectional study included 418 patients diagnosed with axSpA who fulfilled the Assessment of SpondyloArthritis international Society classification criteria. Participants were recruited from 3 Latin American regions: northern (Mexico), Andean (Colombia, Ecuador, Peru, Venezuela), and southern (Argentina, Chile, Paraguay, Uruguay). Collected data included demographic characteristics, HLA-B27 status, extraarticular manifestations, disease activity, radiographic damage, and treatments.

The northern region showed the highest prevalence of HLA-B27 (81%) and uveitis (36.3%), along with lower frequencies of peripheral involvement and fewer patients with magnetic resonance imaging–defined sacroiliitis (7.3%; all P ≤ 0.003). In contrast, the southern region reported a later onset of inflammatory back pain (median 39 vs 22 years; P = 0.01), higher Bath Ankylosing Spondylitis Functional Index scores (median 4.6 vs 3.3, P = 0.005), and a lower response to nonsteroidal antiinflammatory drugs (59.8% vs 79%; P = 0.001). Use of biologic disease-modifying antirheumatic drugs was lowest in the northern region (34.7%) compared with the Andean (57.9%) and southern (53.8%) regions (P ≤ 0.002 for northern vs other regions). The median diagnostic delay was 40.9 (IQR 12.0-121.1) months, with no significant regional differences.

Two clinical phenotypes of axSpA appear to exist in Latin America: a predominantly axial, HLA-B27–positive phenotype in the northern region, and a second phenotype in the Andean and southern regions characterized by greater peripheral involvement and, in the southern region, later symptom onset and worse functional status.

We conducted a retrospective cohort study including all patients with SSc managed at a tertiary SSc clinic between January 2016 and December 2024. Adherence to QIs was assessed across baseline screening (interstitial lung disease and pulmonary hypertension), longitudinal monitoring (pulmonary function testing, echocardiographic follow-up, skin assessment, and clinical documentation), and treatment and referral practices (digital ulcer management and rehabilitation). Multivariable logistic regression identified independent predictors of adherence.

Among 66 patients (mean age 46.2 [SD 12.9] years, 92% female), adherence to baseline screening was high, including high-resolution computed tomography (86%) and transthoracic echocardiography (TTE; 84%). Baseline treatment adherence was also high, with vasodilator therapy for all patients with active digital ulcers (100%). In contrast, longitudinal follow-up adherence was suboptimal, including annual pulmonary function testing (35%), follow-up TTE after a new decline in diffusing lung capacity for carbon monoxide (36%), dyspnea documentation (63%), chest auscultation (27%), annual modified Rodnan skin score (19%), and physical therapy referral (37%). Older age, longer disease duration, diffuse cutaneous subtype, and pulmonary hypertension independently predicted lower adherence.

Despite strong baseline adherence, major gaps persist in longitudinal monitoring, documentation, and rehabilitation, highlighting key targets for quality improvement.

Clinical data from children newly diagnosed with JIA (2017-2021) collected in the Canadian Alliance of Pediatric Rheumatology Investigators (CAPRI) Registry were linked to neighborhood-level food accessibility measures using postal codes. Data were analyzed at enrollment and at 1-year follow-up. Associations were assessed using Spearman rho correlations, Mann-Whitney U test (P < 0.05), and mixed-effects linear regression.

Among 641 patients with JIA, 21.9% were overweight or obese (BMI > 85th percentile) and lived in areas with less access to chain grocery stores (P = 0.02) compared with those with underweight or healthy BMI. At baseline, healthy-weight (P = 0.02) and overweight (P = 0.04) patients had lower disease activity (Clinical Juvenile Arthritis Disease Activity Score in 10 joints) than those with obesity; this association was not observed at 1-year follow-up. At baseline, a greater proportion of fast food restaurants in the neighborhood was linked to fewer active joints (r_s = –0.09, P = 0.04). At 1 year, higher densities of fast food restaurants and convenience stores were associated with lower disease activity (r_s = –0.14, P = 0.02).

Obesity was linked to higher disease activity and reduced access to healthy food in chain grocery stores. However, greater access to both healthy and unhealthy food was associated with lower disease activity, possibly reflecting the general benefits of urban living.

We developed 2 questionnaires, 1 for rheumatologists and a second for PC clinicians, exploring education about the opposite specialty, frequency of advance care planning (ACP) discussions and referrals, and clinician comfort with PC skills in RD. Questionnaires were distributed to clinicians across the US in a variety of clinical practice settings.

In total, 201 rheumatologists and 217 PC clinicians completed the questionnaires. Few clinicians had received more than a lecture about the opposite specialty. Most rheumatologists reported never or rarely discussing ACP (71.6%), many had not referred a patient to PC in the last year in the outpatient (67.2%) or inpatient (47.5%) setting, and they reported low comfort with many PC skills. However, the majority agreed that more of their patients could benefit from PC (66.2%). Most PC clinicians felt less comfortable providing care for rheumatology patients than for other patients in their practice (75.6%), but the majority felt they could be helpful across many common referral indications for people with RD. Clinicians with more advanced education in the opposite specialty reported higher comfort across PC skills.

There is a clear gap in cross-disciplinary education and collaboration between rheumatologists and PC clinicians, with low rates of referral and low rates of clinician comfort. Nonetheless, clinicians feel collaboration would be beneficial. Further partnership is needed to improve this gap.

A cross-sectional study was conducted at 2 tertiary care hospitals among 653 patients with RA. Data on demographics, poor prognostic factors (high erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], rheumatoid factor, anticyclic citrullinated peptide antibody titers, and Disease Activity Score in 28 joints [DAS28] > 5.1), and comorbidities were collected through a structured questionnaire and medical record review. Comorbidities were quantified by the Charlson Comorbidity Index (CCI). Logistic regression analyses were used to identify associated factors.

A total of 646 (98.9%) patients had ≥ 1 comorbidity. The most prevalent were dyslipidemia (75.8%), obesity (58.7%), hypertension (42.7%), type 2 diabetes mellitus (30.3%), and osteoporosis (OP; 15.6%). Age ≥ 45 years was independently associated with coronary artery disease (odds ratio [OR] 9.71, 95% CI 1.91-178.00), OP (OR 19.60, 95% CI 5.96-121.00) and infectious diseases (OR 1.60, 95% CI 1.03-2.54). Female sex was associated with lower cardiovascular risk (OR 0.27, 95% CI 0.11-0.62), whereas female sex was associated with increased odds of OP (OR 3.55, 95% CI 1.71-8.37) and gastrointestinal (GI) disorders (OR 2.18, 95% CI 1.37-3.56). The use of targeted synthetic and biologic disease-modifying antirheumatic drugs increased the risk of infection (OR 14.80 and 4.11, respectively). High DAS28-CRP and ESR values were linked to GI comorbidities. The CCI survival index was significantly lower in older patients (≥ 45 years; mean 68.7 [SD 26.7]) than in younger patients (mean 93.3 [SD 6.7], P < 0.001).

The prevalence of multimorbidity is high among patients with RA in Bangladesh, particularly early cardiovascular disease risk.

We conducted a population-based repeated cross-sectional study using Ontario health administrative databases to assess annual trends from 2000 to 2022. We identified medication claims funded through the Ontario Disability Support Program (ODSP) within the Ontario Drug Benefit (ODB) database. We identified individuals with RA from the Ontario Rheumatoid Arthritis Database. Annual denominators comprised the number of RA individuals between the ages of 20-64 years, alive, with Ontario Health Insurance Plan coverage in the given measurement year. Individuals contributed to annual denominators until death, outmigration, attainment of age 65 (transitioning to ODB Seniors Program) or study end date. Annual numerators comprised the number of RA individuals with at least one ODSP-attributed medication claim for biologic, conventional, or targeted synthetic DMARDs, NSAIDs, opioids, or systemic glucocorticoids. We further quantified the total volume and medication-related costs attributed to these claims funded through ODSP. For comparison, we ascertained disability-related claims (for any medication class) among the general Ontario population aged 20 to 64 years.

Over the 23-year period, the number of RA individuals aged 20-64 years grew from 34,394 to 74,182 individuals, while the number of RA individuals with a disability RA medication claim increased from 2,805 individuals in 2000 to 6,270 individuals in 2022, corresponding to a stable annual disability prevalence of 8-9% of all RA working aged individuals (a pattern driven by individuals transitioning to ODB Senior Program at 65). Regional disability prevalence was lowest in the central region (4.8%) and highest in the Northeast (12.6%). The annual volume of ODSP RA medication claims ranged from 55,611 in 2000 to a peak in 2020 of 255,810 claims, corresponding to annual costs of $1,894,925CAD and $33,215,527CAD respectively (Figure). In contrast, the disability prevalence in the general population ranged from 2.7-3.8% during the study period.

Over 2 decades, the number of working-age RA individuals receiving disability benefits doubled, and RA disability prevalence was twice that of the general population. Nearly 1 in 11 younger RA adults were on disability annually, contributing to substantial medication use and economic costs. Investment in effective, evidence-based care models is needed to preserve work participation and reduce the long-term impacts of RA-related disability.

We gave clinicians access to the QUICK toolkit after 3 months of providing usual care and a training webinar. Six weeks later patients could access the EQUIP toolkit. Toolkit resources included videos, checklists, booklets and QUICK guides and were available to both groups for the duration of the study. We determined toolkit usage through Google analytics and post-intervention questionnaires. Questionnaire data were analyzed descriptively and exploratory analysis performed to examine relationship between toolkit access in past 3 months and adherence to 10 QIs. Analyses were conducted using SAS (V9.4, Cary, NC).

In total, 46 patients participated in the study and 22 of them received THR/TKR rehabilitation during the toolkit implementation and maintenance phases. Of these, 12 completed end of rehabilitation questionnaires and 5 (42%) reported being introduced to the EQUIP toolkit. The most frequently accessed resources were the TKR (64 total views) and THR (48 total views) booklets (Figure 1). Overall, patients rated the QI questionnaire and video as being most helpful; 60% agreed the toolkit helped them understand what to expect during rehabilitation and 80% to engage in and make decisions about their own care. There was no difference in patient-reported QI adherence between those who accessed the toolkit and those who did not (p=0.55). Seven of 14 (50%) of clinicians accessed the QUICK toolkit during maintenance phase. Based on Google analytics, the QUICK toolkit landing page was accessed 237 times and clinicians reported they most often used the QI checklists and QUICK guides (both 86%). Of the clinicians with recent toolkit use, 86% agreed it increased their knowledge of the TJR rehabilitation evidence and 43% said it helped to identify care gaps and areas for improvement. There was no difference in clinicians with improved QI adherence comparing those who accessed the toolkit in previous 3 months and those who did not (p=0.58).

Figure 1

Only a small proportion of patients and clinicians accessed the toolkits and total views, and active users markedly declined during the maintenance phase. We will need to further explore facilitators and barriers to access and develop targeted strategies to improve uptake of the THR/TKR rehabilitation QIs.

[1.] Westby MD. Osteoarthritis Cartilage 2018;26:370-82

In a cohort of 35 SLE patients, we performed whole exome sequencing on FACS-isolated naïve (CD19+, IgD+), memory (MBC; CD19+, IgD–, CD27+), and DN B-cells (CD19+, IgD–, CD27–) from peripheral blood. Patient-matched buccal DNA was used to filter out germline variants, and somatic mutations detected by ≥2 callers (Mutect2, Strelka2, and CaVEMan) were retained. Variant allele frequencies (VAFs) were compared across subsets to assess clonal dynamics. Associations with disease activity (SLEDAI-2 KG), time since diagnosis, and age were evaluated. Pathway enrichment and lymphoma-associated mutations were evaluated by interrogating mutations detected in MBC and DN cells across all patients.

DN and MBC proportions correlated with disease activity (=0.443, p=0.008; =0.354, p=0.037). DN and MBC had significantly higher somatic mutation burdens than naïve cells (p=0.001 and p=0.017), consistent with expansion of antigen-experienced and/or autoreactive compartments under chronic inflammation (Figure 1A-B). Mutation burden in DN correlated with time since diagnosis, but not age, suggesting disease-associated acquisition and/or selective growth of mutated clones (Figure 1C). Among mutations shared between MBC and DN, a disproportionate fraction expanded in DN (Figure 1D), consistent with a competitive advantage of mutated DN subclones. Shared mutations expanded in DN were enriched for B-cell activation and proliferation pathways, including NF-B and B-cell receptor signaling (FDR<0.05; Figure 1E). In patients with high mutation burden, both MBC and DN harbored nonsynonymous variants in lymphoma-associated genes, including IGLL5 and CARD11 (Figure 1F-H).

Our results identify DN B-cells as a clonally evolving population that acquires a high burden of somatic mutations under chronic inflammatory conditions, with some variants affecting genes and pathways relevant to malignant transformation. These results highlight DN cells as a plausible cell of origin for transformation in SLE and underscore the value of DN-focused molecular profiling to identify patients with high-risk clonal features and improve monitoring for progression and lymphoma transformation potential.

[1.] Bernatsky S. J Autoimmun 2013;42:130-5. [2.] Din L. Genet Epidemiol 2019;43:844-63. [3.] Singh M. Cell 2020;180:878-94.

The primary outcome was time to fever resolution, defined as at least 12 months follow-up period after the most recent clinic visit with reported absence of the recurrent fevers and assessed using Kaplan-Meier survival analysis and Cox proportional hazards modeling. Principal Component Analysis (PCA) was applied to explore phenotypic clustering based on symptom patterns.

In this retrospective cohort study, 235 pediatric patients followed at the Autoinflammatory Clinic of The Hospital for Sick Children from 2016 to 2024 were classified as PFAPA (n = 155) or SURF (n = 80) based on validated Eurofever/PRINTO classification criteria for PFAPA and proposed empirical indications for SURF. The median time to fever resolution was significantly longer in the SURF group compared to PFAPA (2,068 vs 1,738 days; log-rank p = 0.037). In a semiparametric Cox regression model, SURF diagnosis was independently associated with a lower likelihood of resolution over time (Hazard Ratio [HR] = 0.683; 95% CI 0.476–0.980; p = 0.038). Inclusion of tonsillectomy status in a multivariable model did not significantly alter the outcome (HR for tonsillectomy = 1.046; p = 0.803). PCA revealed 3 major clusters: a classic PFAPA phenotype (tonsillopharyngitis, cervical adenitis), a GI-dominant cluster (abdominal pain, nausea, diarrhea), and an intermediate group (with mix of the symptoms in lower frequency). The GI cluster was predominantly composed of patients with SURF and correlated with longer disease persistence.

Children with SURF exhibit significantly delayed fever resolution compared to those with PFAPA. PCA-derived clusters support the presence of a gastrointestinal-dominant phenotype within the SURF spectrum, suggesting that these syndromes may exist along a clinical continuum. These findings have implications for prognosis and management, highlighting the need for phenotype-driven approaches in pediatric autoinflammatory conditions.

CITE-seq and TCR-seq were performed to assess the transcriptomic profiles of CD4+ memory T cells in flaring and quiescent SLE patients. CD4+ memory T cells were isolated from PBMCs by negative selection using magnetic sorting, stained with oligo-conjugated antibodies against surface proteins for subset classification, and subsequently partitioned, barcoded, and sequenced. We examined samples from 15 distinct patients at 2 separate clinical visits spaced one year apart, yielding 30 samples. The longitudinal nature of our data allows us to inspect transcriptional changes both between and within patients.

Integrated analysis of 30 samples identified 10 immune cell clusters (Figure 1A). At baseline, flaring patients (n=9) were significantly enriched for Tfh, Th2, Th17 cells, and a Treg subset, while quiescent patients (n=6) had increased Th1 cells. TCR repertoire analyses at baseline revealed a higher proportion of expanded clonotypes in flaring patients, which was not seen in quiescent patients. Interestingly, we also found that there was a higher proportion of expanded clonotypes at follow-up in various subsets of interest, particularly in flaring patients that later became quiescent, suggesting tissue egress and recirculation following resolution of inflammation. Clonal overlap among subsets was markedly greater in flaring patients, suggesting shared antigen specificity and differentiation from common progenitors. More specifically, we identified 2 functionally deviated/exhausted Treg subsets (ISGhi/ISGlo) (Figure 1B) and, at baseline, found notable clonal overlap between the ISGhi Treg subset and Th2/17 cells and between the ISGlo subset and Tfh/Tph cells in flaring patients, which was absent in quiescent patients (Figure 1C). This suggests that there are 2 distinct subsets of cells with shared antigen exposure and/or functional plasticity; one that is exposed to an IFN-rich environment in the tissue, and another that is more involved in T-B cell interactions within lymphoid compartments.

We found abnormal Treg subsets with features of exhaustion and functional deviation that shared antigen specificity with other T helper cells. Their increased prevalence during flares suggests that dysregulated immunoregulation may contribute to SLE pathogenesis.

Baseline sera and clinicodemographic data from IIM patients enrolled in a multicenter registry with routine bio-banked serum samples were included. SIGLEC1 levels were tested using a capture immunoassay (Aviva Systems Biology, San Diego CA). Pulmonary involvement was assessed using pulmonary disease activity defined on the Myositis Disease Activity Assessment Visual Analogue Scales Tool (score≥1.0 cm), parenchymal abnormalities on chest X-ray or high-resolution CT (including ground-glass opacities), and dyspnea due to ILD. Median serum SIGLEC1 levels (ng/mL) were compared between patients with and without these features using the Mann-Whitney U test.

The study included 87 IIM patients (67.8% female, mean age 55.4±14.3 years) with dermatomyositis (DM, n=31), polymyositis (n=4), antisynthetase syndrome (ASyS, n=9), immune-mediated necrotizing myopathy (n=6), inclusion body myositis (n=9), and overlap myositis (OM, n=28). Median serum SIGLEC1 levels were significantly higher in IIM patients with pulmonary disease activity (5.1 vs 2.6 ng/mL; difference 2.5 ng/mL; P<0.05) and parenchymal abnormalities (5.1 vs 2.6 ng/mL; difference 2.5 ng/m; P<0.05) compared with those without these features. There were no significant differences in median serum SIGLEC1 levels between IIM patients with and without dyspnea due to ILD (4.7 vs 3.4 ng/mL; difference 1.3 ng/mL). Higher median serum SIGLEC1 levels differentiated between the presence and absence of pulmonary disease activity (5.2 vs 2.6 ng/mL; difference 2.6 ng/mL; P<0.05) when patients with DM, OM, and ASyS were grouped together. DM patients with pulmonary disease activity (5.3 vs 2.6 ng/mL; difference 2.7 ng/mL), parenchymal abnormalities (5.4 vs 3.2 ng/mL; difference 2.2 ng/mL), and dyspnea due to ILD (7.3 vs 3.8 ng/mL; difference 3.5 ng/mL) had higher median serum SIGLEC1 levels; however, these differences were not significant.

SIGLEC1 levels are a promising biomarker for assessing pulmonary involvement in patients with IIM. This finding reinforces IFN-I activity as a hallmark of IIM-ILD. Future studies are underway to evaluate SIGLEC1 levels as a biomarker of IIM-ILD.

[1.] Fathi M. Arthritis Rheum 2008;59:677-85. [2.] Yu X. Nat Commun 2014;5:4136. [3.] Biesen R. Arthritis Rheum 2008;58:1136-45.

The activity of proteases (NE, PR3, CTG) and various biospecimens were analyzed using fluorogenic substrate after citrullination with PAD2/4 (confirmed by a cit-specific probe). Active protease sites were labeled and visualized using a probe (TAMRA-FP). Degradation of Aggrecan, a proteoglycan found in cartilage, was determined using various biospecimens exposed to PAD isoforms. ACPA targeting cit-proteases was measured in serum from RA patients, ACPA positive and ACPA negative controls with ELISA.

Using both recombinant proteases and neutrophil supernatant, proteolytic activity of NE, PR3 and CTG increased markedly after citrullination with PAD2, and to a lesser extent, PAD4 (Figure 1A). For example, the activity of cit-PR3 increased by 13-fold compared to native PR3. Citrullination level with increasing concentrations of PAD2 correlated strongly with proteolytic activity (R=0.95, p<0.0001). PAD2 citrullination also lead to enhanced stability of proteases, with persistently detectable activity after 72 hours in-vitro, and evidence of protection from autoproteolysis in PR3 and NE, which was not observed with PAD4 (Figure 1B). Protection from Trypsin degradation in cit-PR3 was also observed. In the recombinant proteases, supernatant, and NETs, PAD2 citrullination opened new catalytic sites as demonstrated by labeling using an activity-based probe (Figure 1C), suggestive of a conformational change which was confirmed by in-silico modeling. Aggrecan degradation was enhanced by PAD2-citrullination of NE and NETs. Serum cit-PR3 and serum PR3 activity was higher in RA compared to healthy controls (Figure 1D). In synovial fluid, PR3, NE and CTG activity were all increased in RA compared to OA (Figure 1E). Autoantibodies to PAD4/2 cit-proteases were higher in RA and ACPA positive controls compared to ACPA negative controls (Figure 1F).

PAD enhances neutrophil serine protease activity and stability through conformational changes induced by citrullination, possibly providing a biological advantage for host defense. Enhanced proteolytic activity was apparent in RA biospecimens, leading to degradation of cartilage components and autoantibody formation. PAD isoforms may play functionally distinct roles in the pathogenesis of RA. Best Abstract on Research by Early Career Faculty Award

We analyzed data on female patients with PsA followed in a prospective cohort from 1978 to 2024. Data on PsA disease activity, medications, co-morbidities, and age at menopause were collected using standard protocols. Pre-perimenopause and post-menopause stages were defined as >2 years before and after the final menstrual period (FMP), respectively, while the perimenopause stage was within 2 years (before or after) of the FMP. PsA disease activity was assessed at each visit using Disease Activity in PsA (DAPSA), tender and swollen joint counts, PASI, CRP, and FACIT-fatigue. Disease activity during the perimenopause stage was compared to the pre-perimenopause and post-menopause visits. The association between menopausal stages and PsA disease activity measures was assessed with a Generalized Additive Model with splines (considering time from FMP as continuous) and with linear mixed-effects models (menopausal stages as categorical variables). Each model was adjusted for age, disease duration, and medication use, and accounted for repeated observations via a subject-specific random effect. We assessed the mediating effects of BMI and fatigue on the change in DAPSA across menopause stages.

A total of 477 female patients provided data for 8381 visits over a mean follow-up of 12.1 years. Mean age at first visit was 44.9±13.9 years and mean age at menopause was 48.7 years. Hormone replacement therapy had only been used during 1.5% of visits. A rise in DAPSA scores was found during perimenopause years, followed by a slight drop post menopause (Figure 1A). Linear mixed models found an association between being in perimenopause and higher DAPSA vs pre-perimenopause (β=1.92, p<0.001) and post-menopause stages (β=1.56, p=0.001, Figure 1B). Significantly higher tender and swollen joint counts were found in perimenopause vs both pre- and post-menopause. Higher PASI was found in perimenopause vs post-menopause stage. Increase in fatigue levels during perimenopause only partially mediated the increase in DAPSA score during perimenopause, explaining 12% to 18% of this change. BMI did not have a mediating effect on DAPSA change during perimenopause.

Perimenopause is associated with an increase in PsA disease activity which includes both patient-reported outcomes but also objective measures of activity. These findings may warrant consideration of hormone replacement therapy in perimenopausal PsA patients.

The Lupus in prEGnAnCY (LEGACY) cohort is conducted at SLICC centers in Canada, South Korea, Peru, and Mexico. Pregnant women with SLE are enrolled before 17 weeks and followed in the second (20–24 weeks), third (30–34 weeks) trimesters, and postpartum (8-12 weeks). Since ICP occurs after 20 weeks, only pregnancies with a second-trimester visit were included. Follow-up began at that visit and continued until delivery. AZA exposure was modeled as time varying. The primary outcome was delivery for ICP and/or early-onset ICP (<28 weeks). Multivariable Cox proportional hazards models with frailties adjusted for maternal demographics, co-morbidities, disease activity, and glucocorticoid use. At the Montreal site, thiopurine metabolites and shunting were assessed, using established cut-offs.[3]

Of 127 SLE pregnancies, 46 were AZA-exposed and 81 unexposed (Table 1). Ten ICP cases occurred (each in a distinct woman): 8 among AZA-exposed (17.4%, 95% CI 9.1-30.7) and 2 among unexposed (2.5%, 95% CI 0.7-8.6). AZA was continued until and beyond delivery in most (6/8) exposed ICP cases. All ICP cases required delivery except one AZA-exposed case (who stopped AZA at ICP diagnosis). AZA exposure was associated with a substantially increased risk of ICP (unadjusted HR 9.1, 95% CI 1.9-44.5; adjusted HR 11.9, 95% CI 2.2-65.1). Of note, all ICP cases with metabolite data (4/4) exhibited second-trimester shunting. Among all pregnancies with second-trimester metabolite data (n=22), 36.4% (95% CI 19.7-57.0) were shunting, and 50.0% (95% CI 21.5-78.5) of these developed ICP. No ICP occurred with tacrolimus alone (n=14). All ICP pregnancies resulted in live births, although AZA-exposed cases tended to have higher bile acid levels, earlier delivery, and lower birth weight for gestational age vs unexposed cases. Table 1.

Characteristics of SLE pregnancies at the second trimester visit according to AZA exposure (n=127)

We observed that AZA exposure was strongly associated with ICP in SLE pregnancies. Second-trimester thiopurine shunting may identify women at highest risk, supporting the value of metabolite monitoring.

[1.] Joudaki S, Aliment Pharmacol Ther 2025;61:1430-6. [2.] Nguyen NV. Am J Gastroenterol 2025;121:1183-91. [3.] Lambert-Fliszar F, Lupus Sci Med 2021;8:e000519. Supported by a CIORA grant. Best Abstract by a Post-Graduate Research Trainee Award

Trio whole genome sequencing (WGS) was performed on the proband and both biological parents. Variant annotation and filtering were used to prioritize rare coding variants with predicted functional impact, and segregation was confirmed within the trio. Case-control functional assays on fibroblasts were performed using the proband and 2 independent controls. One was internal laboratory reference control (healthy individual) and the second was a (non-SLE control). diABZI (STING agonist) time-course western blots and an interferon-stimulated gene (ISG) qPCR panel were performed under unstimulated and stimulated conditions.

The patient presented at 6 years of age with fever, malar rash, a Kawasaki-like inflammatory picture and macrophage activation syndrome (MAS). An echocardiogram demonstrated pericardial effusion, and mild left main coronary artery (LMCA) dilation. Following Kawasaki disease therapy with intravenous immunoglobulin, he developed nephrotic-range proteinuria and hypertension, which led to a kidney biopsy confirming class IV lupus nephritis. Laboratory testing showed leukopenia, hemolytic anemia, thrombocytopenia, hypocomplementemia, and positive ANA, anti-dsDNA, anti-Sm, and anti-RNP autoantibodies. He was treated with pulse methylprednisolone, mycophenolate sodium, and ACE inhibition. Neurologic and neurodevelopmental features emerged later in his disease course: absence epilepsy was identified earlier in adolescence (13 years) and was responsive to valproic acid, and upper-motor-neuron–patterned findings (hyperreflexia and clonus) were observed (starting at age 16 years, mild intellectual disability and ADHD became evident around mid-adolescence (15 years). Whole genome sequencing of the proband and parents identified an X-linked hemizygous SAT1 missense variant: NM_002970.3:c.26C>A (p.Ala9Asp) on Xp22 inherited from mom. This variant has a CADD = 31, 5/5 pathogenicity tools deleterious. In functional assays, the proband ISG qPCR panel showed higher induction of several ISGs (IFI44, RSAD2, MX1, IRF7, CXCL1, CCL2) after diABZI compared with controls. In the ISD experiment, the control sample showed stronger pTBK1 and pSTING responses than the proband.

We identified a previously unknown variant in SAT1, with evidence demonstrating its association with early-onset SLE in a male diagnosed at an extreme young age. In addition to bioinformatic tools predicting the variant is deleterious, our functional validation studies provide evidence for downstream immune dysregulation. Our report provides important evidence for the causal nature of this rare variant for monogenic lupus.

[1.] Xu L. Ann Rheum Dis 2022;81:1712-21. [2.] Zhao C. Immunity 2023;56:2508-22.

Provincial formularies and NIHB program were reviewed to compile coverage of bDMARD/sDMARD for the treatment of all JIA subtypes and JIA-associated uveitis. This was compared to the Health Canada (HC) indications for these drugs and current Canadian/American treatment guidelines for polyarticular JIA (pJIA), enthesitis-related arthritis (ERA) systemic JIA (sJIA), and uveitis.[1,2] In the absence of North American guidelines, recently published literature helped us identify recommended evidence-informed treatment strategies for juvenile psoriatic arthritis (JPsA).[3] Health Canada, NIHB and all provinces were evaluated for their overall performance with bDMARD/sDMARD treatment recommendations for JIA and uveitis. A parallel assessment was conducted in adults, focusing on inflammatory arthritis and informed by recently published treatment guidelines.

Overall, Ontario had the highest capacity to follow pediatric bDMARD/sDMARD recommendations followed by HC and Quebec (Figure 1). For JIA subtypes, all pJIA-recommended drugs were indicated and approved by HC, funded through NIHB, and covered by most provinces. For sJIA, HC and half the provinces fully met recommendations, whereas NIHB and remaining provinces ranked lower. Only Ontario met ERA treatment guidelines. HC approved one anti–IL-17 agent for ERA, which is recommended for adult ankylosing spondylitis (AS) but not included in ERA guidelines. However, it remains unfunded by NIHB and all provinces. JPsA treatment recommendations were not met by NIHB nor any province. Notably, HC has approved JPsA indications for anti–IL-17 and tofacitinib, which are included in these recommendations and in adult psoriatic arthritis (PsA) guidelines. Ontario approved half of the drugs recommended in current uveitis treatment guidelines; HC, NIHB, British Columbia and Quebec approved 25% while other provinces did not meet guidelines. Adults with inflammatory arthritis generally fully met treatment guidelines, whereas Adult Stills disease guidelines were not met by NIHB or any province. Figure 1.

Alignment of Drug Coverage with Treatment Recommendations for JIA and Uveitis Across Health Canada, NIHB, and Provincial Formularies. Paediatric recommendations include polyarticular juvenile idiopathic arthritis, systemic juvenile idiopathic arthritis, juvenile psoriatic arthritis, arthritis enthesitis-related arthritis and JIA-associated uveitis. NIHB - Non-Insured Health Benefits; AB – Alberta; BC – British Columbia; MB – Manitoba; NL – Newfoundland and Labrador; NS – Nova Scotia; ON – Ontario; PH – Prince Edward Island; QC – Quebec; SK – Saskatchewan.

Access to publicly funded bDMARDs/sDMARDs for JIA and uveitis is highly variable, with most provinces and NIHB unable to fully meet treatment guidelines. Adults with inflammatory arthritis generally have full access to recommended therapies, highlighting major inequities in pediatric care and a barrier to delivering evidence-based therapies for children.

[1.] Ringold S. Arthritis Care Res 2019;71:717-34. [2.] Onel KB. Arthritis Rheumatol 2022;74:553-69. [3.] Shenoi S. Nat Rev Rheumatol 2024;20:170-81.

Data were extracted from the UK Biobank, including 459 female and 497 male PsA patients. To minimize population stratification, only Caucasian participants were included, resulting in 444 female and 423 male patients, along with 226,198 female and 191,928 male Caucasian controls. A genome-wide association study (GWAS) was conducted, comparing 97,013,422 SNPs between males and females among PsA patients and controls, focusing exclusively on autosomes. Only SNPs with allele frequencies greater than 0.005 in affected cases and controls were included, and associations were considered significant at P < 1 x 10^-6.

In males, 2,596 SNPs were identified across 104 genes, and in females, 4,542 SNPs were associated with 108 genes. Among these genes, 72 were shared between sexes, including PSORS1C1, the strongest genetic associated locus for psoriatic disease. Additionally, 32 unique genes were identified in males, including ERAP-1 and TRAF3IP2, whereas 35 were identified in females, including HLA-DRB1 and HLA-DQA1. Notably, sex-specific genes have been previously documented to exhibit sex-specific differences in immune responses. Ongoing studies are focusing on pathway enrichment analysis of sex-specific genes for both genders.

The identification of unique genes in each sex, alongside shared genetic markers, highlights the complexity of PsA’s genetic landscape. These findings suggest that sex-specific genetic factors may play a role in the manifestation and progression of the disease. Further research is essential to validate these results and explore their clinical and molecular implications, which could ultimately lead to more tailored therapeutic strategies for PsA patients.

This analysis was conducted on PsA patients evaluated in the Gladman Krembil Psoriatic Arthritis Program between July 1, 2024, and July 1, 2025. Patients were classified into C2M/D2M and TR categories according to GRAPPA and EULAR criteria.[1,2] Demographic, clinical, radiographic variables as well as treatment, and comorbidity data were analyzed to characterize the C2M/D2M and TR groups. C2M/D2M patients were compared to non-C2M/D2M, and TR patients compared to C2M/D2M patients who did not meet TR criteria, using both GRAPPA and EULAR classification frameworks.

Of 630 patients assessed, GRAPPA criteria identified 225 (35.7%) as C2M and 81 (12.9%) as TR, while EULAR criteria identified 122 (19.4%) as D2M and 79 (12.5%) as TR. Patients fulfilling C2M/D2M definitions, including TR, showed significantly higher disease activity and treatment intensity compared with non-C2M/D2M groups. These patients had higher patient and physician global assessment scores, increased tender and swollen joint counts (TJC/SJC), higher Psoriasis Area and Severity Index (PASI) scores, and higher entheisitis (tender) point count. C-reactive protein (CRP) and Disease Activity index for Psoriatic Arthritis (DAPSA) were also markedly elevated, accompanied by greater biologic use and a higher number of biologic DMARDs (bDMARDs). The TR subset demonstrated more severe articular involvement (higher TJC/SJC), elevated CRP, and substantially greater treatment exposure, reflected by higher bDMARD use (Figure 1). Female sex and higher BMI were associated with C2M/D2M but not consistently with TR disease.

GRAPPA and EULAR criteria both effectively identify PsA patients with high disease burden but differ in sensitivity and thresholds. GRAPPA captured a broader subset, whereas EULAR applied more stringent definitions. C2M/D2M disease appears multifactorial, potentially driven by non-PsA and comorbidity-related factors such as elevated BMI, while TR disease primarily reflects persistent, objectively active inflammation despite adequate therapeutic exposure.

[1.] Marzo-Ortega H. Ann Rheum Dis 2025;84:e220. [2.] Proft F. Ann Rheum Dis 2025;84(Suppl 1):143–5.

We performed a cross-sectional study of 214 adult SLE patients from a single-center longitudinal cohort who completed both the PDQ-20 and ACR-NB. The PDQ-20 assesses 4 domains—attention/concentration, planning/organization, retrospective memory, and prospective memory—across 20 items scored 0–4 (higher = worse). Objective cognition was evaluated using a modified ACR-NB assessing 6 domains: manual motor speed, attention/processing speed, visuospatial construction, language, learning/memory, and executive function. CI was defined as impairment (z ≤ –1.5) in ≥2 domains. Spearman correlations examined construct validity between PDQ-20 items/domains and ACR-NB tests, while Wilcoxon rank-sum tests compared PDQ-20 scores between CI and non-CI groups.

Participants were predominantly female (90%), with a mean age of 31 ± 17 years; 43% met criteria for objective CI. The mean PDQ-20 score was 31.1 ± 16.9 (out of 80), indicating moderate subjective impairment. The most frequently reported difficulties were "mind wandering," "forgetting names," "losing train of thought," and "forgetting why one entered a room," reflecting deficits in attention and working memory. The highest domain scores were observed in attention/concentration and planning/organization. Correlations between PDQ-20 and ACR-NB scores were generally weak. The strongest associations were between PDQ-20 items related to working memory (eg, Q17 "trouble holding phone numbers," Q4 "trouble organizing") and the ACR-NB Auditory Consonant Trigrams test (r –0.25 to –0.29). No significant difference in PDQ-20 total scores was observed between CI (33.4 ± 17.5) and non-CI (29.3 ± 15.9) groups (p = 0.15), nor were there differences between individual PDQ-20 items (Figure 1).

SLE patients frequently report cognitive challenges, particularly in attention and planning, which correlate only weakly with objective CI. The PDQ-20 captures everyday cognitive experiences not reflected by formal testing, highlighting the need to assess both subjective and objective cognition in SLE. Integrating patient-reported cognitive screening may enhance understanding, monitoring, and support for cognitive health in clinical practice.

Serum samples (n=160) from the Bath Spondyloarthritis Biobank were selected based on availability. All patients had rheumatologist-confirmed diagnoses and met criteria for r-axSpA (n=55), nr-axSpA (n=54), or MBP (n=51). 14-3-3 autoantibody levels were measured using a multiplex assay. Nominal regression modeled the relationship between predictors and diagnosis, generating a probability-based linear score for 3 models: (1) axSpA (n=109), (2) r-axSpA, and (3) nr-axSpA vs MBP. Predictors included age, sex, CRP, and HLA-B27. The r-axSpA vs MBP model was also applied to healthy controls (n=100) for comparison. Statistical significance was set at p < 0.05.

Mean age (SD) was 55 (23) yrs for r-axSpA, 42 (14) yrs for nr-axSpA, and 30 (14) yrs for MBP. Male percentages were 67%, 41%, and 59%, respectively. Disease duration averaged 13 years for r-axSpA and 5 years for nr-axSpA. HLA-B27+ rates were 69% (r-axSpA), 72% (nr-axSpA), and 18% (MBP). ROC AUCs for the 14-3-3 AAb model were 0.77 (all axSpA), 0.78 (r-axSpA), and 0.73 (nr-axSpA). At ~90% specificity, sensitivities were 42%, 47%, and 38%, with PPVs of 88%, 83%, and 83% - all exceeding the SPARTAN target of 33.3%. Adding age and sex to the model improved the diagnostic odds ratio (DxOR) from 5.4 to 18.4, rising to 23.4 with CRP and 63.7 with HLA-B27 (Table 1). Scores for healthy controls matched MBP (p > 0.99). Table 1.

14-3-3 AAb Model Performance by axSpA Subset

Autoantibodies to 14-3-3 AAb differentiates radiographic and nonradiographic-axSpA from MBP, achieves a high PPV and its discrimination improves when age, sex, CRP, and HLA-B27 are added. Alongside these clinical variables, autoantibodies to 14-3-3 may reduce the diagnostic delay at primary care and complement HLA-B27.

Four cohorts were included: the Newfoundland Osteoarthritis Study (NFOAS) as discovery, the Tasmanian Older Adult Cohort Study (TASOAC) and Longitudinal Evaluation in the Arthritis Program: Osteoarthritis Study (LEAP OA) as replications, and the Multicenter Osteoarthritis Study (MOST) for assessing longitudinal prediction. OB+OA+ was defined as either end-stage or radiographic knee OA with BMI≥30 kg/m². Plasma metabolomic profiling and genome-wide genotyping were performed. Regression models were used to identify biomarkers for OB+OA+ and MR for assessing causal relationships.

Metabolome-wide association analysis of 310 OB+OA+ and 99 OB-OA+ patients from the NFOAS identified that acyl-alkyl-phosphatidylcholine C40:6 (PC ae C40:6) was associated with OB+OA+ at metabolome-wide significance (P=1.80x10^-6), which was replicated in the TASOAC including 102 OB+OA+ and 254 OB-OA+ and the LEAP OA including 118 OB+OA+ and 114 OB-OA+ (P≤7.78x10^-3) (Figure 1A). MR analyses showed causal relationships of PC ae C40:6 with knee OA and obesity (Figure 1B). Our longitudinal data showed that the baseline PC ae C40:6 predicted overweight status and BMI at 10-year follow-up in the TASOAC (n=159; P<0.02) and incidence radiographic and symptomatic knee OA at 5-year follow-up in the MOST (n=337; P<0.03) in subjects with baseline normal weight (Figure 1C,D). Furthermore, structural equation modeling analysis in the NFOAS (n=526) revealed that PC ae C40:6 had a significant indirect via obesity and a direct effect on knee OA (all P<0.001).

Our data suggested a causal relationship between PC ae C40:6 and OB+OA+. PC ae C40:6 could be a promising biomarker for monitoring OB+OA+ disease progression and a novel target for developing new therapies.

Patients over age 18 years meeting the Tel HaShomer diagnostic criteria for FMF were recruited from an Autoinflammatory Clinic in Toronto. Clinical records and data were analyzed. Gene panel testing was performed with Next Generation Sequencing at the Hospital for Sick Children. Variants were classified as per the American College of Medical Geneticists criteria. All patients provided written consent to be included in a case series.

A total of 37 patients were included (38% male). The cohort was composed of a variety of ethnicities, predominantly including Middle Eastern (35%), Caucasian (27%) and West Asian (10%). The median age at enrollment was 43 years, symptom onset was 15 years, and diagnosis was 35 years. Thirteen patients had first symptom onset after age 18. The median diagnostic delay was 7 years. Specific triggers for flares were reported in 51% of patients; the most common being stress (42%). The most common symptoms were abdominal pain (97%), fever (83%), and arthritis (73%). CRP was elevated during flares in 80% of patients. Of 36 patients with genetic data; 17 (47%) were homozygous/compound heterozygous, 13 (36%) were heterozygous, and 6 (17%) had no detectable variants in MEFV. The most common variants were V726A (9/36), E148Q and M694V (both in 8/36), and M680I (4/36). All were classified as variants of uncertain significance, or likely/pathogenic. Six patients did not carry any MEFV variants. A positive response to colchicine was observed in 88%, though 33% reported intolerances. IL-1 inhibitors were requested for 11 patients; all applications were denied under public funding, but compassionate access resulted in universal clinical improvement.

FMF remains under-recognized in adults, with significant diagnostic delay (maximum 60 years in our cohort). Colchicine intolerance limits therapy for some, and restricted IL-1 access remains a major barrier. This study adds to the limited Canadian data on adult FMF and highlights the need for greater awareness and advocacy for equitable access to evidence-based biologic therapy. Further studies are needed also to investigate the potential causes of mutation negative FMF.

We isolated peripheral blood mononuclear cells from whole blood obtained from healthy individuals (n=6) and patients with SLE (n=7). We selected patients with SLE with clinically inactive disease, defined as a clinical SLEDAI of 0. Using a previously developed assay to identify autoreactive cells, we isolated ANA+ and ANA– IgG memory B cells using fluorescence-activated cell sorting and cultured them in vitro with CD40L and IL-21.[3] Plasmablast differentiation and immunoglobulin production were subsequently assessed using flow cytometry and IgG ELISA, respectively. Statistical analyses were performed using paired t-test with p<0.05 being significant.

We observed statistically significant group differences in response to T-dependent stimulation with CD40L and IL-21 between ANA+ and ANA– memory B cells in healthy individuals and patients with SLE. ANA+ cells from healthy individuals had significantly less plasma cell differentiation compared to ANA– cells, but this difference was not seen in patients with SLE (p=0.0046 and p=0.7371, respectively) (Figure 1a). Comparable findings were seen in IgG immunoglobulin production between healthy individuals and patients with SLE (p=0.0231 and p=0.9961, respectively) (Figure 1b). Mean age of patients with SLE was 41.0 ± 14.6 years and mean disease duration was 13.1 ± 5.8 years. Mean SLEDAI was 1.86 ± 2.04, mean SDI was 0.29 ± 0.48, and mean PGA was 0.37 ± 0.46. 85.7% (6/7) of patients with SLE were female and 57.1% (4/7) of patients with SLE had serological activity. All patients with SLE were on hydroxychloroquine and 28.6% (2/7) of patients required either immunosuppressive medications or corticosteroids. All healthy controls were ANA negative by Hep-2 IFA testing.

We demonstrate a regulatory checkpoint in healthy individuals which inhibits differentiation of ANA+ IgG memory B cells into plasmablasts using a model of T-dependent stimulation. This checkpoint is not seen in patients with SLE. This abnormality may partially explain the production of deleterious antibodies in patients with SLE.

[1.] Nie Y. Clin Rev Allergy Immunol 2022;62:301-23. [2.] Tsokos GC. N Engl J Med 2011;365:2110-21. [3.] Malkiel S. Arthritis Rheumatol 2016;68:2210-20.

Participants were identified from the SickKids NLE clinic, born between 2012 and 2019, to mothers with positive anti-Ro Ab titers within 1 year and 6 months of their child’s birth. We included the first child seen in the NLE clinic per mother. Clinical details were extracted from the NLE database supplemented by retrospective chart review of both infants and mothers. Ab titers were measured using enzyme-linked immunosorbent assay (ELISA) or chemiluminescent immunoassay (CIA), classified as high (ELISA: 8-100 U/mL, CIA: 20-1685 CU anti-Ro52, 20-1375 CU anti-Ro60) or extremely high (anti-Ro/La titer exceeded upper limit of detection). We excluded infants with cardiac NLE, and tested associations between maternal titer and infant NLE manifestations, jointly adjusting for infant sex, ethnicity, maternal HCQ use during pregnancy, extremely high anti-La Ab titer, and maternal rheumatic disease status.

We identified 282 infants; 59% of mothers had extremely high anti-Ro titers. Hepatitis (27%) was the most prevalent NLE manifestation, followed by cytopenias (24%), rash (12%), and macrocephaly (4%). We excluded 24 infants with cardiac NLE. We observed a significant association between extremely high anti-Ro Ab titer and presence of any non-cardiac NLE manifestations (OR: 1.78, 95% CI 1.06-3.00, P=0.028) (Table), and extremely high anti-La Ab titer and cutaneous NLE (OR: 4.17, 95% CI 1.68-10.15, P=0.002), in multivariable adjusted models. Table.

Association between extremely high anti-Ro/La antibodies and non-cardiac NLE manifestations

Extremely high maternal anti-Ro Ab titer was significantly associated with non-cardiac NLE, and anti-La Ab titer with cutaneous NLE. These associations were significant after adjusting for extremely high titers of the alternate autoantibody and other potential risk factors for NLE. Our findings have important clinical implications, informing family counseling and improving care for infants at risk of NLE and their families. Best Abstract on Research by an Undergraduate Student Award

A cross-sectional analysis of data prospectively captured in the Rheum4U Precision Health Registry. Adults with IA attending rheumatology clinics in Calgary completed Patient-reported Outcomes Measures (PROMs), including the Clinical Health Assessment Questionnaire for functional disability (ClinHAQ; score range 0-3, no to severe disability), EQ-5D-5L for HRQoL (utility range –0.148 to 0.949, worst to perfect health), and Work Productivity and Activity Impairment instrument (WPAI domains: absenteeism, presenteeism, work impairment, and activity impairment; 0-100%, higher scores = greater impairment). Spearman rank correlations assessed associations overall and by IA type at the first registry visit with complete PROMs data (very weak (0–0.19), weak (0.2–0.39), moderate (0.40–0.59), strong (0.6–0.79), and very strong (0.8–1).[1] Partial correlations adjusted for age and sex.

A total of 1,336 patients were included, 68% were women, the median age was 52 [IQR 39-62] years. Among diagnoses, 51% had rheumatoid arthritis, 16% ankylosing spondylitis, and 15% psoriatic arthritis. The median time since diagnosis was 7.3 [IQR 2.8-13.2] years. Higher ClinHAQ scores (greater disability) were significantly associated with lower EQ-5D-5L utilities (poorer HRQoL) and higher WPAI scores (greater work and activity impairment). Absenteeism (r=0.32) showed weak associations, while presenteeism (r=0.58) and overall work impairment (r=0.57) were moderately correlated with disability. The strongest effects were between disability and both activity impairment (r=0.7), and EQ-5D-5L utilities (r= –0.75). EQ-5D-5L utilities were negatively associated with all WPAI domains, with weak relationship for absenteeism (r= –0.31), moderate for presenteeism (r= –0.62) and work impairment (r= –0.61), and strong for activity impairment (r= –0.74). Results were consistent across IA types and remained stable after adjusting for age and sex.

The Rheum4U Precision Health Registry uniquely enabled deciphering the interrelationship of key domains impacted by IA in a large Canadian cohort. Greater disability was associated with poorer HRQoL and increased productivity loss. Similarly, lower HRQoL was related to greater work impairment. The results emphasize the multidimensional, interconnected burden of IA. Day-to-day physical limitations have a more direct impact on participation than missed work alone, highlighting the importance of early, function-preserving interventions. These may yield meaningful benefits across multiple domains of patient well-being.

[1.] Swinscow TDV. https://www.bmj.com/about-bmj/resources-readers/publications/statistics-square-one

We completed a retrospective study of patients with cSLE (diagnosed <18 years of age) followed in the SickKids Lupus clinic from Jan 2022-Dec 2024. Self-reported ethnicity was categorized by Canada census groups. We reviewed electronic medical records for documented MH questionnaire completion, referrals to MH providers, and identified issues at MH visit. Elevated depression and anxiety symptoms were identified by positive screens on the Patient Health Questionnaire 9-item (PHQ-9 score ≥10) and Generalized Anxiety Disorder 7-item (GAD-7 score ≥10). We tested the association between ethnicity and ever completing MH screening and ever screening positive in univariate and multivariable logistic regression models, adjusted for demographic and clinical factors (age, sex, marginalization score, duration of follow-up, neuropsychiatric SLE [NPSLE], lupus nephritis, disease damage) (significance P<0.05).

Our study included 138 cSLE patients; 85% were female with a median age at SLE diagnosis of 13 years (IQR 10-15). The majority of patients were of East Asian (28%), White/European (24%), and South Asian (20%) ethnicity. A total of 107 (78%) patients completed both the PHQ-9 and GAD-7; 28% screened positive on the PHQ-9 and 27% on the GAD-7. In logistic regression models, there was no significant difference in MH screening between ethnic groups. In adjusted models, Black patients had a significantly lower odds of screening positive on the PHQ-9 (OR = 0.07, CI 0.01-0.57, P = 0.01). Increased marginalization (OR = 4.77, CI 1.26-22.61, P = 0.02) and NPSLE (OR = 5.98, CI 1.12-42.77, P = 0.04) were significantly associated with screening positive on the PHQ-9. No significant associations were found between demographic or clinical factors and GAD-7 outcomes (Table 1). For patients that screened positive on the PHQ-9 and/or GAD-7, 89% were referred to as an MH provider, with the most commonly identified issue at MH visit being low mood (39%). Table 1.

Predictors of Ever Screening Positive on PHQ-9 (N=30) and GAD-7 (N=29)

In this multiethnic cSLE cohort, there was no difference in MH screening between ethnic groups. However, Black patients had significantly lower odds of screening positive on the PHQ-9, after adjusting for marginalization and NPSLE. Patients with cSLE experience many MH issues, especially low mood. This study highlights the need to re-evaluate the performance of MH questionnaires in assessing depression and anxiety between ethnic groups, as well as the importance of addressing MH as part of routine care.

This feasibility RCT recruited youth aged 17-18 years with a pediatric-onset rheumatic disease seen at their last pediatric rheumatology visit at McMaster Children’s Hospital and Children’s Hospital in London. Participants were randomized to receive a Youth Transition Roadmap (YTR) only (standard of care), or YTR plus TCI - 8 monthly virtual coaching sessions covering topics from the YTR. At baseline, 8 months and 11 months, collected patient-reported outcomes included measures of transition readiness (Transition-Q, max 100) and PROMIS® Self-Efficacy for Managing Chronic Conditions, which assesses activities of daily living (ADLs), symptoms, medications and treatments, emotions, social interactions, and informational supports.

Of 65 patients approached, 31 (48%) consented and 25 went on to participate (n=12 TCI group). Over 95% of TCI appointments were attended, and 80% of patients completed 8-month follow-up questionnaires. Enrollment was split almost equally between sites. At baseline, 23% of participants in the control group reported being "definitely ready" for transition to adult care, compared to 31% in TCI. At follow-up, comparable values were 10% and 73%, respectively. Mean (SD) Transition-Q scores for the control group at baseline, 8- and 11-month follow-ups were 65.6 (15.9), 73.4 (21.8) and 80.8 (15.5) compared to 71.6 (17.5), 80.1 (12.2) and 90.0 (9.6) for the TCI group, respectively. PROMIS Self-Efficacy scores showed that the TCI group had overall improvements at each timepoint across all domains except for ADLs. The control group showed less consistent improvement, with initial stagnation at 8 months, followed by improvement at 11 months across all domains (Figure 1). Figure 1 A and B:

PROMIS Self-Efficacy scoring at baseline, 8-month, and 11-month follow up

Our results suggest that TCI provides an opportunity to improve skills and confidence in youth transitioning from pediatric to adult rheumatology care. This will inform planning a multicenter RCT to assess effectiveness of a TCI program in supporting youth in their transition to adult care.

[1.] Griffin K. Rheumatol Adv Prac 2024;8:rkae130. [2.] Reesor E. PLoS One 2024;19:e0295174.

RA patients (n = 100) were recruited from an academic rheumatology clinic (Winnipeg, Canada). Healthy controls (n = 137) were recruited through advertising. Thermal images of the dorsal aspects of the hands and feet were captured with a Flir A700 camera. Regions of interest (ROI) were pre-identified as joints commonly affected in RA (Figure 1A). ROIs were manually gated, and the maximum/minimum/average temperatures were extracted. Data analysis was performed in R to identify temperature differences between groups, followed by machine learning classification using ROI-restricted data. Thermograms were also analyzed using a deep learning model which deployed unsupervised feature extraction (DINOV2) and classification (ElasticNet) in Python.

Principal components analysis using ROI thermogram data revealed clear separation between RA and HC (Figure 1B). Differential analysis identified 56 of 114 temperature parameters that were significantly higher in RA patients. For example, the maximum temperatures of the right 5th PIP joint (adjusted p=1.3x10^–8) and right 4th PIP joint (adjusted p=7.6x10^–8) were higher in RA compared to controls. All thermogram parameters (minimum, maximum, average) were increased in joints that were tender or swollen on clinical examination in RA (Figure 1C, all p-values <0.0001). Using thermogram ROI data, XGboost achieved an AUC of.869 to classify RA from control. Rankings of variable importance by SHAP index included average temperatures of several hand joints including the Wrist and 3rd PIP. A computer vision model achieved high performance in classifying RA from controls using entire thermograms (without ROI information), with an AUC of 0.977 and recall of 0.909 (Figure 1D). Principal components from this model were mapped to red, green, and blue channels to visualize thermographic differences between RA and control subjects (Figure 1E).

Thermal imaging is a low-cost, accessible method for detecting synovitis in small joints and can distinguish RA patients from controls. It may enable early detection of subtle joint inflammation at the earliest stages of RA onset, such as in individuals with clinically suspect arthralgia.

[1.] Kow J, Tan YK. Joint Bone Spine 2023;90:105496. Best Abstract on Clinical or Epidemiology Research by a Trainee - Phil Rosen Award

Using a population-based repeated cross-sectional study design, we ascertained medication dispensation claims from the Ontario Drug Benefit (ODB) database from 2000 to 2022, among individuals with RA identified from the Ontario Rheumatoid Arthritis Database. For each year, RA individuals were required to be alive, 20 years or older, with Ontario Health Insurance Plan coverage, and contributed to annual RA population denominators from diagnosis until death, outmigration, or end of study. RA-related medication claims included biologic, conventional synthetic, or targeted DMARDs, NSAIDs, opioids, and systemic glucocorticoids. ODB funding programs included seniors (for 65+), Ontario Disability Support Program, Trillium/Exceptional Access Program (for high-cost medications), Ontario Works (for unemployment), and a combination of other programs. Analyses included trends in annual number of RA medication claims and cumulative medication expenditures, stratified by funding programs and age groups.

From 2000 to 2022, the RA population increased from 60,781 individuals [34,394 aged <65); 26,387 aged 65+] to 154,675 individuals [74,182 aged <65; 80,493 aged 65+)]. Among those under 65, the number of individuals with at least one ODB-related RA medication claim rose from 5,069 (15%) in 2000 to 13,121 (18%) in 2022. For RA individuals aged 65+, the number of individuals with at least one ODB-related RA medication claim increased from 22,476 in 2000 to 63,293 in 2022 (representing 78-86% of eligible RA seniors across all years). Trends in total claim volumes and expenditures by age groups are depicted (Figure 1). Total RA medication expenditures peaked in 2022 at $256,907,248 for all ages ($78M under 65, $179M in 65+). Among funding sources, the ODB Seniors Program accounted for the largest share of claims, followed by the Disability and Trillium programs.

Ontario has seen a significant growth in publicly funded RA medication utilization and spending overtime. Among working-age individuals, nearly 1 in 5 had at least one RA medication claim, while most RA seniors consistently accessed treatment. The substantial increase in RA medication utilization and expenditures alongside the growing RA population underscores the need for more sustainable healthcare planning.

Linked administrative health datasets from the province of Alberta were used to create a combined incident cohort based on validated ICD codes for PsA and axSpA from years 2002-2023. Controls were selected in a 4:1 ratio matched for age and sex. We used the Canadian Institute for Health Information ACSC ICD-10-CA case definitions to identify hospitalizations from the Discharge Abstract Database as our outcome of interest.[1] We calculated incidence rate ratios (IRR) at 3 and 5 years from the date of the first PsA and/or axSpA diagnosis using a multivariable regression model adjusting for age, sex, location of residence, and socioeconomic status using the Pampalon Deprivation Index.

There were 16,054 individuals with incident PsA and/or axSpA over the study period (45% male, mean age 59 years, 78% urban, 31% with both material and social deprivation). Of these, 40.3% (n=6,467) hat at least 1 hospital admission for any reason, with a total of 22,516 unique hospitalizations, compared to 27.2% (n=18,665) of controls with 48,350 unique hospitalizations. ACSC hospitalizations accounted for 6.4% (n=1,433) of all admissions in persons with PsA/axSpA, compared to 8.0% (n=3,856) of all admissions in controls. In both cohorts, chronic lower respiratory diseases were the most frequent reasons for an ACSC admission (40% in cases, 41% in controls). After adjusting for age, sex, location of residence, and socioeconomic status, the IRR for an ACSC hospitalization was increased at 3 years (IRR 1.35, 95% CI 1.16, 1.57) and 5 years (IRR 1.23, 95% CI 1.10, 1.38) in those with PsA and/or axSpA compared to controls (Table 1). Among individual ACSCs, the IRR for diabetes-related admission was increased by 65% (IRR 1.65, 95% CI 1.14, 2.39) and angina-related admissions nearly 3-fold higher (IRR 2.74, 95% CI 1.58, 4.75) at 5 years relative to controls. Table 1.

Incidence rate ratios (95% CI) for Ambulatory Care Sensitive Condition Hospitalizations, in persons meeting the case definition for psoriatic arthritis or axial spondyloarthritis compared to age and sex matched controls

People with PsA and/or axSpA are at a higher risk of being hospitalized for ACSCs compared to the general population, with a signal for higher diabetes and angina-related admissions in established diseases. An enhanced focus on risk reduction is indicated.

[1.] Canadian Institute for Health Information. https://www.cihi.ca/en/indicators/ambulatory-care-sensitive-conditions-hospitalizations

At the ORCHESTRA (Ottawa Rheumatology CompreHEnSive TReatment and Assessment) Clinic, PsA patients initiating a new AT undergo a protocolized ultrasound (US) examination, at baseline and 3 months post therapy assessing 14 entheses for elementary lesions: hypoechogenicity, thickening, and power Doppler signal (inflammatory features), as well as erosions, calcifications, and enthesophytes (damage features), each graded on a 0–3 scale (none, mild, moderate, severe). These were summed to calculate per-patient inflammation and damage scores. Patients were categorized into 3 groups by treatment mechanism: anti-TNF agents (TNFi), JAK inhibitors (JAKi), and IL-17 inhibitors (IL-17i). Due to sample size limitations, JAKi or TNFi were combined when analyzing bio-naïve and bio-experienced subgroups. Baseline and three-month disease activity indices and US scores were compared.

Sixty-two patients who had 3 months follow-up were included, 27 of whom (43.5%) were AT-naïve. 20 patients (32.3%) initiated TNFi, 10 patients (16.1%) initiated JAKi, and 32 patients (51.6%) initiated IL-17i. Baseline disease activity and US findings were similar across groups. However, US-entheseal inflammation scores differed at follow-up (p = 0.025), with lower scores in patients receiving IL17i compared with JAKi (2 [0–6.5] vs 6.5 [3.5–12]; p = 0.036) and a trend of higher reductions in patients receiving IL-17i compared with JAKi or TNFi (Table). Among biologic-experienced patients, despite having similar baseline clinical and US scores, follow-up enthesis inflammation scores were lower with IL-17i (1 [0–4] vs 7 [4.5–11.5]; p = 0.001) with higher reduction at 3 months then others (4 [0–8] vs 0 [–4–4]; p = 0.049). More IL-17i recipients demonstrated reduced entheseal Doppler signal (7 [31.8%] vs 0 [0%]; p = 0.031) (Table). Same differences were not seen in bio-naïve patients (data not shown).

In this real-world cohort of PsA patients initiating AT, IL-17i were associated with greater improvement in US-detected entheseal inflammation compared with JAKi and TNFi, particularly among biologic-experienced patients. These findings support a potential preferential effect of IL-17 blockade on entheseal inflammation, consistent with its pathogenic role. US proved a sensitive tool for detecting early treatment-related changes, highlighting its value in evaluating therapeutic response in PsA.

LEGACY includes Systemic Lupus International Collaborating Clinics in Canada, South Korea, Peru, and Mexico. Pregnant SLE women are consecutively enrolled <17 weeks’ gestation and followed at predefined visits throughout pregnancy and postpartum. At enrollment, plasma was tested for aPS/PT, using ELISA (Werfen, San Diego), with positivity cutoffs for IgG and IgM as >30 chemiluminescent units. LAC testing was performed at each site using validated assays. The present analysis includes the first 98 pregnancies with aPS/PT results. APO were a composite outcome of either: (1) fetal death >20 weeks, (2) neonatal death, (3) placenta-mediated preterm delivery <36 weeks, and/or 4) small for gestational age (<5th percentile). We performed multivariable hazards models with frailties and gestational age as the time axis to assess associations between APO and aPS/PT IgG and/or IgM vs LAC. Maternal covariates at enrollment included age, body mass index, prior nephritis, SLE Pregnancy Disease Activity Index, and medications. We used Harrell’s C-index to assess model discrimination.

Among 98 SLE pregnancies, 9 (9%) were aPS/PT IgG-positive, 25 (26%) were aPS/PT IgM-positive, and 11 (11%) were LAC-positive (Table 1). Eight pregnancies (8%) were positive for both aPS/PT (IgG and/or IgM) and LAC. Thirteen pregnancies (13%) experienced APO, including 5/9 (56%) in the aPS/PT IgG-positive group and 5/11 (46%) in the LAC-positive group. In multivariable analysis, aPS/PT IgG positivity was strongly associated with APO (HR 12.2, 95% CI 1.7-87.2), whereas IgM and/or overall aPS/PT positivity showed nonsignificant trends [HR 1.9 (95% CI 0.3-11.2) and HR 2.2 (95% CI 0.4-11.2), respectively]. LAC positivity was also associated with a substantially higher APO risk (HR 7.8, 95% CI 1.7-35.1), though less strongly than aPS/PT IgG. Discriminative performance was slightly higher for aPS/PT IgG (adjusted C-index 0.80, 95% CI 0.65-0.95) compared with LAC, aPS/PT IgM, and combined aPS/PT IgG and/or IgM models (0.78, 95% CI 0.68-0.89; 0.72, 95% CI 0.59-0.85; and 0.73, 95% CI 0.61-0.86, respectively). Table 1.

Maternal characteristics at baseline and pregnancy outcomes (n=98)

In this preliminary analysis of the LEGACY cohort, aPS/PT IgG demonstrated a stronger independent association with APO and slightly better discriminative performance than LAC. These findings suggest that aPS/PT IgG may outperform LAC in predicting APO and could improve risk stratification in SLE pregnancies. Supported by a CIORA grant.

We optimized an IMC panel to simultaneously evaluate IFI-P expression and characterize immune cell subsets directly within kidney tissue. Paraffin-embedded biopsies from LN patients in the Lupus Nephritis New Emerging Team and University of Toronto Lupus Clinic cohorts were analyzed. A pseudo-tissue composed of IFN-stimulated and unstimulated peripheral blood mononuclear cells in a clot that was embedded paraffin was used as a positive and negative control for antibody specificity. The panel includes 34 metal-conjugated antibodies to detect renal resident cells, infiltrating immune cells (T cells, B cells, monocytes, macrophages, dendritic cells), IFI-Ps, and fibrosis.

The IMC panel successfully detected renal and immune cell subsets, as well as distinct patterns of IFI-P expression in various renal compartments (Figure 1A). IFI-P expression demonstrated a moderate to strong correlation between the different kidney compartments (Figure 1B). Preliminary analysis of 10 LN biopsies revealed a trend to increased IFI-P staining intensity in all of the renal compartments of nonresponders when compared to responders (Figure 1C). This achieved statistical significance (p < 0.05) for IFNAR1, MX1, and PKR in the glomerulus and PKR in the nonproximal tubules, consistent with the concept that elevated renal levels of IFN are associated with poorer response to treatment. Figure 1.

Spatial profiling of interferon-induced proteins in LN kidney biopsies by imaging mass cytometry (IMC). (A) Representative IMC images of kidney biopsies from a treatment responder and non-responder, showing expression of ISG15 (yellow). MX1 (cyan). PKR (green), and IFNAR1 (red) overlaid with DNA (blue). Non-responders exhibited stronger and more diffuse IFI-P staining across renal compartments. Scale bar = 100 μm. (B) Correlation of MX1 expression between kidney compartments demonstrates coordinated interferon activity within tissue. MX1 is shown as a representative IFI-P, with similar correlations observed for the other IFI-P markers. Strong correlation was observed between proximal and non-proximal tubules (R = 0.84. p = 0.0045) and a moderate correlation between proximal tubules and glomeruli (R = 0.64. p = 0.054). (C) Quantitative comparison of mean IFI-P intensity across kidney regions in responders (n = 6) and non-responders (n = 4). Non-responders showed higher expression of IFNAR1 (p= 0.00952), MX1 (p= 0.0381), and PKR (0.0190) in the glomerulus, and increased PKR expression in the non-proximal tubules (p= 0.0381). Asterisks (*) denote statistically significant differences between treatment groups.

This study establishes a validated IMC-based approach for high-resolution spatial profiling of interferon signatures and immune cell subsets in LN kidney biopsies. Preliminary data suggest that elevated IFI-P expression is associated with nonresponse to therapy, supporting further investigation of IFI-Ps as predictive biomarkers. Application of this panel to larger LN cohorts may enable early patient stratification and guide precision treatment strategies to improve renal outcomes.

We studied 87 adult (≥18 years) SLE patients from a Canadian cohort without current LN, all with detailed clinical phenotyping. Serum IgG, IgM, and IgA anti-dsDNA levels were measured by ELISA. Extrarenal disease activity was quantified using the clinical SLEDAI-2K (cSLEDAI; range 0–12). Associations between individual isotypes and isotype ratios (IgM/IgG, IgM/IgA) and cSLEDAI were examined using Spearman’s correlation. Group comparisons across predefined activity categories were performed with Mann-Whitney U tests (2 groups) or Kruskal-Wallis tests with post hoc multiple-comparison correction (>2 groups).

Of 87 non-LN SLE patients, 51 (58%) were clinically active (cSLEDAI ≥1). In this active subgroup, IgM anti-dsDNA levels were inversely correlated with disease activity (r = –0.34, p = 0.016), whereas IgG and IgA anti-dsDNA levels showed no significant correlation with cSLEDAI. A lower IgM/IgA anti-dsDNA ratio was also associated with higher disease activity (r = –0.30, p = 0.033), while the IgM/IgG ratio was not. Patients with high disease activity (cSLEDAI >6) had significantly lower IgM anti-dsDNA levels than those with mild/moderate activity (p = 0.0028). When disease activity was categorized as inactive (cSLEDAI 0), mild/moderate (1-7), and high (≥8), IgM anti-dsDNA levels remained lowest in the high-activity group, with significant differences between inactive vs high (p = 0.046) and mild/moderate vs high (p = 0.0278).

In non-LN SLE, lower IgM anti-dsDNA levels and a reduced IgM/IgA ratio are associated with higher extrarenal disease activity, whereas IgG and IgA anti-dsDNA alone do not track clinical activity. These findings support a potential protective/regulatory role of IgM anti-dsDNA and suggest that IgG-only testing may miss clinically relevant isotype patterns.

Paired serum and saliva samples were collected from SLE patients and healthy controls. Serum was collected by venipuncture and stored at –80°C. Saliva was collected by 1) swab brushing of the gingival crevicular fluid on the gum line, enhancing IgG capture, or 2) passive drooling. Saliva was stored at –20°C. Antinuclear antibodies (ANA) were detected by conventional indirect immunofluorescence on HEp-2 cells (NOVA Lite, Werfen; cut-off >= 1:80), and for a subset of participants, SLE-related antibodies were quantified by QUANTA Lite ELISA for dsDNA (n=6 SLE, n=3 healthy controls), and FIDIS Connective Luminex 100 (Biosynx, Theradiag) for the remaining antibodies, anti-U1-RNP, histone, Jo-1, Pm-Scl, PCNA, Ro62/TROVE2, Ro52/TRIM21, SSB/La, Sm, Sm/RNP, Scl-70, ribosomal P, and centromere B (n=18 SLE, n=6 healthy controls).

We included 19 SLE patients and 6 healthy controls. Among these participants, 16 SLE patients (84.2%) and one (16.7%) healthy control were serum-positive for ANA. With gum line brushing, ANA positivity was observed in 10/16 (62.5%) of serum-positive SLE cases (Figure), and in one (100%) serum-positive healthy control. End-point ANA titers were reduced in saliva-positive cases relative to serum, with an average change of 2 dilution factors. When expert-level ICAP ANA patterns were included, 4/10 (40%) were congruent. There was a trend toward moderate correlation in anti-dsDNA titers between serum and saliva (r=0.65, p=0.06). For the remaining autoantibodies, where the presence or absence of any antibody in the ENA panel was considered a positive or negative ENA, 8/14 (57.1%) of the serum/saliva samples were in agreement. None of the passive drooling samples were ANA, anti-dsDNA, or ENA positive. Figure.

Comparison of antinuclear antibody (ANA) detection by indirect immunofluorescence on HEp-2 cells across paired serum and saliva samples from two systemic lupus erythematosus (SLE) patients. Representative HEp-2 cell images show ANA pattern of AC-5 (nuclear large/coarse speckled) in paired (A) serum (1:1280) and (B) saliva stored at –20°C (1:320) for one SLE patient. ANA pattern of AC-4 (nuclear fine speckled) depicted in paired (C) serum (1:1280) and (D) saliva stored at –20°C (1:160) for a different SLE patient.

Saliva collected by brushing the gum line represents a promising matrix for autoantibody detection in SLE, particularly for ANA screening and anti-dsDNA titers. This minimally invasive approach can be self-administered and easily transported to laboratories equipped for diagnostic testing. Ongoing studies aim to optimize autoantibody detection and further validate the method in larger cohorts.

A retrospective analysis was conducted using data from the Newfoundland and Labrador Centre for Health Information (NLCHI) spanning from 2009 to 2019. Patients diagnosed with PsD were identified using the ICD-9 code 696 and matched with a control group of approximately 75,500 individuals who did not have PsD. From this cohort of around 100,000 patients, those with IBD were identified using ICD-9 codes 555 for Crohn’s disease (CD) and 556 for ulcerative colitis (UC). Data on the number of hospital admissions and total hospitalization costs were collected from the NLCHI database.

A total of 15,100 patients were identified with PsD, and 2,800 patients had IBD. Among these cohorts, 14,368 had PsD alone, 2,068 had IBD alone, and 732 had both conditions. Thus, 4.8% of PsD patients were also diagnosed with IBD, comprising 525 patients (3.4%) with CD and 207 patient (1.4%) with UC. The mean number of admissions for patients with both IMIDs was significantly greater at 6.08 over a ten-year period, compared to 3.09 for those with PsD alone (p < 0.0001) and 5.04 for those with IBD alone (p < 0.001). The total hospitalization costs over 10 years for patients with both conditions amounted to $21,814, significantly higher than the $10,742 for PsD alone (p < 0.001), and numerically, though not statistically, higher than the $17,767 for IBD alone (p = 0.09). Similar numerical trends were observed in hospitalizations primarily due to cardiovascular-related events, with costs for both diseases at $2,476 compared to $1,622 for PsD alone and $1,987 for IBD alone. For mental health-related hospitalizations, the cost was $3,931 for both conditions compared to $1,886 for PsD alone and $3,560 for IBD alone.

These findings highlight the necessity for targeted healthcare strategies that address the complexities of managing multiple IMDs. By focusing on integrated care approaches and efficient resource allocation, healthcare systems can better support patients with these overlapping conditions, ultimately reducing the economic burden and improving patient outcomes.

We conducted a cross-sectional study of people with SSc. Using a standardized questionnaire, trained research assistants conducted telephone interviews collecting information about demographics, disease characteristics, work context, support and accommodation availability, needs and use, disclosure of health needs to supervisors. Workplace outcomes included presenteeism, job disruptions and absenteeism. Linear regressions examined the association of unmet accommodation needs with workplace outcomes.

There were 210 participants (80.9% women) with SSc with 10.5 (SD 8.2) mean years disease duration. Most (n=151, 73.0%) worked full time. Participants worked in education, science, arts, or research (n=75, 35.7%); government, financial, technology, business (n=67, 31.9%); sales, retail, or services (n=40, 19.1%); and utilities, construction, or manufacturing (n=28, 13.3%). Forty-five percent of respondents reported unmet workplace support needs. Participants working in sales, retail or services had the highest proportion of unmet needs (60.0%) compared to those working in government, financial, technology or business (40%). Participants working in government, banking, or insurance who reported unmet needs had significantly higher job disruption scores (on average 1.35 points higher) and higher presenteeism scores (on average 1.26 points higher) than those without unmet needs. Among participants in education, science, arts, or research those with unmet needs reported presenteeism scores (averaging 1.52 points higher). Participants in sales, retail, or service roles with unmet needs had presenteeism scores averaging 2.03 points higher than those without unmet needs (Table 1). Disclosure of the diagnosis of SSc to supervisors did not differ significantly between those with and without unmet needs. Table 1.

Association of unmet workplace accommodations and work productivity

In general, unmet workplace accommodation needs were associated with job productivity across different job sectors. Unmet needs in the sales, retail or services sector appear to be greater than in the government, financial, technology or business sector. To support the productive employment of people with SSc, interventions should target workplace support needs across different job sectors.

We conducted a qualitative study using semistructured interviews with rheumatologists practicing in Ontario, Canada, whose primary practice was a conventional model of care (without IHPs). Participants were purposively sampled to ensure variation in gender, career stage, practice setting, and region. The interview guide was informed by the Theoretical Domains Framework (TDF), an implementation framework used to identify determinants of health-professional behavior. We used content analysis with deductive coding to TDF domains and inductively derived within-domain themes on factors influencing adoption of interdisciplinary care.

We interviewed 14 rheumatologists across Ontario (12 adult, 2 pediatric), of whom 9 were women (64%) and 8 were aged <40 (57%). We identified 6 TDF domains as relevant to rheumatologists’ adoption of interdisciplinary care (Table 1), with barriers and enablers varying by anticipated IHP scope/function. Participants described being optimistic they would be able to feasibly implement an interdisciplinary model with appropriate system supports (1-Optimism) and reported strong self-efficacy for training and supervising IHPs (2-Beliefs about capabilities). Participants perceived that adoption would benefit patients (improved access/equity through shorter wait times, better care coordination, improvements in health outcomes) and rheumatologists (reduced administrative workload and burnout), which they identified as key enablers (3-Beliefs about consequences). Funding was described as the primary system-level barrier. For some, limited physical space to accommodate an IHP was reported to further impede adoption. Participants perceived a shortage of suitably trained IHPs, particularly outside urban centers, as a major barrier to adoption. They anticipated that the substantial time required to train new team members, and the risk of turnover, could create non-recoverable training costs and discourage implementation (4-Environmental context and resources). Rheumatologists reported knowledge gaps regarding IHP training and scope, along with limited business and human-resources skills for recruitment and contracting, as barriers to adoption (5-Knowledge, 6-Skills). Table 1

Adoption of interdisciplinary rheumatology care: TDF domains with themes and illustrative quotes

Among rheumatologists currently practicing in a conventional care model, we identified behavioral determinants of adopting an interdisciplinary model of care. To overcome barriers and strengthen enablers, sustainable funding, workforce development (IHP training), practical implementation resources (business guidance and training), and clear blueprints of successful care models and IHP roles (set-up guidance, team compositions, workflows) are required.

We performed a population-based retrospective study, identifying the annual number of gout ED visits occurring between 2014 to 2023 in Ontario. Annual total and incident ED gout visits and rates were determined, then stratified by sex and age. We described clinical and sociodemographic characteristics and assessed patient-level health care usage factors both preceding and after the gout ED visit. Repeat ED presentations and hospitalizations were determined within 90-days. Among individuals aged ≥66 years, we further assessed dispensations for flare abortive medications, urate lowering therapy and opioids within a 30-day window.

The mean age of individuals presenting to ED was 59.7 (SD 16.4), and 77.5% were male. Between 2014–2023, there were 125,505 gout ED visits in Ontario, including 86,824 incident visits. Annual ED gout encounters peaked in 2018 (14,017 encounters) translating to an annual crude rate of 0.99 (95% CI 0.97–1.01) and male stratified annual rate of 1.56 (95% CI 1.53–1.59) visits per 1000-persons (Figure 1). Older adults had the highest ED visit rates at 3.01 (95% CI 2.89–3.15) visits per 1000-persons in 2015. Patients were highly comorbid with 55.5% of patients with ≥10 Aggregated Diagnosis Groups. Common comorbidities included hypertension (57.7%) and diabetes (24.0%). By 30-days post-ED encounter, 28.3% and 21.3% patients were dispensed a flare abortive medication or attended an ambulatory gout visit respectively, while 10.3% were dispensed an opioid. By 6 months, 38.1% of patients had serum urate testing. By 90-days, 29.9% of encounters led to ED re-presentation, with 9.4% of total encounters representing specifically for gout, culminating in 6.2% (1.5% for gout) of total encounters leading to hospital admission. Findings were comparable for incident ED gout visits.

In what is one of the first Canadian population-based assessments of acute care use for gout, our work suggests that there is a large burden of ED visits, with suboptimal post-ED health services use, marred by under-prescribing of flare medications, over-prescribing of opioids and high acute care representation rates. Quality improvement efforts should be directed at strategies to prevent upstream ED presentations for gout and enhancing appropriate follow-up care. Best Abstract On Quality Care Initiatives In Rheumatology Award

Primary human FLS were cultured and stimulated with native or PTM-modified neutrophil proteases. Cytokine and chemokine secretion (IL-6, IL-1β, TNF-α) was quantified by ELISA and Olink multiplex analysis. Protease-activated receptor (PAR) signaling was assessed using PAR2 inhibitors and phospho-ERK immunoblotting. Serum autoantibody reactivity to citrullinated PR3 was evaluated in RA patients and at-risk relatives.

FLS exposed to PTM-modified neutrophil proteases showed markedly elevated secretion of IL-6, IL-1β, and TNF-α compared with unmodified controls (Figure 1A). This activation was significantly reduced by PAR2 inhibition, implicating a PAR2–ERK signaling axis in FLS inflammatory activation (Figure 1B). Flow cytometric analysis demonstrated rapid ERK phosphorylation following cit-PR3 stimulation, peaking at 15 minutes—much stronger than responses to PR3 (Figure 1C). Western blot confirmed prolonged pERK1/2 activation after cit-PR3 treatment, which was reduced by PAR2 blockade (Figure 1D). Olink proteomic profiling revealed that cit-PR3 shifted the FLS secretome toward a pro-inflammatory, immune-recruiting phenotype, with upregulation of CXCL1, CXCL5, CCL2, CCL3, and enrichment of granulocyte chemotaxis and cytokine-mediated response pathways. PCA distinguished cit-PR3–treated FLS from PR3, reflecting distinct secretome remodeling (Figure 1E-H). Time-course analysis showed persistent IL-6 elevation up to 24 h, consistent with chronic synovial activation (Figure 1I). Autoantibody profiling further revealed stepwise increases in anti-cit-PR3 IgG from ACPA– relatives to ACPA+ relatives to RA patients, linking PR3 modification to early autoimmune responses. Together, these findings identify cit-PR3 as a potent driver of FLS inflammatory signaling and a potential early biomarker for RA. Figure 1:

(A) Cultured fibroblast-like synoviocytes (FLS) stimulated with native or PAD2-citrullinated PR3 show enhanced IL-6 and TNF-α secretion upon cit-PR3 exposure. (B) PAR2 inhibition markedly reduces IL-6 release, implicating PAR2 in protease-mediated inflammatory signaling. (C) Flow cytometry histograms showing time-dependent ERK phosphorylation in FLS, with cit-PR3 inducing stronger and more sustained pERK activation than PR3, LPS, or untreated controls. (D) Western blot demonstrates increased and sustained ERK phosphorylation following cit-PR3 treatment, blunted by PAR2 blockade. (E) Principal component analysis (PCA) demonstrates clear segregation of cit-PR3–treated FLS from PR3 and LPS controls, highlighting distinct secretome remodeling. (F) Volcano plot illustrating significantly upregulated proteins (e.g., CXCL1, CXCL5, CCL2, CCL3, CSF1, TSLP) following cit-PR3 treatment compared with PR3. (G) Heatmap of differentially expressed proteins highlights a distinct pro-inflammatory secretome induced by cit-PR3. (H) Pathway enrichment analysis showing activation of granulocyte chemotaxis and cytokine-mediated signaling pathways. (I) Time-course analysis shows prolonged IL-6 elevation up to 24 h after cit-PR3 stimulation, indicating persistent activation. (J) Anti-cit-PR3 IgG levels increase progressively from ACPA– relatives to ACPA+ relatives and RA patients, supporting its potential as on early autoimmune biomarker.

Our findings establish PTM-modified neutrophil proteases as potent modulators of FLS behavior and contributing amplification of inflammation and autoimmunity in RA. These translational findings will be critical in developing targeted therapies that modulate dysregulated neutrophil function and pathogenic PTMs—broadening the therapeutic arsenal, preventing early disease onset, and ultimately improving patient quality of life.

[1.] Carmona-Rivera C. Curr Osteoporosis Rep 2024;22:280-9. [2.] Pham C. Int J Biochem Cell Biol 2008;40:1317-33. [3.] Suskiewicz MJ. BioEssays 2024;46:202300178.

Urine samples and kidney biopsy data were from the Biobank for Molecular Classification of Kidney Disease from patients with LN (n=14), rAAV (n=10), and healthy controls (n=10). Samples ranged from 14 days pre-biopsy to 238 days post-biopsy. Biomarker levels were quantified using ELISA (usCD163, sC5b9, SIGLEC-1) and Meso Scale Discovery (C3a, C5a) assays and normalized to urine creatinine levels. Mean concentrations were compared between groups, logistic regression generated a combined model, and receiver operating characteristic (ROC) curves assessed performance in predicting complete renal remission (CRR; UPCR<300 mg/g).

UsCD163 and urine-protein creatinine ratio (UPCR) levels were significantly elevated in patients with LN (17.92 ± 14.09 and 241.21 ± 74.41 mg/mmol, respectively) and rAAV (4.27 ± 2.03 and 90.87 ± 30.40 mg/mmol, respectively) compared to healthy controls (0.13 ± 0.01 and 7.53 ± 1.67, respectively), whereas uCAPs and SIGLEC-1 were not. There was a strong positive correlation between UPCR and usCD163 (=0.886, p<0.001), and moderate correlations with C3a (=0.642, p<0.001). C5a (=0.588, p<0.001), and sC5b9 (=0.566, p=<0.001). SIGLEC-1 concentrations showed no significant correlation with UPCR (=0.181, p=0.31). A combined model including usCD163 and uCAPs achieved strong predictive performance for distinguishing patients who achieved complete renal remission from those who did not (AUC=0.91; Figure 1). Among individual biomarkers, usCD163 had the highest discriminative performance (AUC=0.96), while sC5b-9 had the lowest (AUC=0.74; Figure 1). Figure 1.

Receiver operating characteristic (ROC) curve for the prediction of complete renal remission (CRR). ROC analysis was performed for each biomarker- usCD163 (AUC = 0.96), C3a (AUC = 0.82), C5a (AUC = 0.80), and sC5b9 (AUC = 0.74)- as well as a combined model (AUC = 0.91). The combined model, including usCD163 and uCAPS, demonstrated strong predictive performance of distinguishing patients with CRR from non-CRR, with sCD163 having the highest individual discriminative accuracy.

Urinary biomarkers reflecting distinct aspects of renal immune activation have potential to non-invasively monitor disease activity in LN and rAAV. Our findings support usCD163 as an indicator of renal inflammation, correlating closely to disease activity and remission status. A combined model with uCAPs and UPCR improved diagnostic performance further, capturing key immunologic differences in disease pathogenesis. Further validation in a larger, longitudinal cohort is underway.

Single-cell RNA sequencing (Flex Gene Expression) was performed on FFPE ileal samples from SKG wild-type (WT), WT+Curdlan, MIF knockout (MKO), and MKO+Curdlan mice (n=2 per group). UMAP clustering, differential gene expression, and Gene Ontology (GO) analyses were used to assess cellular composition and biological pathways related to immune activation, epithelial integrity, and metabolism.

Distinct transcriptional and cellular changes were observed across groups. Curdlan treatment induced expansion of neutrophil and macrophage populations in both WT and MKO mice. Compared to WT, MIF deficiency led to reduced enterocyte, goblet cell, and Paneth cell populations, indicating epithelial compromise. Under steady-state conditions, GO analysis revealed that MIF deletion caused loss of pathways associated with bacterial defense, epithelial secretion and transport, and epithelial differentiation, consistent with impaired mucosal defense. Upon curdlan challenge, MIF deficiency further suppressed oxidative phosphorylation, mitochondrial electron transport, and ATP synthesis pathways, indicating metabolic dysfunction in the inflamed gut epithelium.

These findings highlight MIF as a critical regulator of intestinal epithelial homeostasis. In its absence, mice exhibit loss of antimicrobial defense and epithelial function under basal conditions and marked impairment of mitochondrial and respiratory metabolism upon inflammatory stimulation, collectively predisposing to gut inflammation and barrier breakdown.

We measured polySia levels in sera from 22 patients with SSc using a specific polySia ELISA and correlated polySia levels with the severity of skin fibrosis using the modified Rodnan skin score (mRSS). We also used primary dermal FB from skin biopsies of healthy controls (HC, age/sex matched), less severe limited cutaneous SSc (lcSSc), dcSSc and post-ASCT patients (N=4-6/per group) and measured the frequency of DSBs, active (nuclear) FOXO1, and polySia levels using immunofluorescence/confocal microscopy and/or immunoblot (IB). We also quantified polySia, ST8SIA2 levels or pro-fibrotic markers (fibronectin and CTGF) using qRT-PCR and/or IB following FOXO1 pharmacological inhibition, ST8SIA2 knockdown via siRNA, or treatment with a polySia elongation inhibitor, 8-keto-Neu5Ac.

Total polySia levels correlated with mRSS (p=0.007, rho=0.560) in SSc patients – highlighting its direct link with fibrosis in SSc. We also observed that FB from dcSSc had a 2-3-fold induction in polySia levels and ST8SIA2 expression compared to FB from lcSSc and age/sex matched HC (p=0.02). Importantly, post-ASCT FB had a substantial reduction in ST8SIA2 (p=0.04) and polySia levels. This was associated with increased DSBs and FOXO1 activation exclusively in dcSSc FB. Finally, FOXO1 inhibition, ST8SIA2 siRNA knockdown, or treatment with 8-keto-Neu5Ac resulted in a 1.9-fold reduction in pro-fibrotic markers and total polySia levels (Figure 1). Figure 1:

A. Graphical abstract of proposed mechanism. In dcSSc fibroblasts, double-stranded DNA breaks activate the transcription factor FOXO1. Upon activation, FOXO1 upregulates the gene expression of the polySia synthetic enzyme ST8SIA2, polySia, and fibrotic mediators such as CTGF and fibronectin, thereby promoting fibrotic remodelling and fibrosis in dcSSc. B. Confocal images showing polySia (green), cis-golgi marker GM130 (red), nucleus (DAPI, blue) in fibroblasts from HC, dcSSc and post-ASCT. C. Spearman correlation analysis comparing serum polySia to mRSS in SSc patients (n = 22).

Our study identifies a novel DSB/FOXO1/polySia pathway as a key driver of fibrosis in SSc. This axis may serve as a biomarker for disease progression and may be indicative of restoration of FB functions post-ASCT. We postulate that targeting the FOXO1/polySia pathway may provide a novel therapeutic approach in dcSSc.

[1.] Khan L. J Autoimmun 2023;140:103110.

Biologic-naïve pts with active PsA were randomized (1:1:1) to GUS 100 mg every 4 weeks (Q4W); GUS 100 mg at W0, W4, then Q8W; or placebo with crossover to GUS 100 mg Q4W at W24. Early (W8) response in joint DA, (based on clinical DA Index for PsA [cDAPSA LDA; ≤13]), was assessed among pts with cDAPSA >13 at BL, without adjustment for sex-specific differences at BL. Multivariate repeated measures mixed models assessed associations between sex and changes in total PsAmodified van der Heijde-Sharp [vdH-S] score through W100 (Figure 1).

Of 739 PsA pts enrolled, 47.5% were female. At BL, female vs male pts were more likely to have dactylitis (60.6% vs 50.3%; p=0.0049), and on average had higher BMI (29.5 vs 28.4 kg/m²; p=0.0144), lower CRP levels (1.6 vs 2.3; p<0.0001), less severe psoriasis (Psoriasis Area and Severity Index [PASI] score: 7.5 vs 12.1; p<0.0001), and more functional disability (Health Assessment Questionnaire–Disability Index [HAQ-DI] score: 1.4 vs 1.2; p<0.0001). BL cDAPSA (46.1 vs 46.4) and PsA-modified vdH-S (26.2 vs 25.5) scores were similar (p>0.05) between sexes. In unadjusted analyses of GUS-treated pts, male sex was associated with greater progression of structural damage through W100 (LSM=1.02; p=0.0260). After adjusting for risk factors of RP, BL characteristics with sex-specific differences in the pooled cohort, disease duration and non-biologic DMARD use at BL, the difference between sexes in RP decreased but remained significant (LSM=0.90; p=0.0406); LSM changes from BL in PsA-modified vdH-S scores in males vs females were 1.36 vs 0.69 (p=0.0502) at W52 and 2.22 vs 1.10 (p=0.0475) at W100 (Figure 1). Early (W8) cDAPSA LDA was achieved by 18.9% of men vs 15.3% of women. In men, this was associated with significantly less RP through W100; in females only, numerical differences were observed.

These results confirm the independent association of male sex with more rapid RP. The previously reported relationship between early improvement in joint DA and diminished RP,[1] was found to be stronger in males than females, which may be due to the lower rate of RP in females.

[1.] Mease PJ. Clin Rheumatol 2024;43(1):241-9.

A total of 703 patients from the Gladman Krembil PsA program were analyzed, with ages at psoriasis and PsA onset recorded. All samples underwent a genome-wide association scan that included over one million single-nucleotide polymorphisms (SNPs). Quality control excluded SNPs with more than 1% missing data and those that did not meet Hardy-Weinberg equilibrium criteria. We treated the age difference between PsA and psoriasis onset as a quantitative trait by subtracting the age at PsA onset from the age at psoriasis onset for each patient. We then performed a quantitative trait locus (QTL) analysis. PsA patients were categorized into 4 groups and compared for genetic differences: (A) PsA occurring at least one year before psoriasis; (B) psoriasis and PsA occurring within one year of each other; (C) PsA occurring one to 10 years after psoriasis; and (D) PsA starting 10 or more years after psoriasis onset.

The QTL analysis identified over 50 SNPs significantly affected the onset of inflammatory arthritis (p < 1 x 10^-5). Most identified loci were associated with a delay in PsA onset in individuals with the mutant allele compared with those with the wild-type allele. Genes associated with delayed PsA included PSORS1C1, CDSN, TXB5, and OSBLV. Conversely, loci on chromosome 15 (in linkage disequilibrium with MYO1E) and chromosome 17 (in LD with CCDC43 and MEIOC) were associated with an earlier onset of PsA. Comparisons among the PsA onset subsets noted above revealed notable differences, particularly between groups A and D (59 SNPs) and between groups A and C (30 SNPs) at a significance level of p < 1 x 10^-5. Development of polygenic risk scores to identify early- and late-onset PsA is ongoing.

This study underscores the significant role of genetic mutations in influencing the variability in the onset of PsA among patients with psoriasis. By identifying over 50 SNPs that significantly impact the timing of PsA onset, our findings highlight the complex genetic landscape that contributes to progression from psoriasis to PsA. Best Abstract On Basic Science Research By A Trainee Award

We used population-based health administrative data from Ontario, Canada to identify all incident IBD cases diagnosed between April 1, 2003 and March 31, 2020 using previously validated age-specific algorithms. Among individuals in this inception cohort of IBD patients, we identified individuals diagnosed with IA either before or after their IBD diagnosis. IA diagnosis (rheumatoid arthritis, axial spondylitis, other seronegative spondyloarthropathies, synovitis) required ≥1 hospitalization or emergency department visit or ≥2 physician claims with an IA diagnosis code, with ≥1 claim made by a rheumatologist (adult or pediatric), internal medicine physician, pediatrician, or gastroenterologist. IA diagnoses could occur at any point during data availability (1991-2024). We calculated the time between the diagnoses of IA and IBD, categorizing time into the intervals (>3 years pre-IBD diagnosis to >10-15 years post-IBD diagnosis). Age- and sex-standardized IA incidence rates were calculated within each interval. Analyses were stratified by IBD type, age at IBD diagnosis (<18y, 18 to 64y, ≥65y), and sex.

We identified 56,776 individuals with incident IBD; 11,814 (20.8%) had an IA diagnosis. The incidence of IA peaked in the 6 months prior to IBD diagnosis (23.1 (95% CI 18.6 to 28.4) per 1000 person-years), then gradually decreased in the time following IBD diagnosis (Figure). This pattern was consistent in all subgroups. Figure.

Incidence of IA among incident IBD cases, stratified by sex

This is the first population-based study to describe the incidence of IA in an inception cohort of people with IBD. The peak in IA diagnosis around the time of IBD diagnosis indicates a need for integrated interprofessional care models to facilitate patient access to both gastroenterology and rheumatology care. Future research will investigate the implications of these co-occurring diagnoses on health services utilization and expenditures.

This retrospective single-center study included patients treated with phonophoresis using fluocinonide 0.05% gel between November 2023 and May 2025. Patients were offered 6 sessions over 2–3 weeks, with some receiving adjunctive dry needling or corticosteroid injections before treatment. Data extracted from the QHR Accuro EMR included demographics, rheumatic and musculoskeletal diagnoses, treatment details, inflammatory markers (when available), Visual Analog Scale (VAS) pain scores, patient-reported outcomes, physical assessments, and adverse effects related to phonophoresis. A clinically meaningful improvement was defined as a ≥2-point reduction in VAS from baseline to the final session. [1] Subgroup analyses compared outcomes by anatomical site, adjunctive therapy use, and overall course duration.

A total of 32 treatment courses were administered to 27 patients (mean ± SD age 59 ± 13 years; 81% female). Thirteen (48.1%) were receiving disease-modifying antirheumatic drugs (DMARDs), and 2 (7.4%) were on biologics at the time of treatment. Across 47 anatomical sites with paired VAS data, the mean VAS reduction (VAS) was 3.18 ± 2.71, with 70.2% achieving clinically meaningful improvement. The Achilles tendon was the most frequently treated site (n = 24), with 62.5% of these sites achieving meaningful improvement, followed by the plantar fascia (n = 9, 66.7%) and peroneal tendon (n = 5, 100%) (Table 1). Sites treated with phonophoresis plus adjunctive dry needling (n = 19) demonstrated higher response rates compared to sites treated with phonophoresis alone (89.5% vs 58.6%) and greater pain reduction (VAS = 3.71 ± 2.37 vs 2.81 ± 2.90). Four patients received corticosteroid injections prior to phonophoresis (3 intramuscular and 1 site-specific), with a mean VAS of 3.75 following phonophoresis and 75% showing clinically meaningful improvement. Most patients completed ≥ 6 sessions within approximately 4–5 weeks. Phonophoresis was well tolerated, with only one mild, self-limiting adverse event reported. Table 1.

Primary outcomes of phonophoresis by anatomical site

Phonophoresis was associated with clinically meaningful pain reduction across most anatomical sites, with adjunctive dry needling further enhancing outcomes. This non-invasive, well-tolerated treatment modality could serve as a useful adjunct for localized enthesitis-related pain, especially in patients unable to receive corticosteroid injections or for whom standard therapies are not ideal.

[1.] Farrar JT. Pain 2000;88:287-94. Best Abstract By A Medical Student Award

We conducted a chart review to validate an Ontario administrative case-identification algorithm for GCA,[1] against the ACR/EULAR GCA Classification Criteria (2022),[3] within Southern Alberta. Our study included patients aged 50 and older diagnosed with GCA from January 1, 2018, to December 31, 2023, in Alberta. We began by applying Ontario’s algorithm for GCA to a linked Alberta health administrative dataset to produce a subset of algorithm-positive cases. This pool was further sampled to generate a random selection of 100 cases within Southern Alberta for chart review. This sample size was calculated using the Wald method and assumed a 95% confidence level, a 5%-10% margin of error, and an expected positive predictive value (PPV) of 81.3% similar to Ontario findings. The 2022 ACR/EULAR GCA classification criteria served as our reference standard and reflected the current GCA diagnostic consensus.[3] As a sensitivity analysis, PPV was also computed using the treating rheumatologist diagnoses as an alternative reference standard. PPV was calculated as True Positives (TP) divided by the number of algorithm-positive charts (n = 100).

1,903 algorithm-positive cases were identified in Alberta using the Ontario case definition and 100 were randomly selected for chart review. When evaluating the performance of the Ontario algorithm in the Southern Alberta cohort (n = 100), the case definition yielded a PPV of 64% (95% Confidence Interval [CI] 54.6-73.4%). In the sensitivity analysis, the Ontario administrative case definition algorithm produced comparable estimates when validated against rheumatologist diagnoses as the alternative reference standard (PPV: 62%, CI 52.5-71.5%).

The Ontario administrative case definition algorithm demonstrated moderate PPV in the Southern Alberta cohort (64%; 95% CI 54.6-73.4%), which was lower than the Ontario cohort estimate (81.3%; 95% CI 73.4-89.1%).[1] The confidence intervals showed minimal overlap, with the upper limit of our CI approaching the lower limit of the Ontario estimate, suggesting possible, but limited, agreement between cohorts. Differences may reflect potential regional or methodological differences including, reference standard selection across studies and sample size. Refinement of the algorithm may improve its performance in Alberta.

[1.] Barra L. Rheumatology (Oxford) 2020;59:3250-8. [2.] Ing EB. Can J Ophthalmol 2019;54:119-24. [3.] Ponte C. Ann Rheum Dis 2022;81:1647-53.

A total of 2,303 patients fulfilling ACR/EULAR classification criteria for SSc were included, comprising 1,976 EoSSc and 327 LoSSc cases. The primary outcome was all-cause mortality from the time of diagnosis, while secondary outcomes included disease-specific manifestations, comorbidity burden, and functional status. Relative risks (RR) with 95% confidence intervals (CI) were calculated for clinical and serological features. Survival analyses were performed using Kaplan-Meier estimates and Cox proportional hazards modeling to identify independent predictors of mortality.

LoSSc patients exhibited distinct clinical characteristics compared with those with earlier onset disease. They were significantly less likely to demonstrate esophageal dysmotility (RR 0.91, 95% CI 0.85–0.97), digital ulcers (RR 0.65, 95% CI 0.53–0.81), or anti-Scl-70 antibody positivity (RR 0.68, 95% CI 0.51–0.91), suggesting a lower prevalence of classic fibrotic and vasculopathic features. In contrast, LoSSc patients demonstrated a higher prevalence of pulmonary arterial hypertension (RR 1.59, 95% CI 1.33–1.89) and a substantially greater burden of age-associated comorbidities, including coronary artery disease, systemic hypertension, diabetes mellitus, hyperlipidemia, peripheral vascular disease, malignancy, stroke, and atrial fibrillation. Functional impairment was also more pronounced, with LoSSc patients more frequently classified as NYHA class II or higher (RR 1.50, 95% CI 1.17–1.92). The risk of multimorbidity was strikingly elevated, with LoSSc patients demonstrating a 27-fold increased likelihood of having 6 or more comorbid conditions. Survival analyses revealed significantly higher mortality in LoSSc at one, 5, and 10 years post-diagnosis (Figure 1). Late-onset disease was an independent predictor of mortality (adjusted HR 4.51, p<0.0001), even after adjustment for key confounders including sex, cardiovascular comorbidities, interstitial lung disease, pulmonary hypertension, renal crisis, and malignancy. Figure 1.

Kaplan Meier survival curves comparing people with SSc diagnosed at age 65 or older (Late-onset Systemic Sclerosis, LoSSc) and those diagnosed before 65 years (Early-onset Systemic Sclerosis, EoSSc).

These findings indicate that LoSSc constitutes a clinically and prognostically distinct phenotype, characterized by increased comorbidity, higher cardiopulmonary complications, and reduced survival. Tailored approaches to screening, management, and prognostication are warranted for older adults with systemic sclerosis.

Patients with ICI-IA enrolled in the Canadian Research Group of Rheumatology in Immuno-Oncology (CanRIO) multicenter prospective cohort who completed a baseline HAQ-DI were included. Demographic, clinical and laboratory data were extracted from the study database. Internal consistency reliability was assessed using Cronbach’s alpha coefficient (≥ 0.7 acceptable). Construct validity was examined by correlating HAQ-DI scores with other measures of disease activity. Responsiveness was evaluated using the standardized response mean (SRM) and effect size (ES) among participants with ≥ 3-point improvement on physician global assessment of disease activity (defined a priori) at 6 month follow-up.

Ninety-six patients from 9 centers were included, 48 female, median age 67 years (range 39-84) with most common malignancies being melanoma (25%) and non-small cell lung cancer (20%). Polyarticular involvement was most frequent (64%) with median tender and swollen joint counts of 6 (range 0–36) and 2 (range 0–30), respectively at baseline. 54% of participants were on systemic glucocorticoids at baseline. Median HAQ-DI was 0.5 (range 0, 3) at baseline and 0.125 (range 0, 2.375) at 6 months (n=66). HAQ-DI scores were higher in those not on immunosuppression (median 0.5 vs 0.375). Floor and ceiling effects were 24% and 1%, respectively. Cronbach’s alpha ranged from 0.72-0.91 across the 8 HAQ-DI domains and was 0.94 for the 20 individual items, suggesting high internal consistency. The HAQ-DI had a significant positive correlation with C-reactive protein, swollen joint count, patient global score and physician global score (Table 1). In those with ≥ 3-point improvement on the physician global score at follow-up (n=23), responsiveness was moderate (SRM =1.4; ES = 0.3). Table 1:

HAQ-DI correlations with clinical/demographic variables

In this prospective cohort study, the HAQ-DI was reliable, valid and sensitive to change in patients with ICI-IA. Over 50% of patients were on baseline immunosuppression likely impacting HAQ-DI scores and responsiveness to change assessment. Future research will explore content validity, the minimal clinically important difference in this population, and correlation to the physical functioning components of cancer-specific patient-reported outcome measures.

We conducted a retrospective study of 21 deceased patients with GPA or MPA followed in our vasculitis center between 2001 and 2022. Clinical characteristics, treatment regimens, organ involvement, infections, and causes of death were extracted from medical records. Cumulative prednisone doses were estimated and described in relation to outcomes.

Among the 21 patients included, 67% had GPA and 33% had MPA. The median follow-up was 986 days. Renal and/or pulmonary involvement occurred in most patients. While 50% of patients had active vasculitis at death, infection was the most common cause of death (52%), exceeding vasculitis-related mortality (19%) (Figure 1). Patients who died from infection had received higher cumulative prednisone doses (median 10.2 grams[g], IQR 4.9–14.1 g) than those who died from other causes (median 5.6 g, IQR 2.5–28.3 g). Long-term glucocorticoid use was associated with metabolic complications and repeated infections.

Infections, rather than active vasculitis, were the leading cause of death in our cohort. These findings underscore the need for individualized immunosuppressive regimens, judicious steroid tapering, and proactive infection risk mitigation in the management of AAV. Future studies should aim to identify predictors and preventive measures of infection-related mortality, while optimizing steroid-sparing strategies.

[1.] Jennette JC. N Engl J Med 1997;337:1512-23. [2.] Stone JH. N Engl J Med 2010;363:221-32. [3.] Wallace ZS. Semin Arthritis Rheum 2016;45:483-9.

We conducted a cohort study of patients with cSLE followed at The Hospital for Sick Children (2016 – 2024) who underwent whole-exome or whole-genome sequencing. Variants were assessed using our internal pipeline with quality control and depth filters. A predefined gene list (36 monogenic lupus genes) was expanded to include genes with established roles in lupus-relevant immune dysregulation. Rare, potentially pathogenic variants were defined as those with minor allele frequency <1% in gnomAD (Genome Aggregation Database) and predicted deleterious by ≥2 in-silico tools with biologic plausibility. Patients harboring ≥1 qualifying variant were classified as variant-positive. Demographic, clinical, treatment and outcome data were abstracted from the dedicated lupus database, supplemented by chart review. This included ACR/EULAR (American College of Rheumatology/European Alliance of Associations for Rheumatology) classification criteria, SLE manifestations, SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) and SLICC-ACR (Systemic Lupus International Collaborating Clinics) damage index scores prospectively collected over time. We also documented complications such as macrophage activation syndrome (MAS) and hospitalizations. We compared the prevalence of irreversible organ damage or major complications, between ‘variant-positive’ and ‘variant-negative’ patients adjusting for demographic and clinical covariates.

151 children and adolescents with cSLE had genome-wide sequencing during the study period; 84% were female, with a median age at diagnosis of 12.8 years (IQR 10.3-15.2). Preliminary review suggests that variant-positive patients are diagnosed at younger age and frequently exhibit classical lupus serology and hypocomplementemia. Identified variants spanned canonical monogenic lupus pathways, including complement genes (eg, C1QA), nucleases and nucleic-acid sensing (eg, DNASE1L3), immune tolerance/lymphoproliferation (eg, CTLA4), and X-linked genes (eg, SAT1). Preliminary review suggests phenotypic heterogeneity across these genetic subgroups with possible differences in treatment intensity and healthcare utilization; full statistical evaluation is ongoing.

In a diverse cohort of children and adolescents with cSLE, and an expanded list of SLE risk genes, we anticipate at least 13% carry rare pathogenic SLE variants. We expect these patients are more likely to sustain irreversible organ damage compared to those who do not carry rare variants. Our findings will extend our understanding of cSLE and improve prognostication.

Study participants with LA were recruited prospectively from a pediatric rheumatology clinic in Halifax, NS. Clinical outcomes were divided into those with resolution of arthritis with 1-2 courses of antibiotics and PILA. Oligoarticular JIA and healthy volunteers served as comparator groups. Reverse-Transcription quantitative Polymerase Chain Reaction (RT-qPCR) of mRNA isolated from peripheral blood mononuclear cells was analyzed to evaluate the expression levels of Type I IFN (IFNA1) and Type I IFN responsive genes (ISG15, IFIT1, OAS1) to create a Type I IFN score, and IFNG as a representative Type II IFN. Standard housekeeping genes ACTINB and UBC were used as reference genes. Fold changes in gene expression within groups were analyzed using the Wilcoxon signed-rank test, and differences between groups with T-tests.

Research cohorts included: 28 antibiotic responders (57%F, age 8.5y ± 3.4y), [19 had resolution after 1 course of antibiotics, 9 after 2 courses], 5 with PILA (75%F, age 10.4y± 1.3y), 5 with JIA (100%F, age 6.8y± 4.0y) and 18 healthy controls ( 43%F, 8.3y±4.9y). Significant expression of IFNA1, ISG15, IFIT1, and OAS1 (p<0.0001) and IFN score (p<0.0001) was observed within the antibiotic responder group, while PILA and JIA groups failed to demonstrate a measurable IFN response. Analysis between groups demonstrated significantly higher IFNA1 expression in the antibiotic responder group compared to PILA (p=0.015).

Our data suggest that robust IFN expression is associated with antibiotic response and disease resolution in children with LA; however, a low IFN signature after Borrelia exposure is associated with persistent joint inflammation despite antibiotics, similar to oligoarticular JIA. Our study is limited by the small number of patients in the PILA group, with sample collection ongoing.

This study is part of a multicenter randomized controlled trial (RCT).[2] We report data from one of 5 sites, which recruited 20 participants randomized to a remote intervention or a wait-list control group. Participants (n=10) in the remote SMP attended 4 60–90-minute Zoom sessions (JIA overview, daily living and exercise, coping strategies, and treatment/lifestyle management) over 8 weeks. Both groups completed questionnaires at baseline (T0) and after the intervention group completed the program (T1). The questionnaires included: (1) the Medical Issues, Exercise, Pain, and Social Support (MEPS); (2) the Children’s Arthritis Self-Efficacy Scale; (3) the Pediatric Quality of Life Inventory 3.0 Rheumatology–Teen Module; (4) the PROMIS (Patient-Reported Outcomes Measurement Information System) Pediatric Pain Interference Scale; and (5) the Readiness for Adult Care in Rheumatology (RACER). After completing the program, participants in the intervention group were invited to take part in an optional semistructured interview to provide feedback. Mann–Whitney U tests compared groups change scores, standardized effect sizes were calculated, and qualitative feedback was analyzed thematically.

Attendance was high, with 80% of participants completing all sessions. 95% completed the baseline and post-intervention questionnaires, and 5 also participated in the optional interview. Participants indicated they would attend again and think other teens would be interested. Feedback highlighted peer connection and the educational value of the sessions. Some participants felt that the sessions were too long, and responses were mixed regarding interactivity. Compared with the control group, the intervention group showed a significant improvement in MEPS (p = 0.027) with a large effect size (r = 0.51). Improvements in the RACER (p = 0.053) and the Self-Efficacy Scale (p = 0.11) trended toward significance, with moderate effect sizes of 0.44 and 0.37, respectively.

This pilot study supports the feasibility and acceptability of a virtual self-management program for adolescents with JIA. The program improved self-management outcomes and showed trends toward greater transition readiness and self-efficacy. These preliminary results warrant further multisite evaluation to confirm effectiveness and optimize engagement. Recruitment is ongoing across sites, with a target enrollment of 100 participants.

[1.] Chomistek K. Discover Health Sys 2025;4(4). [2.] Booth J. JMIR Res Protoc 2025;14:e69539.

Participants were diagnosed and followed in a tertiary care lupus clinic and met SLE classification criteria. Clinical and laboratory data including disease activity and damage indices were prospectively collected and stored in a dedicated database. Participants were genotyped on a multiethnic array and ancestry was genetically inferred. Whole blood was collected prior to treatment initiation with glucocorticoids or other potent immunosuppressants, and whole blood transcriptome wide RNA sequencing was completed. We identified distinct participant clusters based on gene expression profiles using K-means clustering. Clinical and demographic feature differences between clusters were assessed using ANOVA and Fishers exact test. To gain an understanding of the genes driving cluster membership predictive modeling was used. Logistic LASSO regression and random forest supervised models were deployed and the genes most used by the models to aid in prediction of cluster membership were extracted.

The cohort included 75 children and adolescents with cSLE with RNA sequencing on treatment-naïve whole blood samples. Initial K-means plots identified 3 clusters and one outlier which was excluded resulting in the final cohort. The group was 81% female with a median age of SLE diagnosis of 13.8 years (IQR: 12.1, 15.4). The demographic compositions of each cluster did not yield any statistically significant differences. Clusters differed significantly in the proportion of individuals with hypocomplementemia (C3 and/or C4) (Cluster 1= 40%, Cluster 2= 35%, Cluster 3= 100%, P= <0.01), fever (Cluster 1= 55%, Cluster 2= 13%, Cluster 3= 40%, P= <0.01), and Anti-Smith antibodies (Cluster 1= 70%, Cluster 2= 35%, Cluster 3= 40%, P= 0.01). Supervised models successfully identified genes predictive of cluster membership these genes include, but are not limited to IGHG1, IGHG4, INKA2, and SLC39A12-AS1. Cluster 1 was characterized by increased expression of SKA2, ARL1, and SRP68. Cluster 2 showed decreased expression of IGHG1, IGHG4, and IGLV1-44. Cluster 3 displayed increased expression of CD177, ALPL, and SLC4A1.

In a clinically heterogeneous, multiethnic cohort of patients with cSLE, treatment naïve whole blood RNAseq genome-wide expression generated 3 discrete clusters of patients. Genes characterizing cluster membership include IGHG1, SKA2, and CD177. Next steps include gene set enrichment analysis to denote differences in cluster biological processes.

[1.] Tsokos G. N Engl J Med 2011;365:2110-21.

Paired baseline and W76 kidney biopsies from REGENCY participants with biopsy-proven proliferative LN were analyzed. Histological analysis: 64 biopsies (32 OBI+ST, 32 PBO+ST) were evaluated using the 2018 ISN/RPS LN classification, along with the NIH activity (AI) and chronicity indices. The proportion of patients achieving histological or near-histological remission (AI=0 or ≤1) was determined. B-cell analysis: 29 participants (14 OBI+ST, 15 PBO+ST) were assessed. CD79a+/CD138– B cells were quantified by immunofluorescence microscopy and digital whole-slide analysis. Changes in B-cell counts at W76 were compared using an ANCOVA model, adjusting for baseline B-cell counts and stratification factors.

Baseline characteristics were balanced, despite higher tissue B-cell levels in the OBI+ST group. At W76, significantly more patients achieved AI=0 or ≤1 with OBI+ST vs PBO+ST. Among patients not achieving CRR, 52.6% (10/19) in the OBI+ST group had an AI=0 at W76, vs 8.3% (2/24) in the PBO+ST group. Most patients in the OBI+ST group had substantial drops in kidney tissue B-cell counts by W76 (Figure 1). The adjusted mean change in B-cell counts from baseline to W76 was –28.5 (95% CI –33.3 to –23.6) for OBI+ST vs –11.9 (95% CI –16.6 to –7.2) for PBO+ST, a significant difference of –16.6 (95% CI –23.4 to –9.7; P<0.0001). Figure 1.

(A) Proportion of patients achieving AI≤1 and AI=0, (B) change in AI from first to repeat post-W76 biopsy and (C) change in chronicity index from first to repeat post-W76 biopsy

In the largest longitudinal kidney biopsy cohort ever reported for a registrational LN clinical trial, significantly more patients achieved complete or near-complete histological remission with OBI+ST vs PBO+ST. This is the first demonstration of deep kidney tissue B-cell depletion by any anti-CD20 agent, in any glomerular disease. Obinutuzumab’s potent B-cell clearance from kidney tissue may drive kidney function improvement and LN flare reduction. These findings support assessment of histological outcomes in future LN trials and highlight a potential mechanism for obinutuzumab in preserving long-term kidney health.

We analyzed autoimmune serology from 225 asymptomatic ANA-positive or UCTD subjects with longitudinal follow-up (1-7 years) to assess changes over time, seroconversion, and progression to (SARD). ANAs were quantified by indirect IF using the Kallestad® HEp-2 kit and specific autoantibodies measured using the Bioplex® 2200 ANA Screening System which assesses the levels of anti-dsDNA, -chromatin, -Ro, -La, -Sm, -SmRNP, -RNP, -Jo-1, -Scl-70, -centromere and -ribosomal P antibodies.

At baseline, a high ANA titer (≥1:640) predominated in 60% of subjects, with speckled and homogeneous patterns representing the majority of immunofluorescent patterns. The most prevalent baseline autoantibodies were Ro (23.3%) and RNP (15.7%). Among subjects with serial ANA testing (n=77), 60% had initial high titers (≥1:640). Upon follow-up, 53% had declining titers with 6.5% seroconverting to ANA-negative. Of those who seroconverted, 60% had high titers (≥1:640) initially and 40% had a dense fine speckled (DFS) pattern. The median time to ANA loss was 3.3 years. Among the 6 subjects who ever demonstrated a DFS pattern, none of whom progressed to SARD, 33.3% converted to negative, and 33.3% transitioned to other ANA patterns. This variability underscores the dynamic but low-risk nature of DFS pattern. Among the 135 subjects with serial autoantibody profiling, Ro remained the most prevalent antibody (40%) and was usually stably elevated (89% remained persistently positive), showing minimal fluctuation over time. In contrast, RNP (17%) and dsDNA (6.7%) showed the greatest instability, with 44% of dsDNA-positive and 22% of RNP-positive subjects becoming negative. Interestingly, Scl-70, which was positive in 9 patients, also showed instability, with 4 of these patients losing positivity over time. Nine patients progressed to a defined SARD after a median of 31 months. Overall, progressors had high ANA titers (≥1:320), and none became ANA-negative. Among this group, dsDNA (89%) and Ro (SSA) (56%) were the most prevalent autoantibodies.

Many subjects demonstrated immunological improvements. Subjects who achieved ANA negativity typically began with high ANA titers that declined over time. In contrast, progressors showed persistently high ANA titers, frequently accompanied by rising dsDNA and stable Ro reactivity. These findings support the clinical importance of serial ANA and ENA monitoring to differentiate transient autoimmunity from evolving systemic disease.

We analyzed demographic, clinical, and laboratory data from the McGill SLE Research Cohort. Serum NT-proBNP levels were measured yearly from March 2022 to May 2025. We assessed the prevalence of elevated NT-proBNP (≥133 pg/mL),[1] at baseline, and determined baseline variables: age, sex, race/ethnicity, age at SLE diagnosis, SLE duration, smoking, and SLE International Collaborating Clinics (SLICC) Damage Index. Univariate and multivariate linear regressions identified independent associations with baseline log-transformed NT-proBNP (Table 1). Patients were classified into 4 NT-proBNP trajectories: abnormal at baseline and remained abnormal; abnormal and normalized; normal and became abnormal; normal and remained normal. We compared baseline characteristics across trajectories using multivariate logistic regressions. Table 1:

Exponentiated coefficients of univariate vs multivariate linear regression analyses for outcome of log-transformed baseline NT-pro-BNP

We studied 294 patients with ≥2 measurements. At baseline, 101 (34.4%) had elevated NT-proBNP. The mean NT-proBNP levels were 243.6 pg/mL, median 91, interquartile range, IQR 55-171.8. Higher levels were significantly associated with female sex, white race, older age at SLE diagnosis, and longer SLE duration. Cardiovascular damage, pulmonary hypertension, and renal damage were also independently associated with higher NT-proBNP. Of the 101 individuals with abnormal baseline NT-proBNP, 79 (78.2%) remained abnormal at second assessment. Of the 193 with normal baseline levels, 30 (15.5%) became abnormal. No patient with a baseline level ≥350 normalized to <133. Compared to other trajectories, high-risk trajectories (abnormal remained abnormal and normal became abnormal) were more likely to have cardiovascular damage (OR 3.90, 95% CI 1.49-12.48, renal damage (OR 2.87, 95% CI 1.61-5.51), and pulmonary hypertension (OR 31.99, 95% CI 4.59-651.10).

Over one-third of patients had abnormal baseline NT-proBNP, and most (78%) remained abnormal, while over 15% of those with an initially normal value became abnormal. Higher levels were associated with female sex, white race, older age at diagnosis, longer SLE duration, and organ damage. Levels ≥350 pg/mL did not normalize over our evaluation. High-risk trajectories were associated with SLICC damage items (cardiovascular damage, renal damage, and pulmonary hypertension – though the 95% CI for pulmonary hypertension was very wide). Future analyses will examine associations with electrocardiogram and echocardiographic results.

[1.] Sacre K. Rheumatology (Oxford) 2024;63:1739-45. Best Abstract on SLE Research by a Trainee – Ian Watson Award

We analyzed longitudinal data from 1,044 employed SLE patients at the Toronto Lupus Clinic (1996–2024). Patients reported their employment category at every clinical visit and were categorized into 3 exclusive outcomes: WD (permanent or prolonged sick leave), SLE-mortality, and stable employment (actively employed or retiring at/after Canadian retirement age). A Random Forest classifier selected visit-to-visit disease activity measures, treatment regimens, and organ damage features to be used in a Long Short-Term Memory (LSTM) model. Each visit’s data was processed with prior history to create an updated patient health hidden state. The final hidden state was used to classify patients into their most likely final employment outcome. Risk scores for WD were calculated at each visit and early warning alerts were triggered if scores exceeded an optimized threshold. Prediction accuracy and lead time for early detection assessed model effectiveness.

129 patients eventually reported WD, these patients showed more frequent visits to the clinic over longer follow-ups, with higher doses of glucocorticoids and antimalarials, higher disease activity, irreversible damage, and more frequent flares (all p < 0.001) (Table 1). The prediction model achieved 91% balanced accuracy in predicting the final employment states. More significantly, the early warning machine learning algorithm identified 89% of future disability cases, providing a median 28.6-month (IQR: 14.3–42.1) warning before first reporting WD. Table 1.

Characteristics of the Patients by Employment Group at last visit* and Model Results

Predicting workforce exit for SLE patients is critical and our early warning algorithm flagged patients at a risk of disability 2–3 years in advance. Implementing this system would enable timely interventions to help prevent work disability in SLE. By transforming reactive care into pre-emptive action, this prediction model closes a critical gap in SLE management, empowering health care teams to intervene before functional decline becomes permanent WD.

At the ORCHESTRA (Ottawa Rheumatology CompreHEnSive TReatment and Assessment) Clinic, RA patients initiating a new biologic (bDMARD) or targeted synthetic DMARD (tsDMARD) underwent standardized baseline and 3-month follow-up evaluations, including clinical assessments and a comprehensive 36-joint US examination scored using the Global OMERACT-EULAR Synovitis Score (GLOESS). For this analysis, biologic-naïve patients with completed 3-month follow-up were categorized by treatment class: tumor necrosis factor inhibitors (TNFi), Janus kinase inhibitors (JAKi), and other biologics (rituximab, abatacept, or tocilizumab). Demographics, disease activity indices, and US synovitis scores were compared across groups at baseline and follow-up. Changes over time were analyzed to assess early treatment response.

Eighty-six RA patients were included (69.8% female, mean age 55.4 years). Of these, 66 (76.7%) initiated TNFi, 11 (12.8%) JAKi, and 9 (10.5%) other biologics (rituximab: n=2; tocilizumab: n=3; abatacept: n=4). Baseline demographics and clinical features were similar, except that patients in the "other biologics" group were older and baseline deformities were more common among those initiating JAKi (Table). At baseline, disease activity scores and US findings were comparable between treatment groups. After 3 months, all groups demonstrated improvement in both clinical and US measures, with no significant between-group differences. The only observed difference was in the duration of morning stiffness (median: other biologics 0 [0–0] hours; JAKi 0.3 [0–0.5]; TNFi 0.3 [0–0.9]; p = 0.023), primarily driven by differences between TNFi and "other biologics." Numerically more patients on JAKi’s (63.6%) achieved CDAI remission then TNFi’s (47%) and others (44%), although not reached statistical significance. Table-1:

Comparison of sociodemographic characteristics, disease activity indices, and ultrasound scores among treatment groups in the RA cohort

In this real-world cohort of biologic-naïve RA patients, early (3-month) treatment responses assessed by both clinical and US measures were comparable across TNF inhibitors, JAK inhibitors, and other biologics. The findings suggest that short-term improvement in synovial inflammation is largely independent of treatment mechanism. Larger and longer-term studies are warranted to confirm these trends and identify predictors of differential therapeutic response.

Study population included all singleton pregnancies with ≥22 weeks of gestation, July 2008 and December 2024 in Alberta, Canada. Previously validated algorithms based on ICD-10 codes identified women with RA, SpA, PsA and no IMID.[1] We compared maternal characteristics, comorbidities and neonatal outcomes between no IMID and RA/PsA/SpA groups. Dispensation of RA/SpA/PsA medications during pregnancy was evaluated in 2 time periods (2008-2016; 2017-2024). Proportion of days covered (PDC) during pregnancy for each medication was calculated to estimate adherence. In the RA and SpA/PsA groups, logistic regression calculated the odds of delivering preterm and small-for-gestational-age (SGA) infants when exposed to biologics after adjusting for maternal factors.

Among 788,996 pregnancies of 474,197 women, 1627 pregnancies were by women with RA, 1017 with SpA/PsA and 786,352 with no IMID. Among live births, RA pregnancies had higher rates of SGA babies (RA 13%, SpA/PsA 8%, no IMID 10%). RA and SpA/PsA pregnancies had more NICU admissions than without IMID (RA 13%, SpA/PsA 12%, no IMID 10%). Prescription dispensations for RA and SpA/PsA between 2008-2016 and 2017-2024 did not change for corticosteroids (RA 19% to 18%, SpA/PsA 12%), increased in RA for antimalarials (24% to 34%), and pregnancy safe DMARDs (11% to 15%). Biologic uptake and associated mean PDC (SD) increased from 12% (32 (29)) to 23% (58 (33)) in RA and 9% (31(32)) to 26% (71 (31)) in SpA/PsA. In multivariable models, no/low/medium PDC compared to high PDC biologic use was not associated with higher risk of delivering preterm or SGA infants in RA, SpA, and PsA (Table 1). Factors associated with preterm labor in RA women included "Not married" status, preeclampsia and in SpA/PsA - gestational hypertension and pre-eclampsia. Factors associated with SGA included maternal age > 35 years, material deprivation, multiparity, and preclampsia for RA; and multiparity for SpA/PsA. Table 1.

Associations between preterm and small for gestational age deliveries for Albertan women with RA, SpA/PsA* and level of adherence to biologics, and maternal characteristics

Biologic use in the peripartum period has increased in women with RA, SpA, and PsA without negative impacts on preterm labor and SGA. Factors such as pre-eclampsia play a large role in worse peripartum outcomes. Understanding adherence to pregnancy safe medications throughout pregnancy is needed.

[1.] Keeling S. J Rheumatol 2020;47:197-203. Supported by a CIORA grant

We created a cohort of initiators of any advanced IMID therapy using MarketScan administrative health data (2016-2023). Treatment episodes began at initiation and ended after a dispensation/infusion gap of ≥5 half-lives. Episodes were classified as CAT with any 30+ day overlap between advanced therapy classes. Patients were followed from start of the first advanced therapy (time zero) until disenrollment, death, or study end (December 31, 2024). We described baseline characteristics of those exposed to CAT and estimated multivariate hazard ratios (HR) for persistence of the first CAT episode, defined as time until discontinuation of at least one of the combined advanced therapies. We adjusted for baseline age, sex, IMID, comorbidities, conventional synthetic DMARDs (csDMARDs), and glucocorticoids. We also assessed HRs for first serious infection (defined as requiring hospitalization or intravenous antibiotics) comparing person-time on combined vs single advanced therapy, adjusting for the same covariates.

There were 270,198 individuals initiating 693,375 episodes of advanced therapy. Of these, 38,456 individuals (14.2%) initiated 52,212 episodes of CAT. Mean age at CAT initiation was 49 (standard deviation 13.5) years; 62.5% were female. Among 38,456 CAT users, the most common IMIDs were psoriasis, PsO (36.6%), inflammatory bowel disease, IBD (30.0%), rheumatoid arthritis, RA (28.0%) and psoriatic arthritis, PsA (18.9%). Baseline glucocorticoid use was common (44.0%). Among CAT episodes, 51.2% involved TNFα inhibitor exposure (overlapping most commonly with IL17 inhibitors, IL12/23 inhibitors, anti-adhesion molecules, JAK inhibitors or CTLA-4 agonists). Median duration of first CAT exposure was 42 days. Factors associated with lower duration of CAT exposure included RA (HR 1.27, 95% CI 1.24–1.31) and concomitant csDMARDs. Lower HRs were seen with PsO (HR 0.82, 95% CI 0.79–0.84), IBD (HR 0.85, 95% CI 0.83–0.88), and baseline Charlson Comorbidity Index ≥3 (HR 0.77, HR 0.67–0.89). During CAT exposure there were 4.8 serious infections per 100 person-years (95% CI 4.3–5.3). In multivariate analysis, CAT exposure was associated with an increased HR for serious infection (HR 1.20, 95% CI 1.08–1.33) (Table) vs single advanced therapy. Table.

Risk of serious infection associated with combination advanced therapy exposures

In individuals starting advanced IMID therapy, 14.2% had CAT exposures, lasting a median of 42 days. CAT exposure was associated with serious infection risk.

We utilized a mixed-methods approach beginning with a retrospective chart review of all patients seen at the Clinic from January 2022 until June 2025. We concurrently conducted interviews with Clinic rheumatologists, inner-city primary care physicians, and patient representatives to understand specific barriers. Based on these findings, we designed a prospective trial for patients with inflammatory arthritis referred from local inner-city community health centers. The intervention included a $20 honorarium for each follow-up visit they attended with completed bloodwork as well as a Rheumatology-specific outreach service that provided personalized education, advice, and appointment reminders. The primary outcome was the rate of attendance to follow-up visits in the study group compared to historical controls. The study was approved by the UBC REB (H24-03984).

Between January 2022 and June 2025, the Clinic treated 167 unique patients (Table 1). The baseline rate of attendance to follow-up visits was 52.6% overall, and 42.4% among patients with a confirmed systemic autoimmune rheumatic disease. The patient population had high rates of comorbidity: 77% had substance use disorders, while 59% had mental health disorders. Housing instability was nearly universal; 12% of patients were unhoused, while 78% lived in modular, transitional, or single-room occupancy (SRO) housing. At a planned interim analysis of the prospective study (n=9), the rate of adherence to follow-up visits was significantly improved compared to historical controls (90.5% vs 42.4%, p < 0.001). For participants who were previously patients at the Clinic, follow-up rates improved compared to personal priors (87.5% vs 43.5%, p < 0.001). No concerning safety signals were identified.

Standard models of care are often insufficient for marginalized populations. An intervention combining modest financial incentives and specialized outreach support may improve adherence to follow-up in this cohort.

[1.] Rai B. Clin Rheumatol 2022;41:1653-7. [2.] Seta R. Clin Rheumatol 2020;40:413-20. [3.] Vila-Rodriquez F. Am J Psychiatry 2013;170:1413-22. Practice Reflection Award, Best Abstract on Equity Diversity and Inclusion in Rheumatology Award

We conducted a quality improvement project involving postgraduate year (PGY) 4 and 5 rheumatology trainees. Participants completed a baseline survey assessing self-rated confidence in immunology, pathophysiology, drug mechanisms of action (MOA), and exam preparedness on a 5-point Likert scale. Participants also completed a 10-item multiple-choice knowledge test before and after the AI session. Trainees then engaged in 2 20-minute self-directed sessions using ChatGPT with 2 structured prompts focused on disease pathophysiology and pharmacologic mechanisms. Prompts incorporated clinical relevance, analogies, visual metaphors, Socratic questioning, as well as built-in knowledge checks. After completion of the AI session, participants repeated the confidence surveys, knowledge test and provided qualitative feedback via free-text responses. Quantitative results were descriptively analyzed. Qualitative feedback was thematically coded.

Ten trainees completed the study (6 PGY-4, 4 PGY-5). Mean test scores improved from 80% to 98%, with the most substantial gains observed among participants with lower baseline scores. Confidence ratings improved across all domains: immunology (2.2 to 3.2), pathophysiology (2.8 to 3.78), MOA (2.5 to 3.67), and exam preparedness (2.1 to 3.67). Qualitative analysis revealed strong perceived educational value, with participants citing interactivity, real-time feedback, and the ability to simplify complex content as strengths. Areas for improvement included enhanced visuals, interface design, and content accuracy verification.

This pilot study demonstrates the potential of AI-guided educational tools to improve both confidence and knowledge in immunology among rheumatology trainees. While limitations include small sample size and lack of long-term outcome data, findings support further exploration of AI as a scalable and customizable adjunct to traditional instruction. Integration of such tools may enrich specialty training and align medical education with evolving learner needs. Best Abstract By A Rheumatology Resident Award

Consecutive consenting patients with knee pain were recruited from an academic Rheumatology clinic. Each had a knee US and clinical exam, including inspection, bulge sign (BS), balloon/cross-fluctuance (CF), and patellar tap (PT) tests by an experienced rheumatologist. The sonographer was blinded to the clinical findings. Based on published literature, a pathologic knee effusion was defined as a hypoechoic collection measuring >3.2 mm in the lateral recess with quadriceps contraction.[1]

Patients (N=125) had a mean age of 54 + 16 years and 75% were female. Most patients had RA (45%), other inflammatory arthritis (19%), or CTD (14%). Replaced knees (N=4) were excluded. Clinical evidence of effusion was present in 92/246 knees, including 77 with a CF test, either alone (N=42) or in combination with a BS (N=19) or PT (N=16). In 14 knees with a BS alone, 9 were false positive. One knee had a PT alone which was false positive. The prevalence of pathologic knee effusion on US was 35% (87/246). The physical exam (BS, CF &/or PT + for effusion) had moderate sensitivity 71% (95% CI 61, 81), specificity 81% (95% CI 74, 87), PPV 67% (95% CI 57, 77) and NPV 84% (95% CI 77, 89), with an overall accuracy of 78%. False positive results (N=30) were significantly more frequent in patients with BMI > 25 (83%). False negative results occurred mainly with smaller effusions (<6.6 mm). The CF test had the highest agreement (80%) with US (kappa 0.54, p<0.00005) and the best overall performance (ROC area) compared to the BS and PT (p<0.05). The agreement between the physical exam and US was lower if BMI > 25 (kappa 0.44) compared to BMI <25 (kappa 0.64).

The physical exam had moderate diagnostic accuracy for knee effusion. The CF test had the best overall performance in detecting knee effusions in patients with rheumatic diseases, a finding that has not previously been reported. The PT did not add value to the clinical exam in this study. Elevated BMI was associated with reduced accuracy and PPV of the physical exam. Accuracy of knee effusion diagnosis is improved with US, particularly in patients with elevated BMI or small effusions, and is useful for arthrocentesis planning.

[1.] Terslev L. Ultraschall Med 2012;33:E173-E178.

In this 2 phase study, subjects were recruited via a convenience sample of non-rheumatology residents participating in the rheumatology rotation. Phase one consisted of a needs assessment, where surveys were conducted employing open-ended questions as well as quantitative questions using a 5-point Likert scale. Fishbone analysis was completed with relevant stakeholders to outline possible barriers to implementation. Phase 2 consisted of the creation, implementation, and assessment of a novel formal asynchronous learning module using pre and post-completion surveys to obtain qualitative and quantitative feedback to complete a PDSA cycle.

In phase one, 15 residents were surveyed. Over 50% of participants reported both not being exposed to formal teaching during their rotation and not feeling that they had enough formal teaching during their rotation. Basic teaching on common rheumatologic presentations was suggested as the most beneficial topic for teaching. Fishbone analysis (Figure 1) revealed lack of educator’s time, difficulty with scheduling and heterogeneous learning needs as major factors that pose challenges to the implementation of formal teaching that would need to be addressed. In phase 2, preliminary data from 6 residents demonstrated that over 60% of participants rated the content as helpful during their clinical rotation and impacting their clinical practice. Suggested areas for further improvement included the enhancement of topics reviewed and the integration of subspecialty expert opinions.

Historically, non-rheumatology residents have received limited formal teaching during their rheumatology rotations. The implementation of an asynchronous rheumatology curriculum serves as a tool to provide long-term sustainable education to rotating residents. Future work will involve continuing to build curriculum content, and the integration of subspecialist input with iterative PDSA cycles.

[1.] Katz SJ. Clin Rheumatol 2011;30:1081-93.

Medical students and residents completing a rheumatology rotation at the Nova Scotia Rehabilitation and Arthritis Centre were recruited. Participants completed surveys pre- and post-educational module, assessing confidence with knee arthrocentesis, using a five-point Likert scale (1 = strongly disagree, 5 = strongly agree). Participants performed knee arthrocentesis on the 3D knee model twice, once prior to completing an educational module, and again following module completion. Participants were formatively evaluated both pre- and post-learning module, using a standardized grading metric consisting of 18 categories. Pre- and post-module scores were paired and compared using the non-parametric Wilcoxon signed rank test. Descriptive statistics were reported as median and interquartile range (IQR) for non-normal continuous variables and frequency and proportions for categorical variables.

A total of 25 students participated, 12 medical students and 13 residents, ranging from first year medical students to residents in post graduate year 4. Formative assessment scores improved from a median score of 13 out of 18 (IQR 7.5,16) pre-module, to 17 out of 18 (IQR 16,18) post-module (p-value < 0.001) (Figure 1). Within the 18 categories learners scored lowest on "perform pre-procedural time-out" (14% of participants correctly performed) and "post procedure instructions" (24% of participants correctly performed) in the pre module rubric. They improved most in these categories in the post-module rubric, 66% score correctly for "pre-procedural time-out" and 76% score corrected for "post-procedural instructions." Learners’ confidence with arthrocentesis improved from a pre-module median score of 3 out of 5 (IQR 2,4) to post-module median score of 5 (IQR 4,5), with all except 1 study participant showing improvement in post-module scores. Learners rated the use of the module as a valuable learning experience, median 5 (IQR 5, 5) and the use of the 3D arthrocentesis model as valuable to their learning, median 5 (IQR 5, 5). Figure 1.

Box plot of formative evaluation scores pre and post module completion.

The use of a 3D printed knee model for arthrocentesis teaching improved both performance and learner confidence, across various stages of training. Areas of further investigation include assessing retention of knowledge, expansion to other learning sites and utility of other 3D models (other anatomic sites and US compatible models).

The primary question for the SLR was "Which MRI lesion, or combination of lesions, in the SIJ is most sensitive and specific for an MRI considered indicative of axSpA in the SIJ?." Three additional questions addressed an endpoint of clinician diagnosis of axSpA and the extent and location of the lesion(s). The SLR included all studies from January 2017 to July 27, 2025, that included patients with clinically suspected axial SpA undergoing MRI. Studies from a previously published SLR up to January 2017 were also included. Each study selected for data extraction was assessed independently for risk of bias (RoB) by 3 reviewers using the Quality Assessment of Diagnostic Accuracy Studies-2 tool.

Searches in Ovid MEDLINE, Ovid Embase, Scopus, Web of Science Core Collection, and the Cochrane Library gave 1871 unique results for screening in the Covidence tool, of which 35 were selected for data extraction, and 7 were excluded. Only 2 reports described ‘MRI global indicative of axSpA’ as reference criterion for the assessment of MRI lesion definitions and only 5 reports described assessment of MRI lesion definitions in an inception cohort study design. The quantitative component for BME of the ASAS 2009/2016 definitions of a positive MRI lacked specificity. Bone marrow edema (BME) in <4 SIJ quadrants was seen in anterior SIJ slices of antepartum and postpartum women, health individuals, and athletes but in ≥4 SIJ quadrants was specific for axSpA. Erosion and fat lesion were uncommon (<5%) in health individuals and disorders that mimic axSpA (DISH). Erosion in ≥3 SIJ quadrants and fat lesion in ≥5 SIJ quadrants had high specificity for axSpA and was rarely seen in conditions that mimic axSpA. BME adjacent to erosion and/or fat lesion was highly specific for axSpA.

These results reinforce the need to revise previously reported definitions of a positive MRI for axSpA toward more stringent MRI cut-offs that detail the extent and location of MRI lesions.

[1.] Maksymowych W. [Abstract]. Arthritis Rheumatol 2025;77 Suppl 9. https://acrabstracts.org/abstract/the-assessments-in-spondyloarthritis-international-society-asas-and-spondyloarthritis-research-and-treatment-network-spartan-revised-classification-criteria-for-axial-spondyloarthritis-developmen/

The multicenter Screening for Axial Spondyloarthritis in Psoriasis, Iritis, and Colitis (SASPIC) Study at 9 sites is aimed at early detection of axSpA in consecutive patients presenting with undiagnosed back pain to the rheumatologist. Consecutive patients ≤45 years of age with ≥3 months undiagnosed back pain with any 1 of psoriasis, acute anterior uveitis (AAU), or colitis diagnosed by the relevant specialist had routine clinical evaluation by a rheumatologist for axial SpA. The rheumatologist determined the presence or absence of axial SpA at 3 consecutive stages: 1. After clinical evaluation; 2. After results of labs (B27, CRP), radiography; 3. After results of MRI evaluation. All MRI scans were evaluated by 3 central readers whether the MRI was indicative of axSpA. In SASPIC 1 patients had MRI done as deemed appropriate by the rheumatologist, whereas all patients in SASPIC-2 had MRI. Final diagnosis by the rheumatologist was used as gold standard to test the performance of the criteria according to sensitivity and specificity [95% CI], emphasis being on attainment of high specificity.

A total of 363 patients were recruited to the SASPIC cohorts (n=212 SASPIC 1, n=151 SASPIC 2) of whom 308 had MRI evaluation. The proportions of patients diagnosed with axSpA were 46.7%, 61.6%, and 46.8% for those with PsO, AAU, and IBD, respectively, in SASPIC-1, whereas the respective proportions were 23.5%, 57.9%, and 23.3% for SASPIC-2. Patient demographics and disease characteristics were similar between those with and without an MRI scan and with the patients recruited to the 2025 ASAS-SPARTAN cohort from which the criteria were developed. Sensitivity/specificity [95% CI] were 56.5 [47.3-65.3]/98.9 [96.1-99.9] for the entire cohort, and 59.7 [46.4-71.9]/ 97.6 [87.1-99.9], 52.8 [35.5-69.6]/ 100.0 [95.8-100.0], 53.9 [33.4-73.4]/ 98.3 [90.8-100.0] for the subgroups with AAU, IBD, or PsO, respectively. Performance in the 2025 ASAS-SPARTAN cohort using central reader imaging data was 56.6 [49.2, 63.7]/ 98.5 [96.5, 99.4] in testing data and 63.1 [56.1, 69.5]/98.7 [96.8, 99.5] in validation data.

The revised axSpA criteria perform with consistently high specificity in the 2025 ASAS-SPARTAN and SASPIC cohorts.

[1.] Maksymowych W. [Abstract]. Arthritis Rheumatol 2025;77 Suppl 9. https://acrabstracts.org/abstract/the-assessments-in-spondyloarthritis-international-society-asas-and-spondyloarthritis-research-and-treatment-network-spartan-revised-classification-criteria-for-axial-spondyloarthritis-developmen/

Serum samples from 159 patients with a rheumatologist confirmed diagnosis and classified as r-axSpA (AS-modified New York criteria) were tested on the anti-14-3-3 multiplex assay. The serum differential expression of autoantibodies to 14-3-3, CRP and HLA-B27 between patients with r-axSpA and MBP was evaluated by ROC AUC. Regression models combining the auto 14-3-3 AAb Score derived from the Bath study were tested in 2 predictive models: 1 with CRP and HLA-B27 markers only and the other adding Age and Sex variables. Corresponding specificity (SP), sensitivity (SN), predictive values (PPV, NPV), likelihood (LR) and diagnostic odds ratios (DxOR) are provided. The Akaike Information Criterion (AIC) statistical measure was reported to compare the relative quality of predictive models.

Mean age of patients with r-axSpA was 42 (69% male) and for MBP, 30 years (59% male). Differential expressions of each of the biomarkers delivered significant ROC AUCs; 0.70 for autoantibodies to 14-3-3, 0.81 for CRP and 0.84 for HLA-B27. The latter 2 delivered respectively higher DxOR (6.2, 11.1, 24.1) as expected, considering that they were used in patient diagnosis. The model that included the auto 14-3-3 AAb score with CRP and HLA-B27 added had better discrimination of patients with axSpA vs MBP with an AUC of 0.93 and DxOR of 39.6 that further improved to an AUC of 0.94 and DxOR of 95.3 when age and sex variables were added. As shown below (Table 1), the AIC of the predictive models supported the full model as the best fit. Table 1.

Marker and model performance

This study demonstrates that auto 14-3-3 AAb score when added to currently used CRP and HLA-B27 markers, improves the differentiation of people with MBP from established r-axSpA. While the pretest probability of CRP and HLA-B27 performance is higher in this cross-sectional study than would be expected in an early referral cohort, including 14-3-3 AAb score may reduce diagnostic delay and potentially enable more confident and prompt initiation of therapy to improve outcomes.

A mixed-methods design integrating in vitro and in vivo approaches was employed. Bone-marrow-derived macrophages (BMDMs) from C57BL/6 and SKG mice, and human THP-1 macrophages, were stimulated with LPS (100 ng/mL). MOP isoforms (murine: 37, 11, 246; human: 212, 217, 220) and cytokines (IL-1β, IL-10) were quantified by RT-qPCR. Lentiviral constructs (pLenti-MOP 212, 220) were packaged in HEK293T cells (psPAX2 + pMD2.G) and used to transduce THP-1 cells. Phospho-flow cytometry assessed NF-B (p65) and MAPK (ERK1/2) activation, while curdlan-treated SKG mice served as an in vivo model of autoimmune inflammation (Figure 1.2).

Our results demonstrate that MOPs expression were significantly induced upon LPS stimulation in both murine and human macrophages (Figure 1.3-4). In BMDMs, MOP 37, 11, and 246 peaked at 6 h post-LPS, paralleling IL-10 expression. In THP-1 cells, MOP 212 and 217 were progressively upregulated to 48 h. In the SKG in-vivo model, MOPs were elevated, validating the relevance of these pathways (Figure 1.5). MOP-220 overexpression in THP-1 cells selectively enhanced NF-B and reduced ERK signaling (Figure 1.6), leading to upregulation of inflammatory cytokines (IL-1β, TNF-α) at the mRNA level. Together, findings highlight MOPs as potential modulators of inflammatory signaling (Figure 1.7).

This study identifies and characterizes MATH-only proteins (MOPs) as novel regulators of inflammation. MOPs expression is dynamically induced by TLR activation in murine and human systems and correlates with cytokine responses in vivo. These findings suggest that MOPs may modulate NF-B and MAPK-driven cytokine signaling, providing a new molecular framework for immunoregulation. Ongoing MOPs overexpression and knockout studies aim to delineate their mechanisms in chronic inflammation and autoimmune disease.

[1.] Abdul-Sater AA. Nat Immunol 2017;18:26-35. [2.] Nakamura A. Sci Transl Med 2021;13:eabg1210. [3.] Hu YH. Cell Mol Immunol 2021;18:1708-17.

Data from the Rheum4U Precision Health Registry, including adults (> 18 years) with IA receiving care at a rheumatology clinic in Calgary/Canada, were analyzed. The first registry visit with complete Clinical Health Assessment Questionnaire (ClinHAQ) and the Work Productivity and Activity Impairment questionnaire (WPAI) was included. ClinHAQ scores categorized participants into minimal/no, mild, moderate, or severe disability. WPAI domains (absenteeism, presenteeism, overall work impairment, and activity impairment) were scored ranging 0-100%, with higher values indicating greater impairment. Kruskal-Wallis tests evaluated differences across disability levels, and Dunn’s post-hoc tests with Bonferroni correction identified pairwise differences.

Among 1,337 participants (68% women; median age 52 [IQR 39-62] years), 59% had minimal/no disability, 18% mild, 21% moderate, and 2.5% severe functional disability. The median time since diagnosis was 7.2 [IQR 2.5-13.1] years. Significant differences were observed across all WPAI domains (p<0.001), with activity impairment showing the largest differences. Post-hoc analyses revealed that absenteeism, presenteeism, overall work impairment, and activity impairment increased progressively with functional disability, with the most consistent and statistically significant differences observed at moderate levels compared with minimal/no disability. Comparison involving mild disability also showed significant, though smaller, differences relative to minimal/no disability. Differences involving severe disability compared with minimal/no disability were generally smaller or non-significant, likely due to the small number of participants in this group. Activity impairment differed significantly across all disability levels, including comparisons involving severe disability.

In adults with IA, work productivity and activity impairment worsen progressively with increasing functional disability. Most notable productivity declines were detected at moderate ClinHAQ levels. These begin at mild disability but reach a clinically meaningful threshold once functional limitations are moderate. These results offer practical insights for early interventions aimed at preserving physical function. Implementing strategies when patients have minimal/no or mild disability may help maintain productivity and support patients’ participation in daily and work-related activities.

Human spinal tissue from axSpA patients and spinal trauma controls was analyzed by immunohistochemistry (IHC) to localize DRAK2 expression, and by immunofluorescence (IF) to compare expression between CD4⁺ and CD8⁺ T cells. PBMCs from patients and controls were sorted by fluorescence-activated cell sorting (FACS), and STK17B expression in each subset was quantified by qPCR. Parallel IHC was performed on ankle, tail, and ileum of curdlan-treated and PBS-treated SKG mice. To corroborate findings at higher resolution, STK17B expression in mature CD4⁺ and CD8⁺ T cells was queried from our pre-biologic single-cell RNA-sequencing and multiome datasets.

In human spinal tissue, DRAK2⁺ immune infiltrates were more abundant in axSpA than in controls (Figure 1A), with stronger IF staining in CD4⁺ than CD8⁺ T cells. In PBMCs, STK17B was preferentially expressed in CD4⁺ T cells and trended higher in axSpA compared with controls. Single-cell and multiomic analyses confirmed this pattern, showing modest STK17B increases in CD8+ T cells but markedly higher levels in CD4+ T cells of axSpA patients, particularly in effector T cells and Tregs. Notably, pre-biologic STK17B expression was higher among patients who were later identified as non-responders to IL-17i compared with responders (Figure 1B). Consistent with the human findings, curdlan-treated SKG mice exhibited increased DRAK2⁺ infiltrates in ankle, tail, and ileum relative to PBS-treated controls, paralleling the observation in human tissues (Figure 1C). Figure 1.

(A) Histopathology of spinal tissues from AS and control patients with IHC staining for anti-DRAK2. (B) STK17B expression in mature CD4+ T cells of pre-biologic axSpA patients and controls. (C) Histopathology of the tissues from curdlan- vs PBS-SKG mice for anti-DRAK2.

Across humans and mouse models, STK17B/DRAK2 expression is increased in inflammatory lesions and enriched in CD4⁺ effector and regulatory T cells, particularly in patients with inadequate IL-17i response. These findings suggest that DRAK2 upregulation contributes both to axSpA-related inflammation and to treatment resistance, warranting further mechanistic investigation.

[1.] Ramos S. J Immunol 2008;181:7606-16. [2.] Mandarano A. Cell Rep 2023;42:112106. [3.] Talukdar A. [Abstract]. Arthritis Rheumatol 2024;76 Suppl 9.

UPSTAND (NCT04846244) is a 12-month, multi-country observational study in adult patients with axSpA for whom, prior to and independent of the study enrollment, the treating physician has decided to prescribe UPA, per local label. Patients had Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and total back pain scores ≥4 at baseline and an inadequate response or intolerance/contraindication to NSAIDs. Co-primary endpoints are 1) total spinal pain score <4 and ≥2unit improvement from baseline at Week 12, and 2) maintenance up to Week 52 (not available). Secondary endpoint measures include patient assessment of spinal, total back, and nocturnal back pain, painDETECT for capturing neuropathic pain, Widespread Pain Index (WPI) and Symptom Severity Scale (SSS) for capturing nociplastic pain, Ankylosing Spondylitis Disease Activity Score (ASDAS), and BASDAI. This interim analysis reports data through 20-Jun-2024; at cutoff, all patients had completed at least the Week 12 visit. Results are presented as observed cases using descriptive statistics.

A total of 71 Canadian patients were included in this analysis (mean age: 51.3 years [SD: 12.5]; female gender: 52.1%; mainly White [90.1%] or Asian [8.5%]). Most patients had radiographic axSpA (97.1%) and 70.1% experienced symptoms of axSpA for ≥10 years (mean duration 18.3 years). The primary endpoint of a total spinal pain score <4 and a ≥2-point improvement from baseline at Week 12 was achieved by 31.7% (n/N = 13/41) of patients with a baseline score ≥4. The mean total (7.0 to 5.3) and nocturnal (6.6 to 5.0) back pain decreased rapidly over the first 2 weeks of treatment with further reduction up to Week 52 (Figure 1A/B). Treatment with UPA reduced both painDETECT (12.8 to 9.0) and WPI (7.6 to 6.1) from baseline to Week 52 (Figure 1C). Similarly, improvement in axSpA composite measures of disease activity was observed using the ASDAS and BASDAI (Figure 1D). UPA was generally well-tolerated, and its safety profile was consistent with observations made across randomized clinical trials (RCTs). Figure 1.

Effectiveness of Upadacitinib to Improve Pain and Disease Severity in Axial Spondyloarthritis

These interim results show that Canadian patients with axSpA treated with UPA in the real-world setting have rapid and consistent improvement in pain (including measures reflecting neuropathic and nociplastic components) and in disease activity. This improvement in pain and disease control is consistent with data from RCTs.

The study enrolled patients with gastrointestinal conditions (Crohn’s disease [CD], ulcerative colitis [UC]), rheumatological conditions (rheumatoid arthritis [RA], ankylosing spondylitis [AS], psoriatic arthritis [PsA]), or dermatological conditions (hidradenitis suppurativa [HS], psoriasis [PsO]). Participants were eligible if their treating physician had decided to switch them from low-concentration RP or alternative adalimumab biosimilar to AVT02. The study assessed ISP measured via the Visual Analog Scale (VAS), adherence via the compliance rate, patient satisfaction and perception of change in pain via the Likert scale, quality of life based on EQ-5D-5L, and disease activity via the patient and physician global assessment scores for participants up to Day 180 after switching.

The intention-to-treat (ITT) population comprised 324 participants. Following the first administration of AVT02, injection site VAS pain score decreased by an average of –19.9 ± 26.13 across the whole population. Supporting this, 76% of the participants perceived AVT02 as less painful as measured by the 5-Likert scale. Moreover, a significantly lower number of patients experienced ISRs after their first dose of AVT02 (36 patients; 12.4%) compared with their last dose of low-concentration adalimumab (124 patients; 42.3%). Adherence rate was 93.4% overall. The ITT population maintained a high patient satisfaction (more than 74.4% reported being ‘mostly or completely satisfied’) and a high quality of life score (EQ-5D-5L score of >82 on a scale of 1-100) after switching from RP to AVT02. There were generally no changes in patient and physician reported outcomes nor in healthcare utilization.

The results of this study demonstrate that switching from RP or alternative biosimilar adalimumab to AVT02 leads to decreased ISP across all indications, fewer numbers of ISRs, and a maintenance of high adherence rates, patient satisfaction, and quality of life among patients.

[1.] Sacristán JA. PLoS One 2020;15:e0234705. [2.] Kuek A. Postgraduate Medical Journal 2007;83:251. [3.] Feldman SR. BioDrugs 2021;35:735-748.

CLOSE-UP was a prospective, observational post-marketing study conducted at 33 sites in Canada in adults with moderate-to-severe RA who were treated with UPA 15 mg once daily. UPA initiation was decided before study participation. Patients were followed for 24 months after UPA initiation with data collected at routine clinic visits. The primary endpoint was the proportion of patients achieving a Disease Activity Score 28 Joint Count - C-reactive protein (DAS28-CRP) < 2.6 at 6 months. Secondary endpoints included pain score using a visual analog scale, fatigue (FACIT-F), physical function as measured by the Health Assessment Questionnaire-Disability Index (HAQ-DI), and other assessments of disease activity including Clinical Disease Activity Index (CDAI) score. Patients were grouped by prior/most recent exposure to no b/tsDMARDs (bio-naïve), ≤2 bDMARDs but no tsDMARD (bio-experienced), and a maximum of 1 bDMARD followed by a tsDMARD (tsDMARDexperienced). Data are presented as observed and summarized descriptively.

Analysis included 412 patients, with 47.1% identified as bio-naïve, 41.3% as bio- experienced, and 10.7% as tsDMARD-experienced. At baseline, most patients (84.5%) exhibited a DAS28-CRP > 3.2. After 6 months of UPA treatment initiation, 60.7% of patients achieved a DAS28-CRP < 2.6 (primary endpoint) and 75.6% achieved a DAS28-CRP ≤ 3.2 with a response rate maintained for up to 24 months (Figure 1a). Similar trends were observed using CDAI definitions for clinical remission and low disease activity. The type of prior/most recent DMARD exposure did not impact response. Additionally, the proportion of patients achieving a DAS28-CRP < 2.6 at the 6-month visit were similar between those on UPA monotherapy (62.7%) and those on UPA in combination with a csDMARD (60.1%). Improvements in pain score, fatigue, and physical function were observed throughout the study (Figure 1b). At 6 months, 86.5% of patients persisted in their treatment on UPA and 67.5% persisted up to Month 24. The safety profile of UPA was consistent with that seen in Phase 3 trials with no new safety signals.

Consistent with clinical trial findings, this real-world Canadian study demonstrated a reduction in disease activity and improvements in patient-reported outcomes, supporting a favorable benefit-risk profile for patients treated with UPA. Notably, response rates were consistent irrespective of prior bDMARDs/tsDMARDs use or concomitant csDMARD.

BE MOBILE 1/2 (NCT03928704/NCT03928743) included a 16-wk double-blind and 36-wk maintenance period. Patients received BKZ 160mg every 4 wks (Q4W) or placebo (PBO) to Wk16; thereafter, all received BKZ. Sex-stratified outcomes reported to Wk52: ASAS40, ASDAS<2.1, BASDAI, Ankylosing Spondylitis Quality of Life Questionnaire (ASQoL), and objective signs of inflammation (OSI; MRI SPARCC SIJ, MRI Berlin spine, hs-CRP). Wk16 BKZ vs PBO efficacy between males vs females were compared using adjusted relative odds ratios (rOR; logistic regression) and relative differences (RD; ANCOVA). Analyses were post-hoc (no p values).

220/254 BE MOBILE 1 (male: 124/138 [89.9%]; female: 96/116 [82.8%]) and 298/332 BE MOBILE 2 patients (male: 215/240 [89.6%]; female: 83/92 [90.2%]) completed Wk52. At baseline, females had longer mean symptom duration (years; non-radiographic [nr]-axSpA: 11.1 vs 7.2; radiographic [r]-axSpA: 15.0 vs 12.9) and lower HLA-B27 positivity (%) (nr-axSpA: 69.0 vs 84.8; r-axSpA: 78.3 vs 88.3) than males; males had lower mean ASQoL scores (nr-axSpA: BKZ: 8.5 vs 10.8, PBO: 8.6 vs 10.2; r-axSpA: BKZ: 8.3 vs 11.1, PBO: 8.4 vs 9.0), and generally higher OSI values than females. Across ASAS40, ASDAS<2.1, and BASDAI, rORs and RDs demonstrated greater Wk16 BKZ vs PBO treatment effect in males vs females (Figure 1). At Wk52, responses were higher in males with nr-axSpA than females, but comparable in r-axSpA. Overall, at Wk52, both sexes responded well in both trials, with >50% of BKZ-randomized patients achieving ASAS40, >40% achieving ASDAS <2.1, and BASDAI score improvements. For ASQoL, both males and females demonstrated substantial improvements with BKZ at Wk16 (nr-axSpA: –5.5 vs –4.8; r-axSpA: –4.8 vs –5.5) compared with PBO (nr-axSpA: –2.1 vs –2.9; r-axSpA: –3.1 vs –3.7). Improvements continued to Wk52 with BKZ (nr-axSpA: BKZ: –5.7 vs –6.2, PBO/BKZ: –5.5 vs –5.1; r-axSpA: BKZ: –5.4 vs –6.5, PBO/BKZ: –5.5 vs –5.8). For change from baseline in OSI outcomes, RDs indicated a higher Wk16 BKZ vs PBO treatment effect in males than females; absolute OSI values were comparable between males/females and maintained or improved to Wk52 with BKZ. Figure 1.

ASAS40, ASDAS<2.1 and BASDAI to Wk52 and relative odds ratios and relative differences at Wk16, stratified by sex

Wk16 BKZ vs PBO treatment effect trended higher among males than females. By Wk52, females showed improvement in longer-term BKZ response, approaching levels comparable to males. Overall BKZ efficacy was demonstrated across clinical, patient-reported, and OSI outcomes in both sexes across the full axSpA disease spectrum.

We searched MEDLINE and Embase (inception to August 15, 2025) to identify studies of screening tools used to detect SpA in both pediatric and adult IBD patient populations. Review articles, opinion-based articles, conference abstracts, incomplete publications and non-English studies were excluded. Screening of studies for eligibility was performed on Covidence, with conflicts resolved by consensus among 3 reviewers. Data was extracted and synthesized.

Of 568 studies identified, 14 studies were included. All identified studies reported on adults with IBD. Six studies reported on the validation of SpA screening tools, including DETAIL (n=3), IBIS-Q (n=2), and structured clinical screening criteria used in individual studies. Validation studies demonstrated that screening tools such as DETAIL and IBIS-Q showed moderate-high sensitivity ranged 43-92.7% and specificity 62-89.8%, with ≥3 positive items consistently corresponding to a high post-test probability of SpA ranging from 75.0-81.9%. These same scales, along with diagnostic imaging, were used to determine the prevalence of SpA among people with IBD. The prevalence of SpA or sacroiliitis among adults with IBD ranged from approximately 5-30%, with many cases previously unrecognized in routine care. All included studies were conducted in academic or tertiary referral centers.

DETAIL and IBIS-Q are validated tools that can be used for early detection and referral of SpA among adults living with IBD. Study design evaluating the prevalence of SpA using these tools were heterogenous, leading to varied prevalence estimates. All included studies were from referral centers where patients often have more complex IBD presentations which may influence prevalence estimates and limit generalizability to community practice. Coordinated efforts between gastroenterology and rheumatology will be critical to refine, validate, and implement IBD-appropriate tools that support integrated, patient-centered care. This is critical in the pediatric population where there is a complete absence of screening tools.

Following PRISMA guidelines, an initial search was completed on MEDLINE (Ovid) to generate keywords and was followed by extensive searches on MEDLINE, Embase, PsychINFO and CINAHL (1806-August 2025). Eligible studies examined MH concerns for CWJIA and/or their caregivers reporting on the incidence or prevalence of MH disorders, symptoms, cognitive functioning, or positive MH indicators. Four reviewers independently screened and extracted data using Covidence, with quality assessment planned using JBI critical appraisal tools.

A total of 30 studies met the inclusion criteria, with most studies being of cross-sectional design. MH disorders (n=18) and MH symptoms (n=17) were most frequently evaluated. Anxiety and depression were the most reported MH disorders, consistently showing higher prevalence among CWJIA than healthy controls. JIA was shown to impact cognitive functioning (n=7), with several studies exploring its impact on school performance. Positive MH indicators (n=3 studies) such as resilience and adaptive coping emerged as potential protective mechanisms against poor MH outcomes. Caregiver MH was evaluated in 3 studies, all describing elevated distress associated with caring for CWJIA (Figure 1). Figure 1:

Sample results from a subset of included studies for each domain examined.

This systematic review highlights the scarcity of literature describing the burden of MH concerns among CWJIA and their caregivers. The higher prevalence of negative MH indicators in this population, along with the protective effects suggested by positive MH indicators underscores the need for studies of family-centered interventions to strengthen the psychosocial well-being of CWJIA and their caregivers.

[1.] Statistics Canada. https://www.statcan.gc.ca/o1/en/plus/7642-rising-mental-health-concerns-among-youth.

Data are reported for 2 pools, each comprising 1 Phase 2b and 2 Phase 3 studies and their open-label extensions, in patients with axSpA and PsA, respectively (data cut-off in axSpA: September 2024; PsA: August 2024). Uveitis events were identified using the preferred terms "autoimmune uveitis", "iridocyclitis", "iritis", and "uveitis", classified using the MedDRA v19.0; "acute anterior uveitis" was not a specific preferred term available in MedDRA v19.0. Uveitis rates and exposure-adjusted incidence rates (EAIR) per 100 patient-years (PY) for patients who received ≥1 BKZ 160 mg every 4 weeks (Q4W) dose are reported separately for axSpA and PsA, respectively.

Patients with axSpA (N=848) and PsA (N=1,409) had a mean (standard deviation [SD]) age of 40.3 (11.9) and 49.3 (12.4) years, respectively. Mean (SD) time since diagnosis was 6.1 (7.8) years in patients with axSpA and 7.0 (8.0) in patients with PsA. Of patients with axSpA, 130 (15.3%) had a history of uveitis (PsA: 21 [1.5%]). Most patients with axSpA were HLA-B27 positive (717/848 [84.6%]). In patients with axSpA across the pooled Phase 2b/3 data, BKZ exposure was 2,748.9 PY. In total, uveitis occurred in 33/848 (3.9%; EAIR [95% CI]: 1.2/100 PY [0.8, 1.7]) patients overall and in 20/130 (15.4%; 5.0/100 PY [3.0, 7.7]) patients with history of uveitis. In patients without a history of uveitis, 13/718 (1.8%; 0.6/100 PY [0.3, 1.0]) patients had uveitis events (Figure 1). Most events were mild/moderate, 1 was severe; 2 (0.2%) patients discontinued treatment due to uveitis. Incidence of uveitis in patients with PsA was low across the pooled Phase 2b/3 data (total BKZ exposure: 4,264.7 PY); uveitis occurred in 4/1,409 (0.3%; 0.1/100 PY [0.0, 0.2]) patients overall; 2 had a history of uveitis. No uveitis events led to treatment discontinuation. Figure 1.

Incidence of uveitis in patients with axSpA stratified by history of uveitis

Over 3 years of BKZ treatment, the incidence of uveitis in patients with spondyloarthritis receiving BKZ long-term was low.

Nine pregnant individuals with seronegative inflammatory arthritis who were treated with IL-17 inhibitors were identified through the Pregnancy and Rheumatic Diseases Clinics at 2 Canadian centers. Clinical data were prospectively extracted by a trained research assistant using REDCap, electronic medical records, and relevant consult notes. Outcomes of interest included maternal disease activity during pregnancy, pregnancy complications, neonatal outcomes, and the presence of congenital anomalies.

These patients were managed throughout all trimesters of pregnancy and followed for 6 weeks postpartum. The mean maternal age at conception was 34 years. Patient characteristics are summarized in Table 1. Pregnancy complications included gestational diabetes, preeclampsia, chorioamnionitis, gestational hypertension, and COVID-19 infection. Ankyloglossia was noted in 1 infant (P5). Neonatal complications included jaundice not requiring intervention (P4) and transient hypoglycemia and transaminitis (P7) (Table 1). Table 1.

Patient characteristics including: maternal age at conception, diagnosis, gravidity, current biologic therapy, gestational age (GA) at delivery, mode of delivery, fetal birth weight, congenital malformations

In this prospective case series, IL-17 inhibitor exposure during pregnancy was not associated with an increased risk of major congenital anomalies or serious adverse neonatal outcomes. Although encouraging, these results are preliminary and do not establish safety. Confirmation in larger, controlled cohorts is needed. Larger, multicenter studies are needed to confirm these observations and better inform clinical guidance.

This study is part of an ongoing prospective data collection using a single-visit, cross-sectional design. Participants were consecutively recruited from 2 clinical settings within our rheumatology program: (1) the AxSpA Triage Clinic (FASTRAX*), which evaluates patients with suspected AxSpA, and (2) the ORCHESTRA (Ottawa Rheumatology CompreHEnSive TReatment and Assessment) Clinic, which follows patients with established, active AxSpA requiring biologic therapy and managed through a standardized approach. Demographic and clinical data were collected, including place of birth, and symptom duration. Diagnostic confirmation of AxSpA was made by a rheumatologist based on clinical evaluation and imaging findings. The primary outcome was diagnostic delay, defined as the time interval from symptom onset to rheumatologist-confirmed diagnosis of AxSpA. Immigrant status was determined by country of birth (Canada-born vs foreign-born). Comparative analyses were performed between immigrant and non-immigrant patients.

A total of 81 patients were enrolled to date (44 females and 37 males). AxSpA was confirmed in 51 patients, while 30 were determined to have non-SpA back pain. The mean duration from symptom onset to final diagnosis (or exclusion) was 10.1 years (SD ±10.8) overall, 9.6 ±10.8 years among patients diagnosed with AxSpA, and 11.1 ±11.2 years among those with non-SpA back pain. Of the total cohort, 67 patients were Canadian-born and 14 were immigrants. Among Canadian-born patients, 41 were diagnosed with AxSpA, with a mean diagnostic delay of 8.8 years (SD ±10.7). Among immigrants, 10 were diagnosed with AxSpA, with a longer mean diagnostic delay of 12.7 years (SD ±10.9). In parallel, perceived delays in care showed same trends: within immigrant patients, 40% stated moderate-severe delays for access to rheumatology and 30% for imaging, compared to non-immigrants (22% for access to rheumatology; and 7.5% for the imaging) (Table 1). Table 1.

Perceived Delays in Referrals to Rheumatology and Imaging Service

Our pilot data suggest longer diagnostic delays in AxSpA among immigrant patients compared with those born in Canada. Although the sample size is small and lacks statistical power, consistent trends indicate potential inequities in access to rheumatology assessment and imaging. These findings highlight the importance of considering social and systemic factors that may contribute to diagnostic disparities.

The study analyzed genetic summary data from 1,462 AS patients and 164,682 controls, all of whom had undergone genome-wide association scans, as identified from the FinnGen consortium. Large-scale plasma protein quantitative trait locus (pQTL) data were sourced from the UK Biobank Proteomics Project (UKB-PPP; 2,923 unique proteins), the INTERVAL study (2,995 unique proteins), and the Icelandic study (4,719 proteins).[1] Potential protein candidates were identified based on SNP associations with proteins (p < 5x10^-8), followed by linkage disequilibrium (LD) clumping to identify independent pQTLs for each protein (r^2 < 0.001), and defining SNPs when the leading SNP was located within 500kb of the transcription site of the protein-coding gene. A 2-sample MR analysis was then conducted, using the Wald ratio for genes with 1 SNP and inverse variance weighting (IVW) for those genes with multiple SNPs. Sensitivity analyses, including tests for pleiotropy and heterogeneity, were performed to ensure robustness of the causal estimates.

A total of 21 unique proteins were identified as being associated with the risk of AS. In the UKB-PPP dataset, 3 proteins were linked to an increased risk of AS (DXO, LTA, AGER), while 6 proteins associated with a decreased risk (TRIM40, LTB, AIF1, HLA-E, MICB_MICA, CFB). The INTERVAL dataset identified 5 proteins correlated with an elevated risk of AS (IL-23R, TNXB, CFB, MICB, ERAP1) and AGER protein was linked to a reduced risk. From a 2021 dataset,[1] MR identified 8 proteins significantly associated with AS (HLA-DQA2, ERAP1, MICB, BTN3A3, TAPBP, C2, CFB, TNXB and 7 proteins with decreased risk NCR3, HSPA1L, MICA, VARS, APOM, AIF1, AGER). The top 6 Reactome pathways identified from pathway enrichment analysis included Immune system, cytokine signaling, adaptive immune system, adaptive immune system, innate immune system and signaling by interleukins (1 x10^-6).

This proteome-wide MR study identified 21 unique proteins associated with AS risk, offering novel insights into the disease’s pathogenesis. These prioritized proteins also present potential druggable targets, warranting further investigation to explore novel therapeutic opportunities.

[1.] Ferkingstad E. Nat Genet 2021;53:1712-21.

This was a retrospective chart review. Using electronic medical records from 4 community rheumatologists in Southwestern Ontario, a computerized search was performed to identify all patients newly diagnosed with axSpA between January 2011 to January 2021 who had an MRI-axSpA protocol performed at SJHH. MRI reports were reviewed to determine the presence of isolated spondylitis vs sacroiliitis with or without spondylitis. Patient characteristics including age, sex, HLA-B27 status, CRP and ESR at the time of MRI, personal and family history of psoriasis or psoriatic arthritis, personal and family history of inflammatory bowel disease, and family history of axial spondyloarthritis/ankylosing spondylitis, were also extracted. Data analysis was performed using logistic regression with missing data imputed using the CART method.

A total of 1,356 patient charts were identified and 135 patients fulfilled inclusion criteria. The mean age was 42 (± 14) and 55% were female. Of these, 126 patients (93%) had sacroiliitis with or without spondylitis and 9 (7%) had spondylitis alone. A sacroiliac-only protocol would have identified 93% of axSpA cases. Patients with isolated spondylitis were more likely to have a personal or family history of psoriatic arthritis (OR 6.77, 95% CI [1.18, 38.76]). We further approximated cost and time savings to be $700 and 30 minutes per scan, or ~$94,500 and 67.5 hours, respectively, over 10 years for this study cohort.

A sacroiliac-only MRI protocol maintains high diagnostic yield while reducing costs and the time an MRI machine is occupied. However, clinicians should consider spine imaging in select patients specifically those with a personal or family history of psoriasis or psoriatic arthritis. Larger studies are warranted to validate these findings and to better define the role of spinal MRI in patients with suspected axial PsA.

Secukinumab treatment response, as determined using BASDAI50 scoring at week 24, stratified patients into responders (SEC-R) and nonresponders (SEC-NR). Multiome Sequencing was performed on CD4+ T cells from 3 SEC-R patients, 3 SEC-NR patients, and 2 healthy controls.

SEC-R patients had an increased PU.1 CD4+ T cell cluster that had high expression of genes associated with the type 1 interferon (IFN) pathway. SEC-R patients have transcripts elevated in ATP synthesis and cytotoxic molecular functions. SEC-R patients have increased cytotoxic gene transcripts compared to SEC-NR patients. SEC-NR patients appear to have an altered TGFβ signaling pathway likely mediated through RELA and NFKB1. Although SEC-NR Tregs appears more responsive to TGFβ, there is higher expression of IFN genes in the Treg cluster compared to SEC-R.

SEC-NR patients demonstrate enhanced IFN production that is dissociated from cytotoxic potential. This may occur due to increased SMAD7 activation of NFKB1 which prevents cells from differentiating into cytotoxic T cells and maintains a pro-inflammatory effector phenotype. Type 1 IFN is overrepresented in SEC-R patients before secukinumab treatment and elevated after treatment in SEC-NR patients. Regulation of type 1 interferons may therefore play an important role in influencing treatment response to secukinumab in axSpA.

A cross-sectional retrospective study was conducted among children aged 12-18 years diagnosed with JSpA/Enthesitis Related Arthritis (ERA) using the 2019 PRINTO criteria. Patients attending the SickKids JSpA Clinic (Oct 2024-Sept 2025) were screened for mental health symptoms using the Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), and PROMIS 37 v1.1 tools, as part of a hospital-wide measurement-based care initiative. Additional data included demographics, disease characteristics (age of onset, duration, joint/entheseal involvement), disease activity scores (cJADAS, BASDAI), and Physician Global Assessment (MDPGA). Descriptive statistics were calculated, and Spearman correlations determined relationships between PROMIS measures and disease variables. Ethics approval was obtained from the SickKids REB.

Thirty-one patients were included (Table 1). 84% were male, mean ± SD age at onset was 15.7 ± 1.7 years, and mean disease duration was 47 ± 36.4 months. Joint involvement at diagnosis was peripheral (32%), axial (26%), or mixed (39%). Over 90% were on biologics; only 23% had active joints at the screening visit. The PHQ-9 and GAD-7 were completed by n=20, and PROMIS-37 by n=26. Elevated depressive symptoms on the PHQ-9 were reported by 65% (n=13) - 40% mild, 5% moderate and 20% severe. Elevated anxiety symptoms on GAD-7 were reported by 60% (n=12)- 30% mild, 15% moderate, and 15% severe. On average, PROMIS scores indicated good physical functioning and peer relationships. Correlation analysis showed significant positive associations between self-reported disease activity (BASDAI) and depression ( = 0.690, p = 0.001), fatigue ( = 0.807, p < 0.001), pain interference ( = 0.672, p = 0.001) and pain intensity ( = 0.744, p = 0.001). cJADAS scores were significantly correlated with pain intensity ( = 0.734, p = 0.001) and pain interference ( = 0.721, p = 0.001). Anxiety and depression scores were highly correlated with each other ( = 0.880, p < 0.001) and both correlated with fatigue and pain interference (p < 0.001). Table 1

Baseline Characteristics of JSpA/ERA Patients in the Study

Mental health symptoms were highly prevalent in this male predominant cohort of JSpA, even in the context of well-controlled disease. Furthermore, mental health symptoms correlated with self-reported disease-related measures. These findings support routine mental health screening to identify at-risk JSpA patients and provide timely interventions, potentially improving overall outcomes.

Five patients were identified through the Uveitis-Rheumatology Collaborative Program (Toronto, Canada) between 2019 and 2025. Demographic, ophthalmologic, dermatologic, and immunologic data were reviewed, including the timing of tattoo reactivation, uveitis phenotype, systemic work-up, treatment, and outcomes. Infectious and systemic autoimmune etiologies were excluded by comprehensive testing such as angiotensine-converting enzyme (ACE), autoantibodies, chest imaging, tuberculosis screening, and biopsy when indicated.

The cohort comprised 5 adults (3 women, 2 men; mean age 34 years) who all developed ocular inflammation within months of inflammatory changes in long-standing tattoos—manifesting as erythema, induration, or swelling, most often in black or multicolored pigments on the arms, shoulders, or trunk. Latency between tattoo placement and uveitis onset ranged from 6 months to > 5 years (Table 1). Uveitis phenotypes included bilateral anterior (n = 1), anterior-intermediate (n = 1), and panuveitis (n = 3). Two presented with optic-disc edema and 1 with subretinal fluid. Diagnosis was confirmed by biopsy-proven non-caseating granulomas in 2 cases and by elevated ACE with concordant tattoo-ocular activity in 3; none developed systemic sarcoidosis. All received systemic corticosteroids for induction with topical therapy for local control. Methotrexate was first line in 4, with adalimumab escalation in 2 partial responders. One patient required mycophenolate mofetil after steroid-induced hyperglycemia, maintaining remission thereafter. Four achieved ≥12 months of steroid-free quiescence; 1 remains on taper with preserved vision and inactive tattoos. Table 1.

Main Clinical Manifestations of Five Patients with Tattoo-Associated Uveitis Syndrome

TAUS represents a distinctive cutaneous-ocular inflammatory syndrome characterized by concurrent inflammatory activity in tattoos and uveal tissue. Diagnosis relies on the simultaneous inflammation of skin and eye and, although is not always a granulomatous-type inflammation, it is important to rule out this type of involvement with histologic or biochemical evidence due to its particular severity and also to exclude systemic sarcoidosis. Management should combine early systemic corticosteroids with timely transition to steroid-sparing agents—methotrexate or mycophenolate—and escalation to biologics such as adalimumab for refractory or recurrent cases. Continuous communication between ophthalmology, rheumatology, and dermatology is essential. Prompt recognition and multidisciplinary immunosuppression can achieve durable remission, prevent visual loss, and mitigate systemic overtreatment in this pigment-driven disease.

[1.] Kesav NP. J Vitreoretin Dis 2024;8:339-342. [2.] Siebert E. Clin Exp Ophthalmol 2026;54:33-43.

A 51-year-old man presented to rheumatology with severe, progressive inflammatory back pain since age 34, in addition to heel and rib border enthesitis. HLA-B27 was positive. There was a family history of ankylosing spondylitis in his father. MRI of the sacroiliac joints was negative for sacroiliitis. He was diagnosed with clinical spondyloarthritis. Trials of NSAIDs were ineffective. He trialed multiple biologics that were either ineffective or partially effective including etanercept, golimumab, secukinumab, adalimumab, upadacitinib. In November 2024, he presented to clinic with severe hip pain and antalgic gait in spite of upadacitinib and full dose oral diclofenac. In December 2024, repeat MRI SI joints and whole spine showed fatty metaplasia at bilateral SI joints suggestive of chronic sacroiliitis without active inflammation and no evidence of spinal involvement. In April 2025, an MRI bilateral hips and subsequent bone scan revealed an undisplaced right femoral neck stress fracture as well as a 2.4 x 2.5 x 3.2 cm enhancing mixed cystic and solid lesion within the left thigh involving the neurovascular bundle. He underwent open reduction internal fixation of the right femoral fracture in May 2025. A bone density scan revealed osteoporosis (femoral neck T score –3.5). The left thigh mass was biopsied and consistent with a PMT. Endocrinology consultation noted very low serum phosphate (0.45 mmol/L, ref. range 0.70-1.50) and diagnosed TIO. Surgical resection of the tumor was performed in August 2025. The patient noted a dramatic improvement in bone pain following PMT resection and has been able to taper both diclofenac and upadacitinib. There are plans to attempt discontinuation of upadacitinib in the future.

This case demonstrates an example of TIO due to a PMT mimicking spondyloarthropathy. Long-term hypophosphatemic osteomalacia can have axial involvement and cause enthesopathy.[2] This rare diagnosis should be considered in those with suspected spondyloarthropathy who have persistent pain despite biologic therapy, fragility fractures, and hypophosphatemia.

[1.] Drezner M. Rev Endocr Metab Disord 2001;2:175-86. [2.] Álvarez-Rivas N. Bone Reports 2024;21:1-8.

Focus groups were held with adults in English and French. Structured online groups lasting 90 minutes used predefined questions to explore how IA care delivery could be changed to better meet their needs. Transcripts were thematically coded and analyzed to identify patterns to inform new approaches, interventions, and policy.

The 42 adults (English n=30); French n=12) had a mean (SD) age of 64 (13) years and disease duration of 9 (15) years. They were mostly white (88%) women (88%) from BC (21%), AB (10%), ON (29%), QC (36%) and NS (5%) living in urban locations (60%). Most had RA (50%), PsA (14%), axSpA (10%), and/or other rheumatic diseases (26%). Three overarching themes were identified: (1) IA affects all aspects of life. Participants described the physical, mental, and social burden of IA and need for co-ordinated, holistic care - ideally at 1 site. They regarded nurses as essential valued team members providing clinical and psychosocial support. (2) Information needs are dynamic and often go unmet. Patients reported limited preparedness for managing their IA and have difficulty accessing timely, relevant information. They identified opportunities for improved education through online and direct engagement with different rheumatology team members. (3) Care must be individualized. Health care needs and preferences vary based on disease activity and duration, life context, and social determinants. They discussed the need to take into consideration individual circumstances and preferences in addition to results of between-visits remote monitoring.

Advances in IA treatment and access to interprofessional care have significantly improved IA outcomes for many. While physical aspects of IA can be controlled, important gaps persist with emotional and social health needs. Findings will help inform the development and initial testing of FlexCAre, a new IA care model that integrates education, remote monitoring, and flexible visit schedules to better meet the diverse needs of individuals with IA. A patient-informed approach has the potential to improve engagement, equity, and outcomes in Canadian IA care.

Structured online 90-minute focus groups were conducted with HCPs using a predefined question guide to explore opportunities to optimize IA care delivery. Transcripts were thematically coded and analyzed to identify patterns to inform new approaches, interventions, and policy.

The 30 HCPs had a mean (SD) age of 64 (13) years. They included rheumatology nurses (67%), rheumatologists (30%) and pharmacists (3%) in BC (60%) and AB (40%) who had been practicing on average 16 years. Three overarching themes were identified: (1) The challenge of whole person care. HCPs noted that when patients lack access to primary care, providing whole person care can feel overwhelming and limits their ability to focus on complex, dynamic disease-specific needs. Equity gaps are greatest among older adults, racialized groups, individuals with mobility limitations, and in rural areas. Unrealistic patient expectations regarding the scope of services rheumatologists can offer were noted, particularly when patients lack a family doctor and/or mental health services. (2) The need for education and support from IA interprofessionals. Sustaining interprofessional teams remains challenging, even with provincial funding. HCPs emphasized the value of rheumatology team members to educate patients and fill gaps by providing virtual visits, responding to messaging systems, and returning calls. (3) Individualizing care through flexible tools and strategies. HCPs varied in their use of and preferences for virtual care and between-visit monitoring, and tailoring approaches to patient needs, disease status, and life context. Flexibility regarding visit scheduling, type, and monitoring was deemed essential. Several noted that when medication approval depends on symptom assessments, patients are more likely to complete questionnaires. E-health systems can provide disease education and self-management skills training.

HCPs identified key challenges and opportunities to improve IA care delivery. Findings underscore the importance of flexible, integrated, and patient-centered approaches to meet diverse needs, support whole person care, and reduce the burden on providers and meet patient needs. These insights are helping inform the co-design of FlexCAre.

In a single-center cohort of PsA patients fulfilling CASPAR criteria, those initiating systemic therapy for active musculoskeletal disease were invited to an ultrasound sub-study. A retrospective analysis of stored ultrasound scans included participants treated with TNF-α or IL-17 inhibitors. CE was assessed at baseline and 3 months using the SPARCC Enthesitis Index. SE was evaluated at 16 bilateral sites for grayscale and power Doppler abnormalities following a standardized protocol,[2] including quadriceps, distal patella, tibial tuberosity, Achilles, plantar fascia, triceps, lateral epicondyle, and supraspinatus insertions. Elementary lesions (hypoechogenicity, thickening, erosion, enthesophyte, calcification, Doppler signal) were scored individually using a semi-quantitative score, then combined into composite scores representing total lesion burden, inflammation, and structural damage. An active SE count was calculated based on sites with a Doppler signal plus hypoechogenicity or thickening. A multivariable logistic regression model was used to assess associations between baseline SE scores and resolution of CE at follow-up, adjusting for age, sex, baseline SPARCC score, prior advanced therapy, and biologic therapy class.

Seventy-eight patients were included in the analysis, with 42 on TNF-α inhibitors and 36 on IL-17 inhibitors. At baseline, mean SPARCC score was 1.8 (SD 1.8), with 68% showing at least 1 CE site. Mean active SE count was 1.4 (SD 1.7), with 65% showing at least 1 SE site. After 3 months of treatment, mean SPARCC decreased to 1.1 (SD 1.6; p=0.01), and 42% still had at least 1 CE site. None of the SE composite scores, nor biologic class (OR 1.31, 95% CI 0.48-3.58; p=0.603), were significantly associated with CE resolution (Table 1). Table 1:

Association between baseline sonographic enthesitis and resolution of clinical enthesitis at follow-up visit (N=78)

Baseline composite SE scores were not associated with CE responses to treatment, likely reflecting the limited correlation between SE and CE at baseline. Further studies are needed to evaluate associations at individual entheses and determine whether serial sonographic assessments can better capture treatment response.

[1.] Eder L. J Rheumatol 2023;50:258-64. [2.] Eder L. J Rheumatol 2020;96:50-2.

Participants are enrolled into the Rheum4U database. The Rheum4U database was first implemented in 2016 as a longitudinal database of patients with inflammatory arthritis conditions, including rheumatoid arthritis, psoriatic arthritis, axial spondyloarthritis, juvenile idiopathic arthritis, and gout. The database now consists of over 1300 patient profiles. We used a linear mixed effects model to identify the correlation between the Health Assessment Questionnaire (HAQ) score and time since baseline (Table 1).

Table 1

There were 68 patients in the Rheum4U registry who self-identified as Indigenous. From the Rheum4U registry, Indigenous people were identified using self-reported Indigenous status. IA conditions included rheumatoid arthritis, psoriatic arthritis, spondyloarthritis, and juvenile idiopathic arthritis. Patients are 18 years old and older. Median follow-up time per individual is 26 months (IQR 9, 49). Average HAQ at baseline is 0.86 SD (0.79). The average HAQ score at baseline (time 0) is approximately 0.87. As time increases, the HAQ score changes by 0.00076 per month, but this is not statistically significant.

Among Indigenous people with IA conditions, there is no evidence that HAQ scores changed over time.

Participants with IA and symptoms of insomnia were recruited through social media and patient-partner organizations and randomly assigned to the ICBTi treatment group (n= 24; 6 modules over 8 weeks) or the waitlist-control group (n= 26). Participants completed surveys at baseline, 8 weeks (post-treatment), and 3 months later. Treatment group participants completed questions about treatment perceptions. The Insomnia Severity Index (ISI) (maximum score of 28) assessed insomnia symptoms at each time point. Paired sample t-tests were used to analyze changes in ISI scores over time for each group.

The sample included 50 participants with IA and insomnia symptoms (Table 1). Post treatment completion, most participants in the treatment group rated the ICBTi modules as moderately or extremely useful (84%) and were moderately or extremely satisfied (89%) with the program. Seventy-three percent of treatment group participants self-reported moderate or extreme improvements in sleep. However, only 52% of the treatment group completed the entire program. Feedback included wanting more relevance to arthritis and chronic pain, and a guide alongside the intervention. The mean baseline ISI score was 16.7 in the treatment group and 14.9 in the control group. Twenty treatment groups and 24 control group participants completed the 8-week survey. The mean (95% CI) change in ISI scores pre- to post-treatment in the treatment group was –4.95 (–6.77, –3.13), p<.001, and –0.94 (–.38, 2.26) in the control group, a non-significant difference. Eighteen treatment group and 21 control group participants completed the 3-month survey. The mean (95% CI) change in ISI scores from pre-treatment to the 3-month follow-up was –5.28 (–7.62, –2.93, p<.001) in the treatment group and –0.83 (–1.53, 3.20) in the control group, a non-significant difference. Table 1

Characteristics of the Sample

The Internet-delivered CBTi program was acceptable and perceived as useful by most participants but could benefit from further adaptation to arthritis-specific needs. The results suggest efficacy of ICBTi among individuals with arthritis. A larger randomized-controlled trial with a larger, more diverse sample is needed to determine the effectiveness of using ICBTi to help people manage the double-burden of insomnia and arthritis. Supported by a CIORA grant

Data is from the baseline visit of a pilot study of people with inflammatory rheumatic diseases who volunteered for an internet-based intervention to improve sleep. Participants self-reported cannabis use, reasons for consumption, and completed the PROMIS-29 questionnaire (physical function, anxiety, depression, fatigue, sleep disturbance, pain interference, and social participation). Characteristics were compared between cannabis users and non-users using t-test and chi-square. Associations between cannabis use, demographics, and clinical characteristics were examined using multivariable regression.

Our sample had a mean (SD) age of 54 (14) and all were female. Most had RA or PsA, with a mean disease duration of 10 (11) years; many also had OA (30%) (Table 1). One-third reported have used cannabis in the past year, and 24% in the past 3 months (of which 38% used weekly and 31% daily/almost daily). All participations indicated they were using for medicinal reasons only (100%), with primary motivations being to improve pain (19%), sleep (17%), fatigue (<5%) or anxiety (<5%). Nearly half (46%) reported a little improvement in arthritis symptoms with use, 15% reported a lot of improvement, 31% no change, and 8% were unsure. Users reported similar levels of physical function, pain, fatigue, sleep disturbance, and social participation, but significantly higher anxiety (p=.046) and depression (p=.014) than non-users. Table 1.

Sociodemographics, arthritis characteristics, and mean PROMIS-29 scores by cannabis use in the past three months

One in 3 participants in an online intervention to improve sleep reported using cannabis in the past year to improve their arthritis symptoms, with nearly a quarter using cannabis regularly to improve pain, sleep, fatigue and anxiety. Users did not report different PROMIS-29 outcomes, although 61% reported a little to a lot of symptom improvement. Understanding the motivations and health impact of cannabis use can help guide patient counseling and future research on alternative management strategies for pain and mood disorders. Supported by a CIORA grant

Between March and July 2025, we conducted a cross-sectional survey of 410 adults with IA followed at the McGill University Health Centre. Self-reported diagnoses included rheumatoid arthritis (61.5%), spondyloarthritis (13.4%), psoriatic arthritis (9%), systemic lupus erythematosus (7.3%), juvenile idiopathic arthritis (5.1%), and others (3.2%). The primary outcome ‘frequency of AI/ChatGPT use to inquire about their medical condition’ was categorized as an ordered outcome (never rarely/occasionally; somewhat /very frequently) and alternatively as a dichotomous outcome (never used vs ever used AI). The secondary outcome ‘accuracy of information provided by AI’ was categorized dichotomously as rarely/never accurate vs always/mostly accurate. Potential correlates included sociodemographic characteristics, disease duration, prior access to educational resources, reported barriers to education, prior educational resources, and preference for online formats. We built multivariate logistic regressions with either ordered or dichotomous outcomes.

Participants were predominantly middle-aged (mean ± SD 49.6 ± 18.8 years), female (72.7%), urban residents (87.3%), with established IA (77.6%, >5 years). Overall, 59% reported never using AI, 31.7% used it rarely/occasionally, 8.5% used it somewhat/very frequently. In multivariate ordered (logit) models, older age (per-year aOR 0.64, 95% CI 0.51-0.79), established IA (>5 years; aOR 0.51, 95% CI 0.32-0.83), and prior arthritis education (aOR 0.58, 95% CI 0.33-0.99) were associated with lower AI use, while preference for online formats for educational resources predicted greater AI use (aOR 2.06, 95% CI 1.28-3.36). In dichotomous logistic models, female sex (aOR 0.61, 95% CI 0.38-0.97), older age (per-year aOR 0.98, 95% CI 0.97-0.99), and established IA (>5 years; aOR 0.54, 95% CI 0.32-0.89) were associated with lower odds of AI use, whereas online preference again correlated with AI use (aOR 2.25, 95% CI 1.39-3.71). Among AI users, older age was associated with lower perceived information accuracy (per-year aOR 0.96, 95% CI 0.94-0.98). No other covariates were significant.

Many patients with IA use ChatGPT for self-learning, especially younger ones and those preferring online resources. In contrast, women, older patients, those with long-standing disease, or relying on traditional education were less likely to use it. Among users, older age was associated with lower perceived accuracy. Future work should explore how to best integrate AI while ensuring accuracy and equity.

We conducted a cross-sectional survey in Quebec of 410 participants with inflammatory arthritis, including rheumatoid arthritis (61.5%), spondyloarthritis (13.4%), psoriatic arthritis (9.0%), systemic lupus erythematosus (7.3%), and other (8.3%). The primary self-reported outcome was confidence in managing arthritis, categorized as: confident (very/somewhat), neutral, or unconfident (very/somewhat). Potential correlates included sociodemographic characteristics, disease duration, prior use of educational resources, reported barriers to education, and preferred modes of learning. We assessed possible associations of these factors with confidence using multivariate ordered logistic regression.

Participants were predominantly middle aged (mean ± SD: 49.6 ± 18.8 years) female (73%) residing in urban areas (87%) with established arthritis (78% >5 years). Overall, 48% of respondents reported being very confident, 32% somewhat confident, 12% neutral, and 7% somewhat or very unconfident in their ability to manage their condition. The majority (81%) reported at least 1 barrier to accessing or understanding educational materials, most commonly lack of time (31%) and complexity of information (25%). In the multivariable model, prior access to educational resources and preference for online resources as a primary mode of learning were strongly associated with higher confidence in self-management (adjusted OR 2.91, 95% CI 1.29-7.84 and 2.05, 95% CI 1.20-3.52, respectively). Conversely, financial or access-related barriers were negatively associated with higher confidence (adjusted OR 0.56, 95% CI 0.31-0.99). Sex, age, residence, primary language, disease duration, and rheumatoid arthritis diagnosis were not significantly associated with confidence in arthritis self-management.

Prior exposure to educational materials and preference for online learning platforms was associated with confidence in arthritis self-management. In contrast, financial and access barriers negatively correlate with confidence. These findings highlight the importance of improving equitable access to patient education and tailoring delivery formats to align with patient preferences.

Data were sourced from the 2016 Canadian Community Health Survey. Responses from 23,687 individuals with arthritis were analyzed for CRNA, defined as self-reported skipping or not filling prescriptions due to cost in the past 12 months. Sixteen demographic and health/health-system variables were examined using case-weighted random forest models to estimate variable importance (via permutation-based assessment) in the overall and sex-stratified populations. Missing data were imputed using multiple imputations by chained equations. For enhanced interpretability and burden assessment, case-weighted multivariable logistic regression models (overall and sex-stratified) estimated the direction and magnitude of associations. Prevalence estimates and 95% confidence intervals (CIs) were calculated using survey weights and 1,000 bootstrap replicates.

The weighted prevalence of CRNA was 7.5% (95% CI 6.9-8.1), with higher prevalence among females (8.5%, 95% CI 7.7-9.4) than males (6.1%, 95% CI 5.3-6.9). In random forest models, the most influential factors associated with higher probability of CRNA in the overall population were age, insurance coverage, household income, and satisfaction with life (Figure 1). Within the top quartile of factors for both males and females independently were age and insurance coverage. However, remaining top variables differed: among females, household income and education ranked highly, whereas among males, perceived health and satisfaction with life were more prominent (Figure 1). In the multivariable logistic regression, higher odds of CRNA were observed among females (OR=1.37, 95% CI 1.13-1.66), younger adults ≤34 years (OR=5.22, 95% CI 3.53-7.70), non-white individuals (OR=1.53, 95% CI 1.01-2.32), those with lower income (<$20,000; OR=2.49, 95% CI 1.76-3.52), ≥4 chronic conditions (OR=2.22; 95% CI 1.56-3.14), uninsured (OR=3.31, 95% CI 2.72-4.02), and those residing in British Columbia (OR=1.58, 95% CI 1.15-2.18) or the Prairies (OR=1.37, 95% CI 1.0-1.86). Respondents reporting poor/fair health or dissatisfaction with life also had greater odds of nonadherence. Figure 1.

Random Forest Variable Importance Ranking.

Findings highlight socioeconomic and regional disparities in cost-related nonadherence among Canadians with arthritis, with age and insurance coverage being the most influential correlates. While financial and systemic barriers remain central, sex-stratified differences suggest additional psychosocial and health-related factors. Therefore, policies to improve medication affordability and equitable access are warranted.

[1.] Doucet J. Can Oncol Nurs J 2017;27:390-1.

The survey was co-developed by people living with inflammatory arthritis, many with firsthand experience using PSPs. It explored domains such as patient-provider communication, consent, and information sharing, and access to pharmacy and insurance services. The survey was open from June 2023 to January 2024, with 375 respondents across Canada. Descriptive statistics were used to analyze quantitative data, while open-ended comments were thematically reviewed to contextualize experiences and recommendations. Findings were presented to a patient advisory group to co-develop key recommendations for improving PSP design and delivery.

Survey respondents represented diverse rheumatic diseases, including rheumatoid arthritis, psoriatic arthritis, and lupus, with the largest proportion aged 30-49 years. Over half of respondents (57%) received consent forms before PSP enrollment, yet only 60% fully understood the program’s role. Approximately two-thirds felt they received the necessary information about medication use, though 50% reported inadequate nursing support. Respondents emphasized the value of individualized education and consistent points of contact, noting frequent turnover among PSP staff as a barrier to trust and continuity. Key patient-identified recommendations included simplifying insurance systems, improving communication between PSPs and healthcare teams, ensuring informed consent, enhancing patient education, and developing independent monitoring of PSP effectiveness (Figure).[2]

This patient-led review demonstrates that while PSPs fill critical gaps in Canada’s healthcare system, improvements are needed to enhance equity, clarity, and patient-centeredness. People with arthritis and related diseases want programs that prioritize relationship-based care, clear information, and holistic support. Ongoing collaboration between patient organizations, PSP providers, and policymakers can improve these services and ensure they benefit patients in meaningful and impactful ways.

[1.] Grundy Q. CMAJ 2023;195:E1565-76. [2.] Canadian Arthritis Patient Alliance. https://arthritispatient.ca/en/patient-support-programs-survey-results/

This initiative synthesized qualitative findings from multiple Canadian Arthritis Patient Alliance (CAPA) projects led by occupational therapy students. which employed qualitative designs (eg, photovoice) and quantitative design involving an online survey. Participants were individuals living with different forms of arthritis who shared personal stories, photographs, and adaptive "life hacks" demonstrating how they navigate daily challenges. To synthesize the data, we conducted an interpretive, cross-project analysis that merged the qualitative themes generated identifying convergent ideas around adaptation, creativity, and participation. Thematic analysis was guided by Braun and Clarke’s (2012) framework and informed by the PEO model to examine how personal, environmental, and occupational factors intersect to support or hinder participation.

Findings highlighted that people living with arthritis experience functional limitations in a wide range of tasks and occupations, yet they exhibited creativity and resilience when adapting to daily life despite a range of PEO barriers: - Person: Participants reframed loss into adaptation, using creativity as empowerment and self-expression. Emotional resilience, acceptance, and humor were key to sustaining mental health. - Environment: Peer networks, community programs, and digital spaces provided vital social and emotional support, while barriers such as limited OT access, high equipment costs, and stigma persisted. - Occupation: Engagement in meaningful activity—through adaptive tools, modified routines, or personalized strategies—was central to maintaining identity and autonomy. Incremental successes in everyday tasks reinforced confidence and control.

The Hacking Arthritis project demonstrates the power of patient-driven, co-creative approaches that center lived experience in arthritis care. It shows how people with arthritis can struggle with tasks but that those that were interviewed were creative in adapting daily tasks. CAPA will continue to find ways to support people living with arthritis in collaboration with occupational therapists, designers, makers, and others and will add to its repository of tools and life hacks on its website,[1] to provide practical hands-on tools and advice for people with arthritis to live independently.

[1.] Canadian Arthritis Patient Alliance. https://arthritispatient.ca/en/managing-daily-life/#lifehacks

We conducted a retrospective analysis using data from 2 regional CRDS over 4 4-month periods, over 4 consecutive years (n=1768 referrals). We examined the characteristics of rheumatology referrals, including system delays calculated as the interval between the referral receipt date at the CRDS and the date of first appointment allocation. Cox regression models were used to identify factors associated with these delays. Waiting times for initial consultations were compared against CRDS target wait time benchmarks.

Median waiting times were 7 days [3-14] for priority B referrals (target wait time <10 days), 31 days [17-70] for priority C (target <28 days), 286 days [128-464] for priority D (target <90 days), and 548 days [347-548] for priority E (target <365 days). Beyond priority level (p<0.001), several factors were associated with delays in accessing an initial rheumatology consultation. These included the period (p<0.001), with the pandemic year (2020-21) showing longer delays in comparison to the reference year (2019-20); the source of the referral (p<0.001), as referrals originating from family medicine groups having longer waits than those from other practice settings; reason for consultation (p=0.021), with fibromyalgia linked to longer delays and vasculitis and connective tissue disease to shorter ones; sex assigned at birth (p<0.001), with female patients facing longer delays than men; and age (p=0.021), older individuals experiencing longer waits. In the multivariable model, the low priority level, the pandemic period, the referrals from family medicine groups and older age were significantly associated with longer delays.

These results suggest that, beyond medical priority, both patient- and system-level factors may influence delays for rheumatology consultations. The next phase of the study will investigate the circumstances under which these inequities in access arise, by analyzing CRDS demand and supply data, and conducting a comprehensive classification analysis of the additional clinical background and personal history information included in individual referral forms. The findings will inform triage and prioritization strategies in centralized referral systems, including potential extensions and refinements to the standardized referral forms, to support efforts aimed at reducing disparities and promoting equitable access to care. Supported by a CIORA grant

We describe a 77-year-old man with atrial fibrillation and prior stroke who presented with a 3-week history of progressive dyspnea, dry cough, and fatigue unresponsive to outpatient therapy. He had no relevant exposures but reported a 2-year history of Raynaud’s phenomenon. High-resolution CT revealed right-predominant ground-glass opacities with early fibrosis (Figure 1). Serology demonstrated high-titer anti-PL7 and anti-Ro52/TRIM21 antibodies, confirming ASS. Despite initial corticosteroids, his oxygen requirements worsened to 10 L via non-rebreather, prompting escalation to pulse methylprednisolone (250 mg IV x 3 days), cyclophosphamide (500 mg/m² IV monthly), and tacrolimus (target trough 5-10 ng/mL). His respiratory status improved, and by discharge, he required oxygen only with exertion. During admission, workup revealed rectal adenocarcinoma with a hepatic metastasis, for which neoadjuvant FOLFOX chemotherapy was initiated with curative intent. Cyclophosphamide was discontinued to minimize toxicity, while tacrolimus and prednisone were continued. Within 10 weeks, he no longer required supplemental oxygen.

To our knowledge, this represents the first reported case of colorectal cancer-associated anti-PL7/anti-Ro52-positive ASS presenting with rapidly progressive ILD successfully treated with early triple-agent immunosuppression. This case highlights 2 key observations: (1) early combination therapy with corticosteroids, cyclophosphamide, and tacrolimus may be lifesaving in severe, steroid-refractory anti-PL7/anti-Ro52-positive RP-ILD; and (2) The coexistence of metastatic colorectal cancer raises the possibility of a paraneoplastic variant of ASS, a rare but described phenomenon. New-onset ASS should prompt evaluation for underlying malignancy, even in amyopathic presentations.

[1.] Shi J. J Rheumatol 2017;44:1051-7. [2.] Marie I. Eur J Intern Med 2013;24:474-9. [3.] Tsuji H. Arthritis Rheumatol 2020;72:488-98.

We conducted a retrospective chart review of the triplets referred to the Hospital for Sick Children. Peripheral blood DNA of the triplets, as well as unrelated infants with and without cardiac NLE, was run on Infinium methylation EPIC array (at 850,000 methylation sites) analysis. We identified 39 infants seen in the SickKids NLE clinic with and without cardiac NLE, matched for sex, gestational age (GA) at birth, and age at blood sampling. Differential methylation between infants with and without cardiac NLE was performed and methylation changes were visualized using principal component analyses (PCA) and heatmaps.

The MZ female triplets were identified at 18 weeks GA. Triplet A had endocardial fibroelastosis (EFE), a non-nodal manifestation associated with cardiac NLE. Triplet B was healthy, and triplet C had complete heart block (CHB) and EFE. The triplets (blood sampling at 24 days of life) demonstrated segregation on a heatmap based on methylation patterns concordant with cardiac NLE status. The subsequent study included 39 infants (12 cardiac NLE) born to high titer anti-Ro positive mothers, with a mean 37 weeks GA at birth. Ten infants had CHB, 1 had EFE, and 1 had both. PCAs and heatmaps demonstrated segregation of the cardiac NLE infants from those without cardiac manifestations (Figure). The triplets’ methylation patterns were not concordant with methylation segregation patterns observed in the unrelated infants, which may have been a consequence of age differences. Figure.

Differential genome wide DNA methylation differentiating infants with cardiac NLE from those without cardiac NLE

We present the first recorded case of MZ triplets discordant for cardiac NLE and observed differences in methylation profiles between the triplets with and without cardiac NLE. In an epigenetic study of cardiac NLE, we observed segregated methylation profiles between infants with cardiac NLE and healthy infants. We acknowledge that sample collection following cardiac NLE manifestations and treatment may impact results. Further research is required to investigate and validate our findings.

Right sciatic nerve crush injury was performed in male and female C57BL/6 mice (young, age 2 months, n=4; old, 16 months, n=3) on day 0, with euthanasia and bilateral sciatic nerve collection on day 7. Spatial transcriptomics with single cell resolution was performed on both ipsilateral (injured) and contralateral (non-injured) nerves (Xenium, 10x Genomic, Pleasonton, CA, USA). Cells expressing KIF20B were labeled as positive. Chi-square tests were used to compare the proportion of KIF20B positive cells between injured and non-injured nerves, as well as between the nerve segments proximal and distal to the site of injury. Study protocol was approved by the University of Calgary Animal Ethics Committee.

When KIF20B expression was compared across all cell types between injured and non-injured nerves, there was significantly greater expression in injured nerves (2.87%) when compared to non-injured nerves (0.83%; p=0.0000011), (Figure 1). In injured nerves, the proportion of KIF20B expressing cells was significantly increased in the segment distal to site of injury (3.51%) when compared to the proximal segment (1.28%; p=0.000000003), (Figure 1). There was no significant difference in KIF20B expression between non-injured nerves and the proximal segment of injured nerves (proximal, 1.28%; non-injured, 0.83%; p=0.16); (Figure 1). When KIF20B expression was assessed in individual cell types between injured and uninjured nerves, the greatest difference was seen in Schwann cells (injured, 4.90%; non-injured, 1.00%; p=0.0000087). There were no significant differences in KIF20B expression when old and young mice were compared. Figure 1:

KIF20B expression in ipsilateral (injured) and contralateral (non-injured) mouse nerves in both young (2 months) and old (16 months) mice. KIF20B expression (yellow and teal squares) was increased distal to the site of injury in both young and old mice in the ipsilateral nerve when compared to the proximal segment, as well as the contralateral nerve. Nuclei (DAPI stain) denoted by blue dots, Boundary Protein Stain (ATP1A1) denoted by purple dots. D, distal; P, proximal.

KIF20B expression is increased in the distal segment of mouse sciatic nerves following crush injury and these changes are greatest in Schwann cells. Future studies are needed to characterize how Schwann cell expressed KIF20B contributes to peripheral nerve healing, as well as how anti-KIF20B antibodies might disrupt this process and potentially contribute to cranial and peripheral neuropathies in SLE.

[1.] Janisch K. Development 2013;140:4672-82. [2.] Krustev E. Lupus Sci Med 2024. [3.] Krustev E. Arthritis Rheumatol 2021;73:703-6.

Six DM patients from a multicenter inflammatory myopathy registry with available longitudinal biobanked sera were identified. All patients met the 2017 EULAR/ACR criteria for adult idiopathic inflammatory myopathy. Disease activity was categorized based on the International Myositis Assessment and Clinical Study (IMACS) physician global assessment (PhGA) as low (PhGA 0-3) or moderate/high (PhGA 4-10). The IMACS core set measures used for the 2016 ACR/EULAR Total Improvement Score were extracted. Serum samples were analyzed using proximity extension technology (Olink Proteomics Inc., Watertown, MA), simultaneously targeting 92 proteins involved in inflammatory processes. Results were reported as normalized protein expression (NPX) values (log2 scale) with higher NPX values representing higher protein concentrations. Mean NPX difference (NPX) for each protein comparing moderate/high and low disease activity were calculated using paired t-tests with Benjamini-Hochberg correction for multiple testing.

Six female DM patients with ages ranging from 34 to 53 years were included (Table 1). Clinical features at timepoint 1 included rash (n=6), muscle weakness (n=5), interstitial lung disease (n=5), Raynaud’s (n=3), arthritis (n=1) and dysphagia (n=1). CK values ranged from 37-6039 U/L. Autoantibodies included anti-MDA5, -TIF1y, -Mi2, -Ro52, and -Ku. At timepoint 1, 5 patients had moderate/high disease activity and at the timepoint 2, 5 patients had low disease activity. Eleven proteins were significantly upregulated when comparing moderate/high vs low disease activity. The strongest NPX was observed for monocyte chemoattractant proteins, MCP-2 (3.0), MCP-1 (2.4), MCP-4 (2.2) (all adj. p=0.02) and C-X-C motif chemokine 11 (CXCL11, 3.0, adj. p=0.05). Other upregulated proteins included CX3CL1 (1.57), CCL11 (1.42), PD-L1 (1.27), IL-4 (1.1), CD40 (0.92), IL-15RA (0.9) and CSF-1 (0.61) (all adj. p=0.05). Table 1.

Demographic and clinical characteristics

Using serum inflammatory profiles, we identified proteins upregulated in DM patients with moderate/high disease activity compared to low disease activity in a small exploratory cohort. Those included chemokines involved in monocyte and T-cell recruitment that could represent potential biomarkers for disease activity monitoring. Further studies in larger DM cohorts are warranted to evaluate the role of longitudinal proteomic profiling in personalized disease activity monitoring.

Clinical data was abstracted from medical records, including demographics, oncologic history, pre-existing autoimmune conditions, manifestations of disease, laboratory findings, treatment, and outcomes.

18 patients were identified with overlapping myositis and MG. 50% of MG diagnoses were supported by positive electromyography (EMG) or MRI, and 50% were diagnosed clinically by ocular or bulbar symptoms, and/or fatigable muscle weakness. Myositis was diagnosed by CK elevation, MRI or EMG, and physical findings of sustained proximal muscle weakness. All patients received initial high-dose glucocorticoids, with improvement in 12 of 18 patients. In addition to glucocorticoids, 7 received intravenous immunoglobulins, 1 plasma exchange, 8 acetylcholinesterase inhibitor therapy (pyridostigmine), and 3 disease-modifying antirheumatic drug (DMARD) therapy. DMARD therapies included mycophenolate (symptom improvement in 2 of 3 patients), infliximab (improvement in 1 of 3 patients), and rituximab (deterioration in 1 patient). 7 patients received pyridostigmine, of which 6 had symptom improvement. None required ventilatory support. 3 of 18 patients died from MG/myositis syndrome. Mortality was associated with Grade 4 symptom severity, bulbar involvement, and profound muscle weakness. The presence of MG– or myositis associated antibodies did not predict mortality.

This multi-center study characterizes a spectrum of clinical presentations among patients with overlapping immune-related myositis and MG. Mortality was associated with Grade 4 symptom manifestations, bulbar symptoms, and need for ventilatory support, highlighting the critical role of early recognition and aggressive management in severe cases.[1] All patients received high-dose glucocorticoids, with some receiving additional immunosuppressive therapies and supportive care. Addition of acetylcholinesterase inhibitor therapy improved overlap symptoms more than DMARD therapy alone. Among those with EMG-confirmed MG, the majority improved with pyridostigmine, further suggesting true neuromuscular junction pathology and arguing against the interpretation that MG diagnoses merely represent severe myositis, which reinforces the concept of distinct overlap syndrome rather than a single disease spectrum. As in previous studies, clinical outcomes were influenced by disease severity and organ involvement rather than serologic markers, as antibody positivity did not correlate with mortality.[2] These findings support the need for multidisciplinary care, early diagnostic evaluation, and individualized treatment strategies to optimize outcomes in patients with overlap syndromes.

[1.] Haugh A. Expert Opin Drug Saf 2020;19:479-88. [2.] Alghabban A. JTO Clin Res Resp 2024;6:100772.

REGENCY, BLISS-LN and AURORA-1 renal response endpoint definitions were used for analysis of the REGENCY dataset at Week 76. The Cochran-Mantel-Haenszel test, stratified by region and race, was used for treatment comparisons. All patients received oral prednisone as part of ST, tapered to 5 mg/day by Week 24.

At Week 76, 46.4% of patients in the OBI+ST (n=135) and 33.1% in the PBO+ST arm (n=136) achieved CRR (adjusted difference: 13.4%, 95% CI, 2.0 to 24.8%; P=0.0232). The proportions of OBI+ST vs PBO+ST achieving modified BLISS-LN primary efficacy renal response were 51.8% and 39.7% (adjusted difference: 12.1%, 95% CI, 0.5 to 23.8%; P=0.0432); modified BLISS-LN CRR were 48.7% and 33.1% (adjusted difference: 15.7%, 95% CI, 4.3 to 27.2%; P=0.0084); modified AURORA-1 CRR were 48.7% and 33.8% (adjusted difference: 15.0%, 95% CI, 3.6 to 26.5%; P=0.0117). A higher number of patients achieved the individual components of CRR at Week 76 in the OBI vs PBO arm for all 3 components (UPCR <0.5 g/g: 47.4% vs 36.0%; eGFR ≥85% of baseline: 83.7% vs 75.7%; no occurrence of intercurrent events: 88.9% vs 75.0% for OBI+ST and PBO+ST, respectively). In both arms, the main reasons for not attaining CRR were UPCR ≥0.5 or eGFR <85% of baseline (54.8% OBI+ST vs 65.4% PBO+ST). The mean daily prednisone intake was consistently lower in patients in the OBI vs PBO arm from Week 24-76 (Figure 1). The proportions of patients achieving a daily prednisone (or equivalent) dose of ≤5 mg/day were consistently higher in the OBI vs PBO arm from Week 36, reaching a 10 percentage point absolute difference from Week 64-76 (78.5% vs 68.4% for OBI+ST vs PBO+ST; adjusted difference (95% CI): 10.1% (–0.5 to 20.4), P=0.0589). Figure 1.

Mean Daily Dose of Prednisone for Patients Treated with Obinutuzumab or Placebo Plus Standard Therapy

In a post hoc analysis of the REGENCY trial outcomes, OBI showed consistent benefit across patient subgroups, utilizing multiple alternative definitions of CRR and exhibited steroid-sparing properties.

Incidence, severity and attribution of IRRs and hematologic abnormalities, including drug-related neutropenia, were determined based on investigator and NCI CTCAE v5.0 adverse event grading.

The proportion of pts who experienced at least 1 IRR was higher in the OBI+ST vs the PBO+ST arm (21 [15.4%] vs 15 [11.4%]). In the OBI+ST arm, the majority (19 [14.0%]) experienced IRRs of Grade (Gr) 1-2, which resolved. In the OBI+ST arm, 2 pts (1.5%) experienced Gr 3-4 IRRs; both events resolved. No Gr 5 IRRs were observed. The most frequently reported symptoms of IRRs in the OBI vs PBO arms respectively were nausea (4 [2.9%] vs 4 [3.0%]), headache (4 [2.9%] vs 3 [2.3%]) and vomiting (4 [2.9%] vs 2 [1.5%]). IRR incidence and severity was highest at first infusion, with Gr 3-4 observed only then (Table 1). The shifts observed from Gr 1-2 at baseline to Gr 3-4 post-baseline were notably different between the treatment arms for neutrophils and lymphocytes. As lymphopenia is an expected pharmacologic effect of anti-CD20 therapies, this analysis focused on drug-related neutropenia. The proportion of pts who experienced at least 1 drug-related neutropenia was higher in the OBI+ST arm vs the PBO+ST arm (17 [12.5%] vs 5 [3.8%]). Most cases of neutropenia were incidentally detected during routine hematology labs at scheduled study visits. Median time for resolution was 16 days (d) (min-max: 4-378 d) and 50.5 d (min-max: 21-371 d) in the OBI+ST and PBO+ST arm, respectively. Seven pts (4.1%) had Gr 3-4 drug-related neutropenia (including 1 febrile neutropenia), while none occurred in the PBO+ST arm. All drug-related neutropenia resolved with treatment except for 1 PBO pt where it was resolving at clinical cutoff. No Gr 5 neutropenia was observed. Five patients received G-CSF treatment for drug-related neutropenia (4 in the OBI+ST arm vs 1 in the PBO+ST arm). Table 1:

Incidence and Grade of Infusion-Related Reactions by Infusion Visits and Treatment

The incidence of IRRs and drug-related neutropenia was higher in pts receiving OBI+ST but risks remained low overall; many were Gr 1-2, self-limited, easily manageable and without consequence. These data provide insights into adverse events related to OBI.

We report a 48-year-old female first found incidentally at the age of 37 to have renal impairment. Over the past decade, her eGFR had declined to 12mL/min/1.73m², with 3g/L of proteinuria. Renal biopsy in 2020 confirmed widespread AA amyloid deposits with severe interstitial fibrosis and 11/16 glomeruli globally sclerosed, with SAA concentrations exceeding 16,000ng/mL. Throughout her entire course, she had no infectious, rheumatologic or constitutional symptoms. Other than a RF titer of 30 IUx103/L, extensive investigations were negative, including bone marrow biopsy, rheumatologic markers (CCP, ANA, dsDNA, C3/C4, ANCA, ESR, CRP) and infectious serologies (hepatitis, syphilis, schistosoma, strongyloides, whipples, tuberculosis, HIV, HTLV, filariasis). A thorough genetic investigation was also negative including sequencing for the SAA1 gene, panels containing genes associated with hereditary amyloidosis and autoinflammatory diseases, as well as a research exome. A brief trial of colchicine was initially trialed but stopped due to worsening kidney function. Tocilizumab 160mg SC every 2 weeks was initiated in December 2024 in an attempt to suppress hepatic SAA production. A year after, SAA levels fell from >16,000 to 5,427ng/mL. Her GFR stabilized at 13 mL/min/1.73m², and dialysis has not yet been required at the time of writing.

Idiopathic AA amyloidosis is a therapeutic challenge due to the condition’s rarity and lack of standard therapies. While there are numerous publications demonstrating the efficacy of tocilizumab in secondary AA amyloidosis,[1-3] our case is the first we are aware of, describing this therapeutic effect in idiopathic AA amyloidosis. This case underscores the central role of interleukin-6 in SAA production and may form the foundation for future studies with more patients over a longer duration to further explore the disease-modifying benefits of tocilizumab in idiopathic AA amyloidosis.

[1.] Okuda Y. Mod Rheumatol 2019;29:268-74. [2.] Courties A. Amyloid 2015;22:84-92. [3.] Yamagata A. BMC Nephrol 2017;18:377.

Inclusion criteria were age ≥18 years, with unexplained recurrent or chronic inflammation (≥1 of: fevers, serositis, peritonitis, pharyngitis, mucocutaneous ulceration, skin lesions, elevated CRP, response to colchicine or IL-1 blockade). Gene panel testing was performed via Next Generation Sequencing at the Hospital for Sick Children. All patients provided written consent to be included in a case series.

A total of 48 patients were included (85% female). The cohort was ethnically diverse, including Caucasian (77%), South Asian (10%), East Asian, African and Middle Eastern (each 4%). The median age at enrollment was 36 years, and first symptom onset at 25 years. A family history of similar symptoms was present in 23%. Prior to first onset, an antecedent event was recalled in 40% of patients. The most common were concussion (8/48, 17%), and frequent viral infections (6/48, 12.5%). The most common manifestations were joint pain/swelling (83%), dermatologic lesions (77%), and recurrent fevers >38°C (75%). In those with dermatologic lesions, the most subtypes were nonspecific rash (62%), mucocutaneous ulcerations (57%) and urticaria-like lesions (38%). Skin biopsy was performed in 11, with neutrophilic infiltration found in 5. CRP was elevated during flares in 32/39 (82%) of patients, and in 9/48 (19%) at baseline. Autoinflammatory gene variants were found in 40/48 (83%) patients. MEFV variants were present in 30/48 (63%) for which the most common was E148Q (12/30, 40%). NOD2 variants were present in 25/48 (52%), the most common being L1007fs (5/25, 25%). NLRP12 variants were present in 5/48 (10%). Variants were also found (in fewer numbers) in NLRP3, TNFRSF1A, NLRC4, and MVK. Colchicine was beneficial in 32/39 patients. IL-1 inhibitor was trialed in 9 patients, with 8 showing clinical and biochemical improvement.

USAID remains an important area of study given the large number of autoinflammatory patients that lack a monogenic explanation. It remains unclear whether USAID patients have a monogenic disease in a yet unknown gene, or a multifactorial condition with genetic susceptibility factors. Indeed, a ‘2 hit hypothesis’ appears plausible given the significant proportion of patients carrying a genetic variant and recalling a triggering event. Only 1 patient in the cohort denied any antecedent events and lacked autoinflammatory gene variants, highlighting these as likely important factors in disease pathogenesis.

A 66-year-old male was hospitalized with acute fever, headache and back pain 1 month after initiation of rituximab and lenalidomide for relapsed lymphoma. Five years prior after diagnosis of stage IVA follicular lymphoma, he achieved complete radiographic remission with bendamustine and rituximab, and further maintenance was deferred. Six months before his hospitalization, he developed abdominal distension with CT findings of bulky diffuse mesenteric and retroperitoneal lymphadenopathy presumed to reflect lymphoma recurrence. At admission, MRI demonstrated new diffuse pachymeningeal thickening and enhancement with scattered nodularity, and restaging CT noted stable lymphadenopathy but new ill-defined perivascular fat stranding and circumferential wall thickening of the aortic arch and left subclavian artery. At time of lumbar puncture for concern of relapsed lymphoma, he received an empiric single dose of intrathecal methotrexate, cytarabine and hydrocortisone. However, extensive microbiologic and malignancy workup subsequently returned negative including 2 bland CSF samples and an unrevealing retroperitoneal lymph node biopsy. He received no other empiric treatment beyond an initial 3 days of antibiotics. His initial CRP of 255 mg/L steadily decreased and normalized over 2 weeks alongside his symptoms. Repeat imaging at 4 weeks from initial presentation demonstrated a reduction in lymphadenopathy, near resolution of aortitis and no significant dural thickening or enhancement. PET CT body scan subsequently found no abnormal FDG avidity to suggest active large vessel vasculitis, meningitis or malignancy.

The temporal relationship with lenalidomide exposure and a complete clinical, biochemical and radiographic resolution without ongoing aggressive systemic therapy suggests his large vessel vasculitis and pachymeningitis were caused by lenalidomide. This case is particularly unique as neither manifestation is yet described in the literature. Considering the more typical association of pachymeningitis with small vessel vasculitis,[3] our case may reflect variable vessel vasculitis induced by lenalidomide.

[1.] Gribben J. J Clin Oncol 2015;33:2803-11. [2.] Montefusco V. Leuk Lymphoma 2014;55:2032-7. [3.] Mekinian A. Medicine 2018;97:e11413.

We reviewed clinical histories and laboratory findings including genetic testing, in family members across 3 generations. Gene panel testing was performed by next-generation sequencing at the Hospital for Sick Children and variants were classified as per the American College of Medical Geneticists criteria.

The proband (grandmother), aged 71, was initially referred for unexplained and persistently elevated inflammatory markers (ESR 91mm/h, CRP 58-179mg/L). She had no symptoms of any inflammatory disease. Her son suffered from infant onset recurrent painful orogenital ulcers and arthritis, on a background of granuloma annulare and celiac disease. His inflammatory markers were also elevated (CRP 12-17 mg/L). The proband’s daughter was diagnosed in infancy with type 1 diabetes and died from an insulin overdose. Prior to this, she had a son who was also affected by infantile diabetes. Despite having no systemic inflammatory features, he also exhibited elevated CRP (10mg/L). Genetic analysis revealed a heterozygous TNFAIP3 variant, (c.1318G>T, p.Gly440*), in all 3 individuals. This variant was absent from healthy population databases. It has never been documented in the literature and was bioinformatically predicted to create a premature stop codon leading to an absent or dysfunctional A20 protein. As such, it was classified as Likely Pathogenic. The proband’s son was treated initially with colchicine with partial improvement, and later with apremilast, which completely eliminated any further mucocutaneous ulcerations.

We report a novel truncating variant in TNFAIP3 causing HA20 in a multigenerational family. Our case series is in line with the current literature and demonstrates the phenotypic variability of HA20 even within the same family, ranging from silent inflammation to Behcet-like disease to organ-specific autoimmunity. Recognizing the variable expressivity and incomplete penetrance of HA20 is important for early diagnosis, screening of family members, and the use of targeted therapy in affected individuals.

A 21-year-old male first presented in 2012 at the age of 6 with recurrent episodes of transient, non-pruritic urticarial rash, low-grade fever, fatigue, episodic arthritis of the knees and ankles, and enthesitis predominantly involving the Achilles tendon and dorsal foot insertions. During flares, inflammatory markers were elevated (CRP 12-18 mg/L, ESR 31-38 mm/h, serum amyloid A >160,000 ng/mL), with mild normocytic anemia. Autoimmune serologies and complement levels were normal. In 2013, mild unilateral sensorineural hearing loss was identified and remained stable; MRI of the brain and internal auditory canals was normal. Initial genetic testing with a recurrent fever syndrome panel in 2014 and whole-exome sequencing in 2018 were both reported as negative. Anakinra, initiated in 2014, provided partial improvement but was discontinued due to injection-site reactions. In 2018, with worsening symptoms and elevated inflammation (CRP 47 mg/L, ESR 31 mm/h, SAA 55,264 ng/mL), canakinumab was started, leading to rapid and sustained normalization of inflammatory markers and resolution of clinical symptoms. The patient remained in long-term disease quiescence for approximately 4 years (2018-2022), after which the patient discontinued treatment and was lost to follow-up. In 2025, stored DNA was re-analyzed with high-depth sequencing for a panel of 101 known autoinflammatory genes and identified a NLRP3 variant (p. Arg260Pro, Clinvar classification pathogenic) in approximately 5% of reads. Retrospective analysis of existing whole-exome data did not identify this low-level variant.

Consistent with previous reports of NLRP3 mosaicism as a cause of CAPS, this case demonstrates that negative genetic testing does not exclude cryopyrin-associated periodic syndromes and that somatic mosaicism should be considered when the clinical phenotype is compelling. As sequencing technologies evolve, periodic re-analysis offers a critical second opportunity for diagnosis and targeted treatment.

A 65-year-old male was diagnosed with MCTD after presenting with pulmonary arterial hypertension, presumed glomerulonephritis, Raynaud’s phenomenon, and polyarthritis on a background of coronary artery disease and recent NSTEMI requiring stent placement. Investigation revealed a positive ANA (≥1:640, speckled pattern); high-positive anti-RNP-A, Sm/RNP, Ro60/SSA, Ro52/TRIM21, and SSB; and proteinuria. Right heart catheterization and renal biopsy were deferred given dual-antiplatelet therapy and spontaneous renal recovery. He received methylprednisolone prior to a prednisone taper and initiated mycophenolate mofetil (MMF), hydroxychloroquine, macicentan, and tadalafil. He subsequently presented with watery diarrhea, fever (38.5°C), malaise, weight loss and arthralgia. Infectious work-up revealed CMV viremia (serum viral load >4 million/mL) and C. difficile colitis, for which he initiated ganciclovir and oral vancomycin. He was found to have new bicytopenia (hemoglobin 78 g/L, platelet count 175 x10^9/L), hyperferritinemia (peak 6751 μg/L), hypertriglyceridemia (3.47 mmol/L), hypofibrinogenemia (nadir 1.0 g/L), and elevated aspartate aminotransferase (101 units/L). His C-reactive protein was 21.0 mg/L (peak) and his complement C3 and C4 were normal. Both hematology and rheumatology were consulted, and the patient was diagnosed with MAS. Bone marrow biopsy was deferred given overwhelming evidence for MAS. His MMF was held for diarrhea, and he was initiated on methylprednisolone (250 mg daily for 3 consecutive days, followed by taper) and anakinra (100 mg subcutaneously daily, titrated to 3-times daily) with clinical and biochemical improvement.

We found only 2 other published English-language adult cases of MAS in conjunction with MCTD in the context of infection. One case was related to histoplasmosis,[2] and the other to an unspecified infection. [3] It is well known that infections can trigger MAS,[1] and while rare, in the appropriate clinical context, MAS should be considered in patients with MCTD who present with an infection and are not improving with standard treatment and whose biochemical parameters suggest MAS.

[1.] Atteritano M. Eur Rev Medi Pharmacol Sci 2012;16:1414-24. [2.] Kawashima H. Intern Med 2025;64:141-6. [3.] Dhote R. Arthritis Rheum 2003;49:633-9.

A scoping review evaluating the incidence of hypertension in patients receiving ICIs, either as monotherapy or in combination with other anticancer agents, was conducted in accordance with the Joanna Briggs Institute (JBI) methodology and the PRISMA-ScR reporting guidelines. A comprehensive search of PubMed, CINAHL, Embase, and MEDLINE databases was performed for studies published up to June 30, 2025. Eligible studies included adults (≥18 years) with cancer treated with programmed cell death protein-1 (PD-1), programmed death-ligand 1 (PD-L1), or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitors, excluding those with pre-existing hypertension. We identified ICI drug classes, combination regimens, and cancer types that are most frequently associated with hypertension.

A total of 200 studies (n = 226 incidence values) were included in this review. The reported median participant age ranged from 30 to 79 years among patients receiving ICIs in combination with other anticancer agents, and from 54 to 70 years among those treated with ICI monotherapy. The incidence of hypertension demonstrated considerable heterogeneity across studies, with a median of 28.6% (range 0.0-100%) in the combination therapy group (n = 211) and 8.2% (range 0.0-54.3%) in the monotherapy group (n = 15) (Figure 1). Hypertensive events were most reported with PD-1 inhibitors, followed by PD-L1 inhibitors, while CTLA-4 inhibitors demonstrated the lowest reported frequency. Notably, the occurrence of hypertension was more pronounced in combination regimens, particularly those including tyrosine kinase inhibitors (TKIs) or vascular endothelial growth factors (VEGF) inhibitors. Among cancer types, hepatocellular carcinoma and lung cancer were most frequently associated with hypertension in the ICI combination and monotherapy groups, respectively. Figure 1.

Incidence of Hypertension across ICI-based regimens

Our findings demonstrate that ICIs, especially in combination therapy, increases the occurrence of hypertension in cancer patients, suggesting the importance of immune mechanisms in the development of hypertension. Given the limited number of studies characterizing hypertension arising from ICIs, further research is warranted to elucidate underlying mechanisms, refine risk stratification, and inform evidence-based clinical decision-making.

[1.] Cohen Tervaert JW. Hypertension Res 2011;34:443-4. [2.] Pober JS. J Clin Invest 2014;124:4234-6.

This post-hoc, unadjusted, treatment-agnostic analysis included PsA patients from the SPIRIT-P1, -P2, and -H2H studies who were treated with ixekizumab or adalimumab.[1] Patients achieving ACR50 or DAPSA LDA at week 24 (W24) were categorized based on baseline body mass index (BMI): Normal (<25 kg/m2), Overweight (25-<30 kg/m2), and Obesity (≥30 kg/m2). HR-QoL outcomes included Health Assessment Questionnaire-Disability Index (HAQ-DI) and fatigue severity numeric rating scale (NRS). Disease activity was evaluated using pain visual analog scale (VAS), swollen joint count (SJC), tender joint count (TJC), patient global assessment of disease activity (PatGA), physician global assessment of disease activity (PGA), and C-reactive protein (CRP). Observed data were presented. Non-parametric (Mann-Whitney U) test was used to account for non-normal distribution of some parameters; overweight or obesity subgroups were compared to the normal BMI subgroup; p<0.05 denoted statistical significance. No multiplicity testing adjustment was performed. The analysis was not adjusted for baseline assessments of HR-QoL or disease activity.

Among patients who achieved ACR50 by W24, significant differences were observed between obesity and normal BMI subgroups for HAQ-DI, fatigue severity NRS, pain VAS, and PatGA. CRP levels were significantly elevated for obesity and overweight vs the normal BMI subgroup (Table 1). Among patients who achieved DAPSA LDA by W24, patients with obesity had significantly higher fatigue severity NRS vs normal BMI subgroup. Pain VAS scores were significantly higher for the overweight vs normal BMI groups. Differences in PatGA and CRP were statistically significant between obesity and overweight vs normal BMI subgroup. HAQ-DI differences were not significant across BMI subgroups. No significant differences were observed in PGA, SJC, and TJC across BMI subgroups for patients achieving ACR50 or DAPSA LDA at W24. Table 1.

Observed Clinical Assessments and Patient-Reported Outcomes by BMI^a Categories (<25, 25 - <30, ≥30) in Intent-to-Treat Population on Active Biologic Treatment^b

In patients with PsA who achieved stringent treatment targets of ACR50 and DAPSA LDA after 24 weeks of treatment, obesity/overweight is associated with some indicators of negative impact on PsA disease activity (pain, PatGA, CRP) and HR-QoL (fatigue, functional disability). These findings suggest that functional ability, HR-QoL, and other health outcomes in patients with PsA and obesity may be further improved by addressing comorbid obesity.

[1.] Kristensen LE. Rheumatol Ther 2025;12:381-95.

In this retrospective, observational case series, we performed a chart review at the University of British Columbia of 180 IgG4-RD patients. Research Ethics Board approval was obtained. Demographic data, IgG4 serum levels, diagnostic and referral pathways, clinical manifestations and pathological findings were retrieved from patients diagnosed with IgG4-ROD between the Jan 1, 2010 - June 1, 2025, all managed under a unified diagnostic and pathological framework. Descriptive analysis was performed on Excel (Microsoft, Redmond, WA).

Eight representative patients with IgG4-ROD were included in this analysis from a cohort of 51 identified cases. Four patients (50%) had acute inflammatory flare-ups preceding the onset of chronic symptoms later attributed to IgG4-ROD. The median time from chronic symptom onset to expert subspecialty assessment was 15.5 months (range 1-23 months). Patients had a median of 6.5 specialist encounters, 1 diagnostic test panel, 2 biopsies, and 2 diagnostic imaging studies before a definitive diagnosis was established.

This study represents the first health-systems analysis of patients with IgG4-ROD in a Canadian context. We observed prolonged intervals before expert care and a high number of specialist encounters along the diagnostic pathway. In a publicly funded system already burdened by long wait times, these findings highlight the need to streamline triage and referral pathways for IgG4-ROD to enable more efficient, coordinated care.

[1.] Ko J. Ophthalmology 2025;132:995-1004. [2.] Stone J. N Engl J Med 2012;366:539-51.

An online survey based on the 2022 CRA RA guidelines assessed participants’ knowledge, attitudes, and practices, informing the creation of a modified mPAM tool. Participants invited to participate in the pilot project were sampled from current members of the CRA Education and Guidelines Committees. The mPAM guided rheumatologists through a structured mini-audit of their own patient charts, focusing on disease remission rates, medication use, tapering discussions, flare management, and shared decision-making. Each participant received individualized feedback and educational resources, followed by an invitation to complete a re-audit several months later. Quantitative results were analyzed descriptively, and qualitative reflections underwent thematic analysis to identify trends.

Eleven CRA members participated in the pilot; 8 completed both the audit and re-audit. In the initial audit, 60% of patients were in remission, predominantly managed with conventional synthetic DMARDs (69%), while biologic or targeted synthetic therapies accounted for 23%. Identified guideline gaps included documentation of tapering (45%), flare discussions (38%), and shared decision-making (38%). Thematic analysis highlighted inconsistent documentation and limited detail regarding medication and patient communication. Re-audit reflections demonstrated increased awareness of documentation practices, improved incorporation of guideline elements, and reported adoption of strategies such as explicit patient communication on management plans. Participants described the mPAM as relevant, practical, and aligned with Maintenance of Certification (MOC) objectives.

The Mini-Practice Audit Model (mPAM) provides a feasible, effective approach to engage rheumatologists in self-assessment and continuing professional development aligned with disease specific treatment guidelines. By promoting reflective practice through personalized feedback and iterative auditing, the mPAM enhanced participants’ awareness of clinical documentation and guideline adherence. The pilot demonstrated potential for broader application across rheumatology and other specialties.

[1.] Yates M. Rheumatology (Oxford) 2020;59;8:2035-42. [2.] Eva KW. Acad Med 2005;80:S46-54. [3.] Wooster D. JVU 2007;31:207-10. Practice Reflection Award

A 57-year-old man with relapsing-remitting MS on Tecfidera presented with a 1-year history of symptoms beginning with sudden-onset bilateral hand numbness, nocturnal heat sensations, plantar fasciitis, and mild foot drop while traveling internationally. Upon returning, nerve conduction studies confirmed bilateral carpal tunnel syndrome, and he underwent right carpal tunnel release without symptomatic improvement. Spinal MRI showed 2 new MS lesions at C4 and T3, though neither accounted for his symptoms. Over the following months, his musculoskeletal symptoms progressed to weakness, frequent dropping of objects, impaired fine motor control, stiffness in all extremities, and restricted mobility. He also reported a 3-month history of constitutional symptoms, including unintentional weight loss of 30 pounds, occasional night sweats, and generalized pruritus. On examination during his initial Rheumatology consultation, he was noted to have positive groove sign over the forearms and calves, lower extremity hyperpigmentation, erythema over the dorsum of the feet, flexor contractures of the fingers with a positive prayer sign, inability to make a fist, diminished bilateral grip strength, and restricted ability to kneel or cross the legs due to fascial tightening. In terms of investigations, comprehensive malignancy screening (pan-CT, PET, colonoscopy, esophagogastroduodenoscopy) was negative. Serologic testing revealed modest CRP elevation and weakly positive anti-Mup44 antibody. Muscle biopsy demonstrated myofasciitis, confirming the diagnosis. The patient provided consent for publication.

The patient was started on prednisone, resulting in prompt symptomatic improvement. In collaboration with Neurology, rituximab was initiated to manage both myofasciitis and MS concurrently. The weakly positive anti-Mup44 antibody, which is typically associated with inclusion body myositis (IBM), was considered to be clinically insignificant given that the clinical course and rapid response to prednisone were not in keeping with IBM. To our knowledge, this is the first report on a case of myofasciitis in an MS patient. This case highlights the importance of careful physical examination, expedited tissue diagnosis and close interdisciplinary collaboration between neurology and rheumatology for the workup of myopathies in patients with underlying neurological disease.

A 30-year-old man of East Asian ancestry presents with a 2-month history of heliotrope rash, puffy eyes, periungal erythema, bilateral polyarthritis, as well as muscle weakness progressing to dysphagia and dyspnea. His Initial CK was 993 with a negative ANA, RF, CCP, and a CRP of 12. On his myositis panel, he was positive for anti-MDA-5 (51), anti-Ku positivity (42). His pulmonary function test had decreased DLCO (61%) but increased residual volume (133%), favoring neuromuscular restriction, with only a small non-specific ground glass opacity on CT Chest with no specific ILD signs. He was started on IVIg 2 g/kg as well as methylprednisolone 500 mg 3-day pulse (Figure 1 for full therapeutic course). He also received an initial Rituximab 1g dose 4 days after admission. On day 4, he was planned for discharge, however, his ferritin continued to rise from admission 3,779 ug/L to a peak of 6,412 ug/L on post-admission day 13, with increasing Triglycerides to peak of 2.62 mmol/L, a mid-100s range transaminitis, worsening weakness and therefore there was a concern for macrophage activation syndrome (MAS). Peak H-score was 146, however, no signs of primary HLH was seen on bone marrow biopsy. Soluble CD163 receptor (1467 ng/ml, cutoff was 1217) was positive as well as was sIL2 (360 ng/ml, cutoff was 666)s. He was started on Tofacitinib 11 mg daily and re-pulsed with Methylprednisolone 500 mg for 3 days again. He was also later (see Figure 1) given Anakinra 100 mg q8H and pulsed again with Methylprednisolone 500 mg for 3 days and also received a second Rituximab 1g dose and IVIG 2g/kg course. Multiple attempts to taper steroids were unsuccessful with MRI on post-admission day 31 demonstrating thigh hematoma and worsening myositis despite treatment, with the hematoma felt due to myositis which lead to a third course of IVIG (2g/kg) and he improved and MDA-5 level continued to reduce until discharge when it was 17. Ultimately, he was discharged on Anakinra, Prednisone, and Tofacitinib. He remained stable with Prednisone and Anakinra down-taper and was stable at a 6-month follow-up on only Tofacitinib 10 mg BID and Anakinra 100 mg sc on alternating days.

Here we present a novel case of MDA-5 overlap with MAS, in a patient without radiographic ILD, successfully treated by immunosuppression including Tofacitinib and Anakinra. This builds on past work treating MDA-5 with ILD with a triple regimen (Methylprednisolone, Rituximab, Tofacitinib) [2] and further supports the role of Tofacitinib.[3]

[1.] Lu X. Nat Rev Rheumatol 2024;20:48-62. [2.] Manghani M. Rheumatol Autoimmun 2024;4:122-5. [3.] Yanagihara T. Eur Respir J 2025;65:2500458.

Our patient is a 76-year-old male, presenting with lower limb myalgias, weakness, and elevated inflammatory markers. He was initially treated by his other physicians as PMR with moderate dose prednisone when we met. Despite therapy with moderate dose prednisone, he did not experience significant improvement, and his symptoms were largely proximal lower extremity, with no upper extremity symptoms. He had no skin rash, or other connective tissue disease symptoms. His lower extremity symptoms were not due to inflammatory arthritis in the lower extremity joints. He had no respiratory or renal disease on history or current symptoms. He did endorse a 1-year history of chronic nasal congestion, altered taste, reduced appetite, fatigue and night sweats. He was initially on a statin which was discontinued, given a concern for possible statin induced myopathy. Imaging for malignancy was negative. Auto-antibody testing was performed, which eventually identified positive anti-SRP and positive anti-MPO ANCA, as well as elevated rheumatoid factor. While his CK had been found to be within normal limits, serum aldolase levels were found to be elevated. EMG-NCS performed by neuromuscular neurology supported a myopathic process and sensorimotor axonal polyneuropathy likely secondary to his diabetes. Ultimately muscle biopsy confirmed presence of a subacute to chronic destructive vasculitic process involving arterioles and small arteries. With these findings, the unifying diagnosis of ANCA-related small vessel vasculitis involving mainly the lower extremity skeletal muscles was made.

Small vessel vasculitis involving mainly skeletal muscle is an uncommon presentation of ANCA associated vasculitis. The low titer positivity of multiple antibodies supporting entities which can cause similar symptoms contributed to this patient being a diagnostic dilemma. This case serves as an example of the value of consideration for small vessel vasculitis of skeletal muscle as a cause of weakness, and the importance of tissue biopsy to help confirm diagnoses.

[1.] Conticini E. Autoimmun Rev 2022;21:103029. [2.] Ruffer N. J Neurol 2025;272:496. [3.] Shimojima Y. Autoimmun Rev 2024;23:103602.

We assessed sera from pregnancies with CHB outcome compared with anti-Ro-positive pregnancies without CHB. We used solubilized proteins from fetal heart tissue, and from developmentally immature stem cell-derived cardiomyocytes, to characterize the targets of maternal serum antibodies from affected pregnancies, compared to those from unaffected pregnancies. Targets were identified on 2D gels of cardiac proteins exposed to maternal sera and confirmed using single-lane westerns.[1,2] A targeted 4-peptide ELISA was developed based on the identified cardiac protein epitopes and is being assessed. Additional cohorts from Canada, Germany, Italy, Spain and U.S. are being assessed to refine and validate our assays. (Table 1) In collaboration with EuroImmun AG, we are developing a standardized research assay that can be translated to a laboratory-developed test for clinical care.

TABLE 1

Pregnancies with prior CHB were assessed separately (Table 1, Columns 11 to 13). For no prior CHB, sera from 7 affected and 5 unaffected pregnancies identified expanding autoantibody target cardiac proteins (beyond Ro and La) throughout CHB pregnancies, which were absent in unaffected pregnancies. (7/7 vs 0/5; p=0.0013, Fisher Exact Test [FET]) The earliest target was AT1A1 (sodium/potassium pump alpha 1 subunit), and western blots identified these autoantibodies. (7/7 vs 0/5; p=0.0013, FET) A Padua cohort identified the same autoantibody fingerprint, and same AT1A1 reactivity by both western and ELISA. (20/20 vs 0/25; p<0.00001, FET). A Toronto (validation) cohort had equivalent results for 2/3 methods. (16/16 vs 0/24; p<0.00001, FET). In pregnancies with a prior CHB child, the antibody pattern and anti-AT1A1 ELISA were occasionally positive despite no CHB resulting in a reduced positive predictive value (0.429). Negative predictive value remained at 1.0. Ro-negative autoimmune CHB[3] provided equivalent results. Six additional cohorts are under evaluation.

We have identified AT1A1 as a robust auto-antibody target associated with autoimmune CHB outcome. This marker demonstrates strong discriminatory performance across multiple cohorts. Ongoing multicenter validation and assay development with commercial partner EuroImmun AG will support translation of these findings into a clinical diagnostic test aimed at improving CHB risk prediction.

[1.] Benjamin S. Lancet Rheumatol 2025;7:e554-64. [2.] Benjamin S. [Abstract]. Arthritis Rheumatol 2022;74 Suppl 9. https://acrabstracts.org/abstract/fetal-cardiac-targets-identify-the-autoantibodies-associated-with-congenital-heart-block/. [3.] Brucato A. J Rheumatol 2009;36:1744-8.

Blood samples were collected from 45 patients with new onset (< 5 yrs), positive ANAs, and suspected SLE at Brigham and Women’s Hospital Lupus Center. At baseline, none met SLE or other SARD classification criteria. All received prednisone <10mg/day and no immunosuppressants. Using baseline samples, soluble SIGLEC1 was measured by ELISA and a comprehensive autoantibody profile was performed: ANA by indirect immunofluorescence assay on HEp-2 cells and patterns classified according to the International Consensus on ANA Pattern anti-cell (AC) nomenclature, SLE-related autoantibodies, including anti-DFS70 by a fully automated multi-analyte system using particle-based multi-analyte technology, and anti-C1q and anti-phospholipid antibodies by ELISA. To examine patterns of autoantibodies, we used hierarchical clustering and investigated their relationships with disease progression, LLAS (sum of standardized proportions of each of 5 lymphocyte subsets above), and SIGLEC1 levels.

Of 45 patients, 36 had multiple visits with a mean follow-up of 13.6 months. In follow-up, 3 patients were diagnosed with SLE and met 2012 SLICC or 2019 EULAR/ACR criteria; 4 were diagnosed with or suspected of new dermatomyositis or Sjögren disease. We identified 5 clusters of suspected SLE patients based on autoantibody profiles (Figure 1A). Cluster A (AC-4 nuclear speckled with multiple autoantibody reactivity including anti-RNP, -dsDNA, -anti-Ro60/SSA) was more likely to progress or develop a CTD including SLE (OR 1.94, 95% CI 0.42-3.46) than others (Figure 1B), particularly compared to Cluster C (no autoantibodies). Cluster A also had significantly higher SIGLEC1 vs Cluster E (Figure 1C). There was no difference in LLAS by autoantibody cluster (Figure 1D).

Fig 1A) Five autoantibody clusters (A-E) based on baseline samples of 45 suspected SLE (L to R): Cluster A (n=11) nuclear speckled pattern (AC-4) with the greatest autoantibody reactivity including anti-RNP, anti-dsDNA, and anti-TROVE2/Ro60, Cluster B (n=4) nuclear large speckled pattern (AC-5), Cluster C (n=9) negative ANA (AC-0) with rare autoantibodies at low titers, Cluster D (n=9) isolated anti-DFS70 antibody with dense fine speckled (AC2) pattern, and Cluster E (n=12) nuclear speckled with mitotic plate staining (AC-30). Fig 1B) Cluster A (AC-4 nuclear speckled pattern and multiple autoantibody reactivity) had largest N with disease progression +/– definite SLE or other SARD at follow-up. *denotes a significant difference in proportion of patients who had disease progression +/– definite SLE or other CTD at follow-up (Cluster A vs. C, diff. 43.43%, 95%CI 0.08%-0.79%). Fig 1C) 5 autoAb clusters of suspected SLE patients and median SIGLEC1. Cluster A had higher median SIGLEC1 than others. Fig 1D) Lupus Lymphocyte Activation Score (LLAS) not statistically different across autoAb clusters

Autoantibody profile characterized by nuclear speckled with multiple autoantibody reactivity, including anti-RNP, -dsDNA, and -Ro60/SSA, was predictive of SARD development. This cluster also had higher baseline SIGLEC1 vs those with monospecific DFS70 antibodies or no autoantibodies. Further analyses will assess whether LLAS, SIGLEC1, and autoantibodies are complementary, and when combined, could enhance the prediction of SLE development.

[1.] Horisberger A. [Abstract]. Arthritis Rheumatol 2024;76 Suppl 9.

A 48-year-old male was referred for early childhood onset, recurrent 3-5-day febrile episodes accompanied by severe abdominal pain, large joint arthralgias and myalgias. He was treated intermittently with corticosteroids and NSAIDs, with incomplete response. At 43 years old he developed chronic kidney disease with renal biopsy compatible with amyloidosis. This eventually progressed to ESRD requiring hemodialysis. Genetic testing was performed when he was 48 years old and revealed a heterozygous missense variant in TNFRSF1A (c.214_215delinsCT, p.Cys72Leu). The mutation resides in exon 3 within the extracellular cysteine-rich domain, and was predicted to disrupt disulfide bond formation, resulting in misfolded receptor protein and defective TNFα signaling. Substitutions at the same residue (Cys72Arg, Cys72Ser) had been previously demonstrated to be causative for TRAPS.[2] His asymptomatic parents did not carry the mutation. As such, this de novo Cys72Leu variant was classified as Likely Pathogenic, and the patient was diagnosed with TRAPS. Anakinra 100 mg SC daily was started which prevented further attacks. However, he remains on hemodialysis and is on the waitlist for renal transplant.

In summary, our case highlights the importance of early recognition of autoinflammatory diseases like TRAPS, in order to initiate targeted treatment and prevent life altering complications such as amyloidosis and ESRD. We report a novel variant in the TNFRSF1A gene, adding to the literature of mutations causing TRAPS. Further studies are needed to functionally characterize the biological impact of Cys72Leu, as well as to elucidate the complex mechanisms between TNF receptor dysfunction and IL-1 signaling.

[1.] Gaggiano C. Mediators Inflamm 2020;7:8562485. [2.] Lachmann HJ. Ann Rheum Dis 2014;73:2160-7.

In this longitudinal study, consecutive adult English-speaking SLE patients were invited to participate. Patients completed an assessment using PROMIS CAT’s 13 domains (physical function, mobility, pain behavior, pain interference, ability to participate in social roles, satisfaction with social roles and activities, fatigue, sleep disturbance, sleep-related impairment, applied cognition-abilities, anger, anxiety, and depression) and corresponding legacy instruments at baseline and at 3 and 6 months. The generic anchor question was asked to identify those with symptom severity change. Domain-specific anchor questions were asked at 6 months with responses graded from –7 (greatest worsening) to +7 (greatest improvement), and 0 representing no change. For domain-specific anchors, improvement was defined as >1 and worsening as < –1. Area Under the Curve (AUC) and 95% confidence intervals for each of the 13 domains were calculated and minimal important differences (MID) were derived from the above AUC analysis, also called Anchor-based approach.

108 patients (90.7% female) were included. MIDs for PROMIS Physical Function were calculated to be –1.84 in patients that improved and –6.17 in patients who worsened over 6 months (Figure 1). MID for Satisfaction with Social Roles and Activities was –4.40 in patients that improved over 6 months (Figure 1). AUC was considered significant (> 0.7) in PROMIS Physical Function (improved), Satisfaction with Social Roles and Activities (improved), Pain Interference (worsened), fatigue (worsened) and sleep disturbance (worsened). Figure 1:

AUC and Anchor-based MID in patients reported worsening and improvement in anchor Q1 (at 6 months)

In summary, MID for PROMIS CAT in SLE cohort varied significantly among categories. Given patients did not demonstrate very significant change over 6 months as expected in the absence of intervention or change in therapy, MID is to be interpreted cautiously in this setting. Physical function and Satisfaction with Social Roles and Activities were domains in which MID could be derived.

[1.] Moazzami M. Lupus 2021;30:2102-13.

This case series features 5 male patients (Table 1). The median age at disease onset was 65 (range 50-77) years. The median delay in diagnosis was 18 (range 1-46) months. The median disease duration was 44 (range 20-79) months. All patients had somatic UBA1 variants: p.Met41Val (n=2), p.Met41Thr, p.Met41Leu, and 1 uncharacterized p.? variant (Table 1). All patients reported constitutional symptoms. Initial working diagnoses included unspecified inflammatory condition, adult-onset Still’s disease, relapsing polychondritis (n=2), and atypical polyarteritis nodosa vs undifferentiated connective tissue disease (Table 1). Elevated inflammatory markers were observed in all patients (CRP frequently >100 mg/L). Vacuoles were confirmed on bone marrow biopsy in 4 patients. Three patients presented with, and 1 later developed, macrocytic anemia, whereas 1 patient had intermittent normocytic anemia. Thrombocytopenia and lymphopenia were each observed in 3 patients. Two patients developed myelodysplastic syndrome following diagnosis of VEXAS. Patients trialed several different therapies including hydroxychloroquine, methotrexate, azathioprine, mycophenolate, rituximab, anakinra, tocilizumab, tofacitinib, ruxolitinib, colchicine and dapsone with limited or no sustained benefit. Corticosteroids were required at moderate-to-high doses in most patients. At present, patient A is maintained on prednisone 35 mg daily. Patient B is taking prednisone 15 mg daily and ruxolitinib 20 mg twice daily. Patient C underwent alloHSCT in April 2025 with resolution of symptoms and discontinuation of prior medications (prednisone and ruxolitinib). Repeat bone marrow biopsy showed <0.5% UBA1. Patient D continues with prednisone 5-6 mg daily and azacitidine. Patient E underwent alloHSCT in August 2023. He developed chronic graft-versus-host disease requiring treatment with prednisone 7 mg daily and belumosudil. There was no evidence of UBA1 mutation on repeat bone marrow biopsy.

In conclusion, this case series highlights the multisystem nature of VEXAS syndrome and the substantial diagnostic delay often encountered in clinical practice. We recommend considering VEXAS syndrome in patients with treatment-resistant autoinflammatory syndrome and cytopenias, especially macrocytic anemia. While conventional immunosuppressive medications have provided limited benefit, allogeneic hematopoietic stem cell transplant may be promising for select patients.

[1.] Beck D. N Engl J Med 2020;383:2628-38. [2.] Williams S. J Rheumatol 2024;51:734-7.

Data was collected prospectively and analyzed retrospectively from a Newfoundland PsA cohort started in 2007. Patients were indexed on the date they first initiated secukinumab or izekizumab. Retention was assessed at 6, 12, 24, and 36 months using clinical and laboratory data including TJC28, SJC28, health assessment questionnaire (HAQ), patient and physician global assessments, PASI scores, and CRP levels. Serologic HLA class I typing was performed. IBM SPSS v.28.0 was used to calculate Kaplan-Meier survival curves and 2-tailed Spearman correlation coefficients.

30 patients were included. All were b/tsDMARD experienced. 60% of patients were female. The mean BMI was 31.3 kg/m2 and 33.3% of participants had a smoking history. PsA was diagnosed at a mean age of 42.3 (21-60) years. On index, patients had a mean CRP of 11.5 mg/mL, TJC28 of 6.7, SJC28 of 4.7, and HAQ of 1.5. Overall retention was estimated at 50.3% at 36 months. 23 patients had HLA class I analysis performed. The most common haplotypes were HLA A1 (43.5%), A2 (52.2%), B8 (30.4%), B27 (39.1%), Bw4 (39.1%), and Bw6 (47.8%). HLA Bw4 was negatively associated with retention to IL-17A inhibitors secukinumab and ixekizumab with Spearman correlation coefficient (r) –0.639 (p= 0.025) (Table). Although not statistically significant, in those who discontinued IL-17A antagonists before 36 months, HLA A2 and B27 showed tendency for negative association with r –0.418 (p= 0.177) and –0.123 (p= 0.704), respectively. We did not find any definitive association with HLA class I profile and response outcome measures such as CRP or HAQ. There was also no association with discontinuation due to lack of efficacy or side effects. The small nature of the study limited the ability to assess for a difference in response to treatment with either agent. Table 2.

Correlation between time to discontinuation of interleukin 17A antagonists, CRP at index, and HLA class I type.

In patients with psoriatic arthritis, HLA class I type may be associated with various responses to treatment with the IL-17A antagonists secukinumab or ixekizumab. This cohort study is limited by small sample size and has significant potential for error, but further exploration with larger studies is warranted.

[1.] Rahman P. J Rheumatol 2012;39:431-3.

The HHS SAID registry was established to describe and follow patients with systemic autoinflammatory diseases at Hamilton Health Sciences. Patients enrolled in the registry from February 2023 to April 2025 (N=94) were stratified by consultation clinic (Autoinflammatory Clinic [AC] or Pediatric Rheumatology Clinic [PRC]) and by diagnosis (Periodic fever, Aphthous stomatitis, Pharyngitis, and Adenitis [PFAPA]; Syndrome of Undifferentiated Recurrent Fever [SURF]; Familial Mediterranean Fever [FMF]; Other Monogenic Autoinflammatory Syndromes [OMAS]; and systemic Juvenile Idiopathic Arthritis [sJIA]). Descriptive statistics were generated using an available-case approach to summarize demographic, referral, and time-interval data. Group differences were assessed using chi-square or Fisher’s exact tests for categorical variables and Mann-Whitney U or Kruskal-Wallis tests with post hoc pairwise comparisons for continuous variables.

Ninety-four participants were included (50 male, 44 female). Sixty pediatric participants were seen through PRC (median age=5.2yr, IQR=6.0yr) and 24 pediatric and adult participants were seen through AC (median=15.4yr, IQR=33.8yr) (p=0.000). Diagnosis stratification amounted to 39 PFAPA (41.5%), 21 FMF (22.3%), 14 OMAS (14.9%), 13 SURF (13.8%), and 7 sJIA (7.5%). Besides sJIA, all other groups had similar referral to consultation times (median range=3.0-4.1mo, p>0.05). From consultation to diagnosis, PFAPA (median=0.0mo) and sJIA (median=0.1mo) showed near-immediate diagnosis, unlike FMF (median=3.0mo, IQR=5.3mo), SURF (median=4.6mo, IQR=14.1mo), and OMAS (median=12.8mo, IQR=33.1mo) (p=0.000). From symptom onset to diagnosis, OMAS (median=47.5mo, IQR=21.7mo, p=0.002), SURF (median=26.2mo, IQR=39.5mo, p=0.001) and PFAPA (median=14.8mo, IQR=18.9mo, p=0.014) had the longest durations (Table 1). Referrals lacked key information in 91.7% (22) of AC and 74.6% (44) of PRC cases. Within the AC, missing information on fever/episode duration (OR=4.5, p=0.003) and symptom onset (OR=3.3, p=0.047) were significantly higher vs the PRC. OMAS was the only group predominantly referred by other specialists (64.3%, p=0.005). All disease groups showed high missing referral information rates on symptom onset, episode duration, and frequency: lowest in PFAPA (61.5%) and >90% in others. Table 1.

Summary of Age and Time-to-Diagnosis Intervals Stratified by Clinic and Diagnosis Groups.

Except for sJIA, all autoinflammatory diseases had long referral, consultation, and diagnostic intervals, most notably SURF and OMAS, reflecting diagnostic uncertainty and referral inefficiencies. High rates of missing referral details may have contributed to these diagnostic delays. Standardized referral templates and clinician education on diverse autoinflammatory presentations may help reduce diagnostic latency and improve timely specialist care.

This case involves a 30-year-old gentleman with minimal past medical history, who presented at age 25 to an emergency department with a 12-month history of constitutional symptoms, including nearly 100-pound weight loss, fatigue, night sweats, and fevers. This was accompanied by musculoskeletal features such as mid and lower back pain, peripheral edema, and multifocal skin and soft tissue nodules suspected to be in fitting with diffuse lymphadenopathy. After extensive diagnostic workup, it was found that he had extensive fulminant systemic sarcoidosis, proven with excisional biopsy of a mediastinal lymph node. Also present was osseous involvement of the in the hands, feet, pelvic bones, and vertebral bodies of the thoracic and lumbar spine (Figure 1). He experienced rapid improvement with a tapering course of prednisone, which was completed after a total of 14 months of therapy. Recovery was complicated by a generalized tonic-clonic seizure 1 month after prednisone taper. Investigations yielded neurologic involvement, including parafalcine mass and leptomeningeal sarcoid involvement, as well as involvement of the spinal parenchyma of the thoracic and lumbar spine. Immunosuppression with infliximab and methotrexate (MTX) was initiated. Following 2 years of clinical stability, MTX was discontinued. He continues to experience clinical stability on infliximab infusions every 6 weeks. He had interdisciplinary follow up including with a neuroimmunology clinic. The patient reported feeling back to pre-illness state and is able to function as a caregiver to his young child. Figure 1:

Radiographic manifestations of systemic sarcoidosis in this patient. A-C: plain radiographs of bilateral feet and left hand with reticular lacelike lucency thought to represent osseous sarcoidosis, D: plain radiograph of the chest showing bilateral hilar adenopathy, E: MR thoracic spine (sagittal, T1 image) showing multiple irregularly enhancing lesions concerning for osseous (vertebral) sarcoid and cord involvement.

This case illustrates the heterogeneity of systemic sarcoidosis, manifesting in this patient predominantly with both neurosarcoidosis and musculoskeletal manifestations. Systemic immunosuppression can be beneficial for cases with severe/ systemic manifestations. Early recognition and multidisciplinary management are critical for outcomes and to prevent irreversible organ dysfunction.

[1.] Barreras P. J Neuroimmunol 2022;368:577871. [2.] Fidler LM. Eur Respir J 2019;54:1900444.

Twenty-eight patients with CNSLBP and Twenty-eight age and sex-matched asymptomatic participants were selected according to specific inclusion and exclusion criteria. Saliva samples were collected, and total RNA was isolated. Reverse transcription and qPCR were performed using the Quant Studio 3 Real-Time PCR system, ThermoFisher Scientific. Bioinformatics analysis was performed using the STRING database to explore cytokine protein-protein interaction (PPI) and miRNet for miRNA network analysis.

The expression levels of IL-18, TNFα, IL-6, HMGB1, IFNG, IL-2, IL-8, and IL-1β were increased in the saliva of LBP patients compared to the control group. A STRING database analysis of IL-18 protein-protein interactions (PPI) reveals that the PPI enrichment is highly significant, with a p-value < 1.0e-16, and the gene ontology biological process revealed its role in regulating the inflammatory response and other cytokine production. miRNet analysis showed that multiple miRNAs can target more than 1 cytokine.

The expression levels of inflammatory mediators including IL-18, TNFα, IL-6, HMGB1, IFNG, IL-2, IL-8, and IL-1β were increased in the saliva of CNSLBP patients compared to the control group. A STRING database analysis of IL-18 protein-protein interactions (PPI) reveals that the PPI enrichment is highly significant, with a p-value < 1.0e-16. IL-18 interacts with other cytokines including IL-6, TNF, IL-1B, IFNG, and IL-8. Gene ontology (biological process) revealed its role in regulating the inflammatory response and the production of other cytokines and chemokines. miRNet analysis showed that multiple miRNAs can target both IL-1B and IL-6 including hsa-let-7a-5p, hsa-let-7c-5p, hsa-let-7d-5p, hsa-miR-21-5p, hsa-miR-23a-3p, hsa-miR-25-3p, hsa-miR-26a-5p, and hsa-miR-26b-5p.

Primary OA patients who underwent total knee or hip arthroplasty were assessed for their postoperative pain at least 1-year after surgery using the WOMAC Likert 3.0 pain subscale. Three pain phenotypes were defined: sustained pain (pain on all 5 questions), pain while active (pain while walking and taking stairs), and pain at rest (pain while sitting/lying and at night while in bed). Patients reporting no pain were classified as controls. Plasma proteomic profiling was performed using the Olink® Explore HT platform. Associations between postoperative joint pain and protein expression were assessed using logistic regression adjusted for age, sex, and body mass index. Functional enrichment analysis was conducted using KEGG and GO databases. Protein-protein interaction network was constructed using the STRING database and visualized in Cytoscape 3.10.4 to identify hub proteins. Bonferroni correction was applied to control for multiple testing across 5416 proteins and 3 pain phenotypes (α=3.08x10-6).

A total of 149 patients were included. The prevalence of sustained pain, pain while active, and pain at rest 4 years after TJA was 5, 13, and 7%, respectively; 81% reported no pain, thereby served as controls (Figure 1A). No individual protein remained significant after multiple testing correction. However, 246, 332, and 260 proteins were nominally associated (p<0.05) with sustained pain, pain while active, and pain at rest, respectively. For sustained pain and pain at rest, the associated proteins were enriched in the MAPK signaling pathway, extracellular matrix, and growth factor activity. Hub proteins included CCL2, ERBB4, SHC1, NCAM1, MMP9, HRAS, FGF3, and NTRK2 for sustained pain, CD86, NCAM1, and ANXA5 for pain at rest (Figure 1B, 1D). Proteins associated with pain while active were enriched in the interleukin 17 signaling pathway, myeloid leukocyte mediated immunity, and cytokine activity. Hub proteins included ITGB2, CASP8, and CCL2 (Figure 1C).

Figure 1.

Our data showed distinct molecular signatures for different postoperative pain phenotypes following TJA. While sustained and rest pain shared enrichment in MAPK-related and extracellular matrix pathways, pain while active appeared to involve immune and inflammatory mechanisms. These findings highlight potential protein biomarkers and pathways contributing to heterogeneous postoperative pain experience in OA patients.

Primary OA patients who underwent total knee or hip arthroplasty were included. Plasma proteomic profiling was performed using the Olink® Explore HT platform, and plasma metabolomic profiling was conducted using the Biocrates MxP Quant 500 kit. Associations between early revision after TJA and protein expression were evaluated using logistic regression adjusted for age, sex, and body mass index. Functional enrichment analysis was conducted using KEGG and GO databases. Protein-protein interaction network was constructed via the STRING database, visualized in Cytoscape 3.10.4, and hub proteins were identified using the CytoHubba plug-in. Metabolites associated with hub proteins were identified using Spearman correlation analysis. Bonferroni correction was applied for multiple testing (α=9.23x10^-6 for 5,416 proteins; α=2.70x^10-5 for 622 metabolites and 3 hub proteins).

A total of 168 patients were included, with revision data extracted an average of 10.5 years after primary TJA. The early revision rate was 3% (Figure 1A), with a mean time to revision of 2.6 years. No individual protein reached significance after multiple testing correction. However, 337 proteins were nominally associated with early revision (p<0.05). These proteins were enriched in complement and coagulation cascades, hematopoietic cell lineage, and regulation of angiogenesis and vasculature development pathways (Figure 1B,C). FLT3, IL10, and NRAS were identified as hub proteins (Figure 1D), among which FLT3 and NRAS were negatively associated with early revision TJA, while IL10 was positively associated. Although no metabolite reached multiple-testing corrected significance, 28, 17, and 18 metabolites were nominally correlated (p<0.05) with FLT3, IL10, and NRAS, respectively, predominantly long-chain diglycerides, triglycerides, and phosphatidylcholines.

Figure 1

Multi-omics integration of plasma proteomics and metabolomic data revealed that dysregulation of angiogenesis and lipid metabolic pathways may contribute to the risk of early revision TJA in patients with primary OA. These pathways and their key molecular mediators warrant further validation as potential predictive biomarkers or therapeutic targets.

All inpatient consultations done from March 1, 2024, to February 28, 2025, were summarized. The various categories of data collected included demographic information, consulting services, reason for referral, clinical impact of rheumatology consult, use of joint aspirations/steroid injections, POCUS utilization, urgency of referral, and time followed under the rheumatology service. Findings were also compared to previous 12-month period from June 2011- July 2012 looking at similar data to show changes in the patient population and rheumatology consults over time, significant differences are summarized (Table 1).

Table 1

A total of 268 consults were completed during the study period, representing a 13% increase since 2012 (n=238). Due to some missing data, the reported figures underestimate the true number of patients and diagnosis seen. Female patients accounted for 58% of all consults compared to 50% in 2012. Referrals were most commonly from general internal medicine (n, 39.6%), cardiology (n, 7.5%), and neurology (n, 8.2%). Patients had a wide variety of rheumatic diseases, but the most common conditions seen were gout (n, 9.7%), osteoarthritis (n, 8.6 %), and systemic lupus erythematous (SLE) (n, 6.3%). Interestingly, the number of consults for SLE and osteoarthritis have increased dramatically compared to 2012 (n, 2.9% and n, 5.9% respectively). Patients were admitted in hospital for an average of 17 days, followed under rheumatology for an average of 5 days, and 54% of all cases were emergent/urgent. Joint aspirations and/or steroid injections were performed in 57 cases, and point-of-care ultrasound was used in 37 cases. Across 268 consultations, rheumatologists helped make the diagnosis in 202 cases (n, 75%) and confirmed diagnosis in 37 (n, 14%) cases (Table 1). Consults also commonly involved suggesting medications (n, 83%) and ordering investigations (n, 79%).

Rheumatology consultations are predominantly urgent/emergent and complex, and rheumatologists play a large role impacting diagnosis, patient management and improving outcomes. As the number of in-patient rheumatology consults increases, access to rheumatology care is vital to treat patients in a timely manner and improve patient’s quality of life.

CITE-Seq was conducted on innate immune cells from 24 patients including healthy controls (HC, n=5), non-progressor (NP, n=6) IFN high or low, progressors (P, n=5) or SARD (n=8) patients. Differential gene expression analysis was performed to identify genes of interest. Spectral flow cytometry and plasma ELISAs were conducted in an expanded group of patients to validate differences in CITE-Seq genes of interest. A monocyte cell line (THP-1) was used to investigate the kinetics of 1 gene identified by CITE-Seq to gain a better understanding of potential functional implications.

Non-progressors (NP) exhibited increased gene expression of heat shock proteins (HSPs) like HSP70 and CD52 compared to P (Figure 1A). Both proteins are proposed to promote immune regulation through tolerogenic effects on innate immune cells. Conversely, P exhibited increased gene expression of MHC class II alleles, which are associated with immune activation. Using flow cytometry, we confirmed the differences between groups of surface expression of CD52 and MHC class II on innate immune cells (Figure 1B). Little is known about how HSPs are regulated and expressed. To better understand the kinetics of HSP70, THP-1 cells were heat shocked. Gene expression showed rapid and transient upregulation which was attenuated by 18h, while soluble HSP70 increased steadily following activation of the heat shock response (Figure 1C). Protein HSP70 was decreased at the 12h timepoint using immunofluorescence (Figure 1D), following heat shock, suggesting the release of HSP70. We therefore measured plasma HSP70 in our patient cohort and found that soluble HSP70 was increased in NP compared to P (Figure 1E), in support of our CITE-Seq results. Ongoing experiments are being conducted to evaluate the release of HSP70 by purified innate immune cells from our patient cohort. Figure 1.

Innate immune cells during the progression of SARD. A) Feature plots from CITE-Seq of monocytes and DCs shotting HSPA1A (HSP70), CD52 (CD52) and HLA-DRB5 (MHC Class II). B) Spectral flow cytometry showing representative results from classical monocytes tor HLA-DR and CD52 protein expression. C) Gene expression of HSPA1A (HSP70) by RT-qPCR and soluble HSP70 (sHSP70) concentration by supernatant ELISAs measured in a THP-1 monocyte cell line. Cells were heat shocked (43°C for 1h) and subsequently rested for 6h, 12h, 18h, 24h before collection. E) Heat shocked THP-1 cells were rested for 12h and used for cytospin with subsequent immunofluorescence staining with DAPI for cell nuclei and HSP70 (scale bar = 50 μm). E) Plasma ELISAs for soluble HSP70 in patient cohort. Data was analyzed using a Kruskal-Wallis test with Dunn post hoe and Bonferroni correction (* = p-value < 0.05).

Our data shows that NPs exhibit mechanisms of immune suppression that are decreased in P. Importantly, P exhibits immune dysregulation prior to clinical progression. These results will allow us to further investigate the immunological differences in innate cells that may drive or inhibit progression in SARD.

[1.] Goldblatt F. Lancet 2013;382:797-808. [2.] Wither J. Arthritis Res Ther 2017;19:41.

In this study we proposed to conjugate a commercial anti-TNF-α antibody (Yuflima, containing adalimumab; Celltrion) with a radiomaker 89 zirconium coupled with a DFO chelator. The 89Zr-DFO-Adalumimab will be used in PET (positron emission tomography) imagery to identify RA patients expressing elevated level of TNf-α in the joint.

We successfully conjugated the radiomarker Zirconium 89 to the Adalumimab antibody. Preliminary results show that the conjugate DFO-Adalumimab is still able to target TNF-α with the same affinity as the commercial adalimumab.

These promising findings will enable us to test 89Zr-DFO-adalimumab in a collagen-induced arthritis (CIA) mouse model (DBA/1 strain) to assess inflammation at the join levels using PET imaging.

[1.] Government of Canada. https://www.canada.ca/en/public-health/services/publications/diseases-conditions/rheumatoid-arthritis.html [2.] Babaahmadi M. Stem Cell Res Ther 2023;14:268. [3.] Wang Z. Front Immunol 2021;12:755844.

This study was conducted on serum samples collected from 107 DMARD- and steroid-free RA patients (48 seronegative, 59 seropositive) enrolled in the EUPA cohort (NCT00512239), between 2005 and 2019, at the CIUSSS de l’Estrie-CHUS, Québec, Canada.[2] Serial sera collected at baseline and at the 12-month follow-up visit were analyzed by DIA-MS. MS data were analyzed using DIA-NN software for peptides/proteins identification and quantification. Statistical analyses were performed using R: Differentially abundant proteins (DAPs) across clusters were identified by Mann-Whitney U test with Bonferroni correction. KEGG enrichment analyses were conducted using the PathfindR R package, with BH correction. Generalized estimating equations (GEE) models were adjusted for age, sex, serology, and symptom duration, with FDR correction using Storey’s q-value.

Proteomic profiling quantified 869 serum proteins, of which 368 passed quality control and filtering for downstream statistical analyses. 1-Principal component analysis (PCA) followed by hierarchical clustering of baseline (Figure 1A), and 12-month proteomic data suggested patients could be grouped into 2 clusters. 2-KEGG pathway analysis of DAPs between patient clusters showed significant enrichment of complement and coagulation cascades pathway. 3-These clusters exhibited distinct serum levels of complement-related proteins (Figure 1B). 4-C68omparison of patient trajectories between baseline and 12-month serum-based clusters (Figure 1C), revealed that transitions between clusters were accompanied by significant modulation of complement-related protein levels (Figure 1D). 5-GEE models identified 29 proteins (q-value ≤0.05) associated with binomial 12-month disease activity, defined as DAS28-CRP ≤2.6 or ≥3.2, which were enriched for KEGG complement and coagulation cascades pathway. Figure 1.

A) Hierarchical Clustering on PCA was performed on RA patients’ baseline serum proteome. B) Baseline serum complement pathway (KEGG hsa04610) protein levels were normalized by z-scores. Average z-scores per patient are shown as a color gradient over PCA plot. C) Sankey plot of patient trajectories between baseline and 12-month proteome-based clusters. D) Average serum complement proteins z-scores of patients grouped by cluster trajectories BH-adjusted p ≤ 0.05 = * and ≤ 0.001 = ***.

This study highlights the heterogeneity of circulating complement components in early RA patients, suggesting that complement protein profiles may reflect underlying disease mechanisms beyond general inflammation and could inform future biomarker-driven approaches to RA management.

[1.] Carrasco-Zanini J. Nat Med 2024;30:2489-98. [2.] Carrier N. J Rheumatol 2024;52:119-27.

A CyTOF panel was developed to quantify IFN-induced proteins (IIPs) across peripheral blood immune populations. A composite IIP score (mean expression of 6 IIPs) was generated for each cell population as a surrogate for IFN exposure. 15 healthy controls (HCs), 26 quiescent (clinical SLEDAI > 0 for 1 year with no increase in immunosuppressive treatment, ≤ 10 mg prednisone) and 42 recently flaring (<1 month, change in clinical SLEDAI-2K ≥ 1 requiring escalation of therapy) were analyzed. To assess the direct effects of IFN, naïve B cells from HCs were isolated and stimulated with IFNα, IFNβ, or IFN. Cells were cultured under conditions that either promoted or inhibited ABC differentiation, including IL-21, anti-CD40, Fab2, CpG, or IL-4.

CyTOF identified 7 B cell subsets, all of which exhibited higher IIP levels and greater activation in flaring vs quiescent patients (Figure 1A). ABCs were more abundant in flaring patients, and their frequency correlated with the global IIP signature (Figure 1B,C). Expression of activation markers (CD86, TLR7, TLR9, HLA-DR, Ki67) was strongly associated with IIP score, but not disease status, indicating that IFN, rather than flare alone, drives B cell activation (Figure 1D). Importantly, the association between activation and IFN exposure was evident even within individual patients, where the top 10% of IFN-experienced B cells had significantly higher activation than the bottom 10%. In vitro, IFNα and IFNβ directly induced expression of activation markers within 18-24 hours. In isolated naïve B cells, all 3 IFNs increased ABC differentiation, even without canonical ABC-inducing signals (Figure 1E). Notably, IFN overcame IL-4-mediated suppression of ABC differentiation, in part by reducing IL-4Rα and inducing TLR7 expression. In SLE patients treated with the IFN-blocking therapy Anifrolumab, ABC frequency and IIP signatures decreased (Figure 1F). Figure 1.

A) IIP score for HCs, quiescent, and flaring SLE patients in B cell subsets. Higher IIP scores were found in flaring versus quiescent, and SLE patients versus HCs. (Mann Whitney U test with BH correction for multiple tests)

B) Frequency of B cell subsets displayed as the proportion of CD19+ B cells. Flaring patients had more ABCs than quiescent patients and HCs. (Mann Whitney U test with BH correction for multiple tests)

C) Correlation between cellular abundance and IFN signature. The proportion of ABCs were correlated with IIP score as well as IFN-stimulated genes (ISGs). IIP score also correlated with the proportion of PBs. (Spearman correlation)

D) Correlation of IIP score and markers of activation. The expression of activation markers correlated with IIP score for SLE patients. (Spearman correlation)

E) ABC differentiation from purified naïve B cells. 5 days of incubation with IFNα, IFNβ, or IFN caused significantly more differentiation of ABCs, irrespective of the incubation conditions (+/– IL-21, IL-4, anti-CD40, CpG). Results are displayed as the fold change from the respective non-IFN conditions. (Student’s T test with Holm correction for multiple comparisons post Shapiro-Wilk test to assess for normality)

F) The ABC profile of patients treated with Anifrolumab versus standard-of-care. Both the IIP score and proportion of ABCs were significantly reduced in Anifrolumab-treated patients. (Mann Whitney U test) In Anifrolumab-treated patients, the frequency of ABCs showed a trend to correlation with the IIP score. (Spearman correlation)

IFN exposure drives human B-cell activation and promotes differentiation of ABCs. Our results identify a mechanistic link between IFN signaling and pathogenic B-cell development, and support IFN blockade as a strategy to reduce pathogenic ABCs and prevent SLE flares.

We used whole exome sequencing (WES) to characterize the mutational frequencies and their associated signatures in dcSSc patients who did not undergo ASCT (dcSSc, N=35) and those who did (post-ASCT, N=9). We also generated DFs from dcSSc, post-AHSCT (or age/sex matched healthy controls (HC), (N=8-10 patients/group), and quantified the frequency of DSBs via -H2AX levels (immunoblot (IB)), and DSB nuclear foci (confocal microscopy). We measured the relative ROS levels, mitochondrial membrane potential, and phospho-PERK (active) in DFs to mechanistically link DSB with PERK activation using flow cytometry and/or IB, respectively. We also determined the downstream effects of PERK activation on mitochondria (eg, mitochondrial dynamics and biogenesis). Then, we measured FOXO1 activation via nuclear translocation, IB, and expression of its downstream mRNA target SOD2. Finally, mitochondrial-dependent resistance-to-apoptosis was determined at baseline, and following treatment with cyclophosphamide, a PERK or a FOXO1-inhibitor using TUNEL and cleaved caspase 9/3 levels (IB).

dcSSc patients’ DFs had increased genomic instability and DSBs compared to patients treated with ASCT. dcSSc DFs had increased indicators associated with PERK activation (phospho-PERK, ROS, and mitochondrial membrane potential). This was associated with increased mitochondrial remodeling, mitochondrial biogenesis, and mitochondrial fusion. Importantly, FOXO1 was exclusively activated in dcSSc, but not HC or post-ASCT DFs. Inhibition of PERK or FOXO1 resulted in increased mitochondrial-dependent apoptosis.

Our study highlights a novel mechanism whereby genotoxic signals in dcSSc promote cell survival via a PERK/FOXO1-dependent axis and associated metabolic remodeling (Figure 1). It also provides mechanistic insights related to how changes to the mutational landscape reduce pro-fibrotic signals in DF after ASCT. Future studies targeting this dysregulated pathway may provide an additional rationale for exploring it therapeutically in patients with dcSSc.

[1.] Gniadecki R. J Autoimmun 2022;131:102847.

Clinical gene panel sequencing (Invitae) identified the variant in the proband. Sanger sequencing confirmed homozygosity in the proband and his asymptomatic younger brother, and heterozygosity in both parents. Three-dimensional protein modeling using PyMol to predict confirmation changes. HEK293T cells overexpressing wild-type and mutant DNASE1L3 constructs were assessed for expression, secretion, and nuclease activity by Western blotting and plasmid/chromatin digestion assays. Single-cell RNA sequencing (scRNA-seq) was performed on PBMCs from both parents, the asymptomatic sibling, and 2 time points from the patient to explore downstream immune effects.

A homozygous missense variant (c.678C>T; p.T224M) in DNASE1L3 (NM_004944.2) was identified in the affected patient. Structural modeling suggested that the substitution destabilizes the Mg²⁺-binding site for enzymatic function. Overexpression studies demonstrated that T224M DNASE1L3 is normally expressed and secreted but exhibits markedly reduced nuclease activity compared to wild-type and known pathogenic variants (R206C, W215Gfs*2). Patient sera-based validation studies are underway. Preliminary scRNA-seq analysis revealed elevated expression of IFN-stimulated genes in the patient and mild increases of T, B and NK cell populations in the asymptomatic sibling with the same homozygous variant, suggesting early immune activation and potential predisposition to IFN-I pathway dysregulation.

We have identified a novel homozygous missense mutation in DNASE1L3, encoding an endonuclease previously implicated in mSLE, in a pediatric patient with HVUS and lupus nephritis. We demonstrated that this mutation has normal extracellular secretion but impaired nuclease activity, which implies poor clearance of extracellular nuclear debris likely resulting in type 1 IFN pathway stimulation, and thus leading to autoimmune disease like SLE as well as highlighting the importance of longitudinal monitoring in at-risk family members.

The search strategy for this umbrella review was developed and executed in collaboration with a medical librarian, using MEDLINE, Embase, CINAHL, and Cochrane Library from inception to August 2025. Quality of included reviews was assessed using AMSTAR 2, and evidence for each intervention was assessed using GRADE methodology.

2,715 results were retrieved and after removing duplicates, 2,218 unique results remained for title and abstract screening. 270 full-text records were assessed for eligibility, and 49 systematic reviews and meta-analyses were included. Among these, 6 reviews were rated high quality, 22 moderate, 9 low, and 12 critically low. Conditions included are fibromyalgia, systemic lupus erythematosus, rheumatoid arthritis, psoriatic arthritis, spondyloarthritis, Sjögren’s disease, and dermatomyositis. The certainty of evidence ranges from very low to moderate (Table). Table:

Assessment of evidence quality for each intervention.

There is moderate quality evidence to support Vitamin D supplementation, at 1,200 IU/day to 50,000 IU/week, and Fib-19-01 phytotherapy for fatigue management in rheumatic diseases. These interventions offer a new therapeutic opportunity for patients with intractable fatigue or desire to pursue natural therapies. Remaining evidence shows potential, but the low quality highlights a need for further research with rigorous study design. Furthermore, only patients with fibromyalgia and systemic lupus erythematosus are represented within the moderate quality evidence. Although shared pathways underlie fatigue in various rheumatic diseases, supporting generalizability of our findings, it remains important to create a representative evidence base to inform treatment.[3]

[1.] Overman C. Clin Rheumatol 2016;35:409-15. [2.] van Eeden C. Expert Rev Clin Immunol 2022;18:1049-70. [3.] Davies K. Nature Rev Rheumatol 2021;17:651-64.

This study assessed the quality of 250 consecutive referrals received at Sunnyside Rheumatology Clinic in Kingston Ontario. We defined our audit standards based on the OMA and CPSO referral recommendations, with the standard that referrals meet 100% of the outlined criteria.

While the standard expectation is that referrals meet 100% of the outlined criteria, the analysis of 250 referrals revealed substantial deficiencies in key areas. Notably, 40% of referrals did not include a clearly stated reason for referral, and 60% failed to provide an adequate physical examination. Additionally, 38% of referrals lacked even a description of relevant symptoms. Further gaps included missing personal health history in 10% of referrals, absence of family history in 68%, no allergy documentation in 15%, and missing current or previous medications in 16%. Relevant laboratory work was absent in 26% of referrals, while 34% lacked appropriate imaging. 21% of referrals contained redundant or excessive information. 22% of referrals were returned to the referring physicians with requests for additional information to enable proper triage. Many referrals were rejected outright due to being clearly inappropriate for rheumatology assessment.

This study highlights significant gaps in the quality and completeness of rheumatology referrals, underscoring the need for enhanced collaboration among referring physicians regarding appropriate and acceptable referral practices. In addition to improving adherence to established guidelines, there is a need to educate providers on when it is clinically appropriate to refer patients to rheumatology. By targeting services to patients most likely to benefit and improving the referral process, we can enhance workflow efficiency and ultimately improve patient outcomes and unnecessary burdens on consulting physicians.

Participants were recruited from the Montreal site of the Lupus in prEGnAnCY (LEGACY) cohort, a multicenter prospective cohort enrolling SLE pregnancies at < 17 gestational weeks. APO was evaluated at each trimester and postpartum, and included: 1) gestational hypertension, preeclampsia and/or eclampsia, 2) placental insufficiency, 3) placental abruption, and/or 4) small for gestational age (SGA ≤ 5 percentile). Neonatal cardiac function was assessed ≤4 weeks postpartum using STE, with global longitudinal strain (GLS) reported via apical endocardial or apical 4-chamber peak longitudinal strain. GLS is expressed as a negative percentage, with more negative values indicating better myocardial contractile function. We evaluated GLS with univariable and multivariable regression analysis adjusting for neonatal age and birth weight.

This study included 26 pregnant women with SLE, of mean maternal age 35.9± 4.7 years and disease duration 9.9 ± 7.4 years. Most were in Lupus Low Disease Activity State (LLDAS) at baseline (85%), and 65% (15/26) maintained LLDAS throughout pregnancy. Live birth occurred in 89% (23/26), among which APO occurred in 42% (11/26). Out of live births, 3 missed the STE assessment and 4 had suboptimal images preventing GLS estimation. Thus, GLS was assessed in 16 neonates of mean age 11.8 ± 26.2 days at STE (Table 1). HCQ was used by all mothers (16/16), with mean cumulative gestational exposure of 1103.2 ± 294.6 mg x days/kg. Mean GLS was-26.3 ± 4.2%, with term neonates at –26.2 ± 4.3%. Lower mean GLS was observed in neonates born to mothers with APO (–25.2 ± 4.3%) and anti-Ro antibodies (–24.8 ± 4.5) vs their respective counterparts (–27.2 ± 4.1% and –27.9 ± 3.4%). GLS was not significantly associated with APO, or anti-Ro positivity in multivariable models. Table 1.

Maternal and neonatal characteristics of mother–newborn dyads with neonatal GLS assessments, stratified by anti-Ro antibodies status

We observed lower GLS in neonates born to SLE mothers with anti-Ro antibodies and those with APO. Though not statistically significant, potentially due to small sample size, the trends may reflect subclinical cardiac alterations. These findings support the need for larger studies to clarify the impact of maternal antibodies, APO, and HCQ on fetal cardiac health.

We conducted a retrospective chart review of JIA patients transitioning from pediatric care to the YARD clinic between 2013 and 2023. Inclusion criteria: patients >17 years with ≥ 1 pediatric visit 12 months prior to YARD transfer, ≥1 YARD visit, and 1 12-month YARD follow-up (FU). Descriptive statistics assessed demographics, disease activity, medications and healthcare utilization (ED = emergency department, HA = hospital admission) 1 year pre- and post-transition. For study purposes, "transition" equates to the first YARD visit.

68 patients (n=47, 69% female) met inclusion criteria: enthesitis-related arthritis (21/68), oligoarticular extended (6/68), oligoarticular persistent (9/68), polyarticular RF-negative (7/68), polyarticular RF-positive (7/68), psoriatic (8/68), systemic (4/68), unclassified (4/68), and rheumatoid arthritis (2/68). The YARD clinic received 122 JIA patient referrals. Median transition age was 18 years. 13.24% of patients had pre-existing uveitis. Median time from last pediatric visit to first YARD visit was 4.45 months (2.96-6.06). Patients attended an average of 3.54 FU visits 12 months pre-transition and 2.76 visits 12 months post-transition. Median missed rheumatology visits: 0 (0-1) pre- and 0 (0-1) post-transition (Table 1). Median PGA scores were 2 (IQR 0-2, n=64) pre-transition and 0 (0-2, n=53) post-transition. ED visits occurred in 4/68 patients pre- and 3/53 post- transition (Table 1). HA occurred in 3/68 and 1/53 patients pre- and post-transition. Post-transition, 15 patients were discharged <12 months due to repeated missed appointments (3/15), distance/transportation challenges (3/15), refusal of care (2/15), relocation for work/education (2/15), and unspecified reasons (5/15). 7/15 patients were transferred to adult rheumatologists and 5/15 to family physicians. Table 1:

Disease Activity and Healthcare Utilization Across Transition Intervals

JIA patients transitioning to the YARD clinic maintained stable rates of ED use and HA in the first year, suggesting minimal acute complications. Missed visit rates remained similar, and clinical disease activity improved. Early discharge was moderately high, primarily due to geographic challenges and patient preferences. These results show that youth with JIA can maintain healthcare engagement and stable outcomes in this model, supporting its efficacy. Further research assessing long-term healthcare utilization and disease control following transfer to adult care is needed.

[1.] Chhabra A. Rheumatology (Oxford) 2020;59:3727-30.

Linked administrative health datasets from the province of Alberta were used to create an incident cohort based on validated ICD codes for gout from years 2002-2023. Controls were selected in a 1:1 ratio matched for age and sex. We used the Canadian Institute for Health Information ACSC ICD-10-CA case definitions to identify hospitalizations from the Discharge Abstract Database as our outcome of interest.[1] We calculated incidence rate ratios (IRR) at 3 and 5 years from the date of the first gout diagnosis using a multivariable regression model adjusting for age, sex, location of residence, and socioeconomic status.

There were 129,378 individuals with incident gout over the study period (66% male, mean age 71 years, 79% urban, 34% with material and social deprivation). Of these, 42.6% (n=55,085) had at least 1 hospital admission for any reason, with a total of 180,696 unique hospitalizations, compared to 31.2% (n=40,373) of controls with 111,102 unique hospitalizations. ACSC hospitalizations accounted for 12% (n=20,889) of all admissions in persons with gout, compared to 10% (n=10,607) of all admissions in controls. This was driven primarily by hospitalizations for heart failure and pulmonary edema in the gout cohort (50.5%) and chronic lower respiratory diseases in the matched cohort (43.4%). After adjusting for age, sex, location of residence, and socioeconomic status, the IRR for an ACSC hospitalization was increased at 3 years (IRR 1.15, 95% CI 1.09, 1.22) and 5 years (IRR 1.18, 95% CI 1.13, 1.23) in those with gout compared to controls (Table 1). Among individual ACSCs, the IRR for heart failure and pulmonary edema admissions was increased by 34% at 5 years in those with gout (IRR 1.34, 95% CI 1.23, 1.45) relative to controls. Table 1.

Incidence rate ratios (95% CI) for Ambulatory Care Sensitive Condition Hospitalizations, in persons meeting the case definition for gout compared to age and sex matched controls

The risk for potentially preventable hospital admissions is increased in people with gout, primarily driven by heart failure and pulmonary edema. Access to high quality ambulatory care with optimization of comorbidity management is indicated to improve outcomes.

[1.] Canadian Institute for Health Information. https://www.cihi.ca/en/indicatorsambulatory-care-sensitive-conditions-hospitalizations

We used linked population-based administrative datasets to retrospectively assess ED use for any reason by persons meeting the case definition for incident gout over a 10-year period (2007/2008-2017/2018). We estimated the annual frequency of ED use and assigned the most responsible diagnosis code to broader diagnostic groupings. We analyzed visit characteristics, acuity at presentation using the Canadian Triage Acuity Scale (CTAS), and disposition using descriptive statistics. All results were additionally stratified by biological sex (male/female) and geographic location of residence (urban/rural).

646,926 ED visits were made by 88,373 individuals with gout in Alberta. We observed a 69% increase in ED use over the study period by the cohort although the mean number of visits per person per year decreased over the 10-year period, from 1.06 (95% CI 1.03, 1.09) in fiscal year 2008 to 0.79 (95% CI 0.77, 0.80) in fiscal year 2017. The majority of visits for any diagnosis were assessed at CTAS 3 "Urgent" (32.5%) and CTAS 4 "Less urgent" (32.2%). The proportion of visits triaged as ‘Urgent’ increased over the 10-year period, from 25.9% of all visits in 2008, to 37.9% in 2017. Visits specifically for gout accounted for 5.7% of all visits, primarily triaged as CTAS 3 (23.2%) and CTAS 4 (56%). Injuries and infection each accounted for ~11% of all visits. Almost 1 in 5 (17%) visits resulted in admission, although just 1.3% of admissions were for gout flares specifically. About one-fifth (19.6%) of individuals discharged from an initial ED visit had a minimum of 1 ED return visit within 72 hours. Where the first visit was coded as inflammatory arthritis, 42.2% of return visits were for the same diagnosis. Female patients more frequently required hospital admission (20.4% vs males 15.7%), and while urban residents had an increased frequency of ED visits (25.6% vs 9.2%), they were less likely to be admitted to hospital than rural residents (11.4% vs rural 20.0%).

Acute care utilization by persons with gout has increased significantly over time, with lower-acuity presentations dominating out-related ED visits suggesting unmet ambulatory care needs.

This retrospective cross-sectional study analyzed US scans from PsA patients and non-psoriatic controls collected in a single center following standard protocol. All PsA patients met the DUET enrollment criteria including PsA duration <5 years and were not using biologics. Controls had no psoriasis or other autoimmune disease. Enthesis US scans of the quadriceps, proximal and distal patellar tendons, triceps and Achilles were scored by a single reader blinded to the diagnosis for entheseal elementary lesions including hypoechogenicity, thickening, Doppler signal, enthesophytes, calcifications and erosions. We evaluated 7 candidate DUET scores, each incorporating different combinations of entheseal sites and elementary lesions. Models were refitted using coefficients estimated in the discovery cohort. Model performance was also stratified by age group.

In our validation cohort of 102 PsA patients and 69 controls, the 7 candidate DUET risk scores yielded areas under the curve (AUCs) ranging from 0.660 to 0.764 (Figure 1). Stratifying the risk scores by age with a cutoff of 55 years enhanced AUCs to 0.781 (under 55) and 0.753 (over 55). Figure 1.

ROC curve of candidate DUET scores

The candidate DUET scores demonstrated discriminative ability in an external validation cohort, with additional improvement following age stratification. These findings will guide further refinement of the selected DUET score and inform its integration into clinical and research settings. Best Abstract on Spondyloarthritis Research Award

Pooled post hoc analysis was conducted for data from BE OPTIMAL (NCT03895203; biologic DMARD [bDMARD]-naïve) and BE COMPLETE (NCT03896581; TNF inhibitor inadequate response/intolerance [TNFi-IR]). Both studies assessed subcutaneous BKZ 160 mg every 4 wks in patients with PsA and were PBO-controlled to Wk16, then PBO patients switched to BKZ (PBO/BKZ). BE COMPLETE Wk16 completers could enter BE VITAL (NCT04009499; open-label extension), in which all patients received BKZ. Efficacy outcomes are reported by BL patient characteristic subgroups. Efficacy outcomes included ≥50% improvement from BL in ACR response criteria (ACR50), the composite outcome minimal disease activity (MDA), complete resolution of swollen joint count (SJC=0), and 100% improvement from BL in Psoriasis Area and Severity Index (PASI100; in patients with BL psoriasis ≥3% body surface area). Data are reported by randomization group at Wk16; for the BKZ Total group (PBO/BKZ and BKZ-randomized) at Wk52. The association of BKZ-treated vs PBO patients achieving Wk16 response overall and for each subgroup was estimated via odds ratios using logistic regression with factors for treatment, study, region, subgroup, and treatment by subgroup interaction (subgroup and interaction excluded in the overall). All p values are nominal and generated for the treatment by subgroup interaction term; missing data used non-responder imputation.

Of the 1,112 patients randomized to PBO (n=414) or BKZ (n=698), 1,073 (96.5%) completed Wk16 and 1,002 (90.1%) completed Wk52. Overall BL demographics and disease characteristics were generally similar between treatment groups. Achievement of ACR50, MDA, SJC=0, and PASI100 responses were greater with BKZ vs PBO within all patient subgroups at Wk16, with consistent efficacy responses with BKZ treatment for most patient subgroups. Younger patients (<45 years) treated with BKZ were significantly more likely than older patients (≥45 years) to achieve ACR50 (p=0.001), MDA (p=0.006), and SJC=0 (p=0.035) at Wk16. Males were significantly more likely than females to attain ACR50 (p<0.001). Improved efficacy responses with BKZ treatment were sustained or increased from Wk16 to Wk52 across all subgroups (Figure 1); (SJC=0 and PASI100 data not shown). Figure 1.

ACR50 and MDA response rates at Week 16 and Week 52 by baselines demographics and disease characteristics (NRI)

BKZ demonstrated durable and greater improvements in clinical joint, skin, and composite outcomes measures vs PBO at Wk16, which were sustained to 1 year, regardless of patient demographics and clinical presentation at BL.

Mean log fold-changes (logFC) in serum β-Defensin-2 (BD-2), IL-22, IL-17A and IL-17F levels were summarized for FRONTIER patients. Improvements ≥5-points in PROMIS-29 domains scores (or ≥2 for pain), and physical/mental component summary (PCS/MCS) scores, are considered clinically meaningful. ICO PsA Phase 3 sample sizes were informed by estimates from model-based analyses, including a meta-analysis that bridged FRONTIER 1 to PASI75 to expected American College of Rheumatology 20% improvement (ACR20) at Week (W)16 and meta-regression modeling that bridged ACR20 to secondary endpoints.

23/91 (25%) FRONTIER 1 patients had PsO+PsA (ICO, n=20; placebo, n=3). Among patients with biomarker data, mean logFC in serum BD-2, IL-22, IL-17A and IL-17F (data not shown) over time indicated consistent ICO pharmacodynamic effect between patients with PsO only and with PsO+PsA. ICO-treated PsO+PsA patients reported numerically greater mean changes from baseline (BL) at W16 vs placebo across PsA relevant PROMIS-29 domains, ie, improvements in physical function (7.7 vs 1) and reductions in fatigue (–7.4 vs 2.3 [worsening]), pain interference (–10.7 vs –1.3), and pain intensity (–3.5 vs –1.5). In 20 ICO-treated patients with PsO+PsA, 45% and 70% reported ≥5 point improvement from BL in PROMIS-29 PCS and MCS scores, respectively, vs no patients receiving placebo. ICONIC-PsA 1&2 sample sizes of 540 (5:5:5:3 to ICO Dose 1/2/placebo/active reference arm) and 750 (1:1:1 to ICO Dose 1/2/placebo) (Figure) were estimated to provide ≥90% power to detect significant differences between ICO and placebo. Given minorities are often under-recruited in PsA trials, the ICO PsA program aims to assess diverse populations. Figure 2:

ICONIC PsA-1 (biologic-naïve [A]) and ICONIC PsA-2 (biologic-experienced [B]) study designs

Exploratory assessments from FRONTIER 1 showed comparable ICO pharmacodynamic effects between patients with PsO only, and with PsO+PsA. ICO-treated patients with PsO+PsA reported numerically greater improvements in PsA-relevant PROMIS-29 domains vs placebo. Informed by these post-hoc analyses and model-based meta-analyses, the multicenter, double-blind, placebo-controlled ICONIC-PsA 1 and ICONIC-PsA 2 studies will evaluate ICO in active PsA.

Post hoc analysis assessed subcutaneous BKZ 160mg every 4 weeks (wks; Q4W) in patients with PsA and varying BL joint involvement. Patients were grouped by BL swollen joint count (SJC) based on quartiles: SJC ≤5, 6-≤7, 8-≤12, >12. Due to few patients with BL SJC 3/4, patients with SJC 5 were included in first quartile; quartile sizes vary. Patients were pooled from BE OPTIMAL (NCT03895203; biologic DMARD [bDMARD]-naïve) and BE COMPLETE (NCT03896581; TNF inhibitor inadequate response/intolerance [TNFi-IR]). Unequal trial sizes (BE OPTIMAL 431 BKZ, 281 PBO; BE COMPLETE 267 BKZ, 133 PBO) yielded unequal quartile proportions. Both trials required ≥3 tender and swollen joints and had 16-wk double-blind, placebo (PBO)-controlled periods. Completers of BE OPTIMAL Wk52 or BE COMPLETE Wk16 could enter BE VITAL (NCT04009499; open-label extension), with all patients receiving BKZ. BE OPTIMAL included a reference arm (adalimumab 40mg Q2W); data not reported due to small patient numbers in SJC quartiles. Outcomes reported: ACR ≥50% improvement, Psoriasis Area and Severity Index 100% improvement, minimal disease activity, SJC=0, Pain visual analog scale ≥50/70% improvement from BL, Health Assessment Questionnaire - Disability Index minimal clinically important difference (≥0.35 decrease from BL in patients with BL score ≥0.35). Data were pooled across trials and reported by randomization group at Wk16, Year 1 (Wk52), and Year 2 (Wk104/100 from BE OPTIMAL/BE COMPLETE).

At BL, SJC distributions were: ≤5 (n=370), 6-≤7 (n=215), 8-≤12 (n=275), >12 (n=252). At Wk16, BKZ-treated patients demonstrated numerically greater improvements in joint, skin, composite, and patient-reported outcomes vs PBO, across patients with varying BL joint involvement. For all domains assessed, improvements were sustained to 2 years in BKZ-randomized patients, with robust efficacy across patients with varying BL joint involvement (Figure 1); (patient-reported outcome data not shown). For patients who switched from PBO to BKZ at Wk16, improvements in efficacy similar to BKZ-randomized patients with varying BL joint involvement were reported to Year 1 and sustained to Year 2. Figure 1.

(A) ACR50, (B) PASI100, (C) MDA, and (D) SJC=0 responders at Week 16, Year 1, and Year 2, reported by baseline joint involvement (NRI, OC)

In patients with PsA and varying BL joint involvement, BKZ treatment demonstrated greater improvements vs PBO across disease domains at Wk16, and improvements were sustained to 2 years. Efficacy was robust across all groups of patients with varying BL joint involvement, reflecting the broader range of patients seen in clinical practice.

Patients who completed treatment in the parent study, achieved ACR20 response at W52, and had sufficient clinical benefit per the investigator were eligible for the LTE. Patients received tildrakizumab 200 mg every 4 weeks, 200 mg every 12 weeks (Q12W), or 100 mg Q12W until parent study database lock (≥52 weeks of treatment), after which all patients received tildrakizumab 100 mg Q12W through W208. Safety was assessed in all patients who entered the LTE and received ≥1 dose of tildrakizumab based on frequency and severity of adverse events (AEs); frequency of serious AEs (SAEs), AEs of special interest (AESIs) and clinical interest (AECIs); and presence of antidrug antibodies (ADAs) to tildrakizumab. Analyses were based on the treatment received.

Of 281 patients who entered the LTE, 205 completed treatments through W208. Any AEs, treatment-related AEs (TRAEs), SAEs, and treatment-related SAEs occurred in 224/281 (79.7%), 55/281 (19.6%), 40/281 (14.2%), and 2/281 (0.7%) patients, respectively (Table). The most common TRAEs were upper respiratory tract infection (3.2%) and nasopharyngitis (2.5%). Overall, 17/281 (6.0%) and 7/281 (2.5%) patients discontinued the study due to AEs and TRAEs, respectively, chiefly infections and infestations. AESIs were reported in 13/281 (4.6%) patients and included infections and infestations (1.8%); cardiac disorders (1.1%; not treatment related); malignancies (n = 2; 0.7%); respiratory, thoracic, and mediastinal disorders (n = 2; 0.7%); and vascular disorders (n = 1; 0.4%). Only 1 AECI occurred during the LTE. Two patients died due to AEs (1 aortic dissection and 1 metastatic adenocarcinoma, neither treatment related). Non-treatment-emergent (TE) and TE ADAs were detected in 2.8% and 1.1% and non-TE and TE neutralizing ADAs in 0.7% and 0.4% of patients, respectively. Patients’ ADA status was not associated with AEs of hypersensitivity or injection-site reactions, AESIs, or AECIs. Table.

Summary of AEs in the LTE study

The safety profile of tildrakizumab was maintained through extension W208 in patients with PsA. These data support continued development of tildrakizumab to treat patients with active PsA.

[1.] Mease PJ. Ann Rheum Dis 2021;13:1147-57.

M3©-JIA is a 3-site, parallel, randomized controlled trial recruiting caregiver-child dyads (ages 4-12) into either an 8-week M3© intervention or wait-list control. Weekly online sessions are led by trained facilitators, with caregivers and children attending separate groups. The M3© program incorporates neuropsychology, social-emotional learning and positive psychology. Quantitative data includes demographics, attendance, and pre-/post-intervention questionnaires assessing mindfulness and parenting practices; qualitative feedback was collected through open-text responses.

Of 67 dyads screened to date, 22 (33%) were randomized (11 intervention, 11 control). Most caregivers were mothers (86%), mean age 40.6 ± 6.5 years. Children were predominantly female (82%) with a mean age at enrollment of 9.3 ± 2.7 years and disease duration of 5.3 ± 3.1 years. Attendance was higher among caregivers than children (≥80% session attendance: 75% vs 50%), with strong engagement in both groups (camera on ≥85% of session: 75% vs 88%). Post-intervention, children reported greater awareness and use of mindfulness skills—for example, knowledge of "breathing breaks" increased from 42% to 100%, and understanding emotional regulation from 50% to 95%. Caregivers showed improvements in mindfulness and parenting confidence (eg, practicing mindfulness regularly: 31% to 63%; confidence in helping their child calm down: 69% to 90%) (Table 1). Qualitative feedback highlighted enjoyment, connection, and the value of creative, hands-on activities. Table 1.

Participant demographics, adherence and satisfaction of the M3© program

Preliminary findings demonstrate that M3© is feasible, engaging, and positively received by children with JIA and their caregivers. Early data suggest improvements in mindfulness awareness and parenting practices. While primarily scheduling challenges limited randomization rates, strong adherence and satisfaction support the promise of M3© as a scalable mental health support strategy within JIA care.

We included 1072 patients (0-18 years old) enrolled within 3 months of diagnosis in the Canadian Alliance of Pediatric Rheumatology Investigators (CAPRI) Registry. The treating rheumatologist assigned JIA categories using ILAR classification criteria. Descriptive statistics summarized patient characteristics at baseline and at 1 year. Psychosocial impact was measured utilizing the psychosocial domain (22 items) within the Juvenile Arthritis Quality of Life Questionnaire (JAQQ). Boxplots visualized changes in JAQQ-psychosocial median scores over time, and Wilcoxon ranked-sum tests highlighted significant differences for JIA categories. Hierarchical clustering of patients using the standardized scores (Z-scores) of 22 JAQQ-psychosocial items produced heatmaps for JIA categories (baseline and 1 year), as well as a heatmap for JIA patients at enrollment (Figure 1). Spearman correlations investigated factors associated with psychosocial impact, and univariate and multivariate regressions quantified the relationship between factors and psychosocial impact. Analyses were conducted using STATA 15 and Python 3.13. Figure 1.

Heatmap at enrollment of the 22-JAQQ psychosocial items (y-axis) graphed against patients (x-axis).

Descriptive statistics showed oligoarthritis was the most frequent category (45.4% of patients) and polyarthritis RF-positive was the less frequent (3.8%). Significant improvements in JAQQ-psychosocial scores from enrollment to 1 year were observed for polyarthritis RF-negative, polyarthritis RF-positive, psoriatic, and systemic arthritis (p<0.05). Hierarchical clustering of JIA patients at enrollment (n=1072) revealed 4 patient clusters by psychosocial impact: minimal (51.0%), mild (30.6%), moderate (9.3%), and severe (9.0%). JAQQ-psychosocial items clustered into externalizing behaviors, internalizing behaviors, and school-related problems (Figure 1). Heatmaps at enrollment across JIA categories (excluding undifferentiated) showed polyarthritis RF-positive with the highest percentage of patients with severe psychosocial impact (12.5%, mean Z-score 2.24). Oligoarthritis patients exhibited a continuum of psychosocial impact, while psoriatic arthritis patients clustered at minimal or severe extremes. Spearman correlations showed moderate associations between psychosocial impact and functional disability, fatigue, pain, and other JAQQ domains at baseline and at 1 year (correlations=0.4-0.6). CHAQ disability index, fatigue, and pain interference were significant predictors of psychosocial impact in multivariate regression.

Our findings suggest that patients diagnosed with certain JIA categories are at higher risk for greater psychosocial impact, especially polyarthritis RF-positive. Exploring the category-specific psychosocial burdens is vital for targeted, tailored psychosocial interventions to complement medical treatment for JIA.

We retrospectively and prospectively reviewed the medical records of patients with childhood-onset inflammatory myositis who experienced persistent disease activity and were treated with anifrolumab. This study involved 2 tertiary medical centers: Hospital Sant Joan de Déu in Barcelona and the Hospital for Sick Children in Toronto. Data on demographics, disease manifestations and severity, laboratory findings, treatment details, and responses to therapy were collected.

Four patients, 3 females and 1 male, aged 3.5 to 10 years at the time of diagnosis, were identified (Table 1). The median time from diagnosis to starting anifrolumab was 12 months (IQR 7.8 to 31). All presented with muscle weakness and cutaneous features, and patient 1 also had ulcerative skin disease, bowel perforation, and pulmonary infections. Patients 1 and 4 were positive for anti-NXP2 antibody, while patients 2 and 3 had positive anti-p155. Prior to commencing on anifrolumab infusions, all patients received prednisone, methylprednisolone pulses, and intravenous immunoglobulins (IVIG), along with 2 or more of methotrexate, tacrolimus, mycophenolate mofetil (MMF), and cyclophosphamide. Patient 1 also needed 3 surgeries due to bowel perforation. Clinical responses were evaluated after 6 anifrolumab infusions (5mg/kg q4 weeks) for patient 1, 3 infusions for patients 2 and 4, and 2 infusions for patient 3. All 4 patients demonstrated clinically meaningful improvement in their skin involvement and overall disease activity. Patient 4 experienced a halt in the progression of the calcinosis lesion, while patient 1 also saw significant improvement in muscle strength and no recurrence of gastrointestinal involvement. The prednisone dosage was substantially reduced in patients 2 and 3, while it was discontinued in case 1. No anifrolumab-related adverse effects were observed. Table 1:

Demographics, Clinical Characteristics and Treatment History of Patients

This study highlights the promising efficacy of anifrolumab in the management of refractory JDM, with clinically meaningful improvement in cutaneous and other involvement, along with a favorable safety profile. These findings provide additional support for the systemic inhibition of type I interferon in managing the disease and emphasize the need for prospective studies.

[1.] Barrutia-Etxebarria A. Pediatr Dermatol 2026;43:116-20.

We retrospectively reviewed the medical records of patients who developed thrombocytopenia (platelet count < 100 x10^9/L) and were diagnosed with cSLE and followed in the rheumatology clinic at The Hospital for Sick Children (SickKids) between January 2005 and December 2024. In this clinic, structured data, including disease activity (assessed by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)), are prospectively collected at every visit. Definite cSLE was defined by the 2019 EULAR/ACR classification criteria, while patients with incipient cSLE had clinical features of evolving SLE but achieved a EULAR/ACR score below 10. A complete response was defined as a platelet count >100 x10^9/L with no bleeding. Partial response was defined as a platelet count >30 x10^9/L with at least a 2-fold increase from the lowest count and no bleeding. Descriptive statistics were used to characterize the study groups and outcomes.

Of the 798 patient records reviewed, 207 (26%) of patients had thrombocytopenia. One hundred sixty-one patients (78% female) with a median age of 12.7 years (IQR 10.1-14.5) and a median platelet count of 22 x10^9/L (IQR 7-59) at the time of thrombocytopenia diagnosis were included (Figure 1).[1] The median lowest platelet count was 11 x10^9/L (IQR 2-41). 131 patients (81%) had definite, and 30 (19%) had incipient cSLE (Table 1). One hundred nine (67%) of patients were treated with corticosteroids, and 80 (50%) of them received IVIG prior to commencing on HCQ (Table 2). Seventy-three (45%) patients achieved complete or partial responses before initiating HCQ. 147 (91%) patients were treated with HCQ, initiated at a median of 6 months (IQR 2.7-12.2) after thrombocytopenia diagnosis, at a median platelet count of 77 x 10^9/L (IQR 32.5-198.0). Of those, 35 (24%) patients were treated with HCQ monotherapy (Table 3). All 35 responded; 30 had complete responses after a median follow-up of 52 months (IQR 33-75). Of the 147 patients who received HCQ during their disease course, 11 experienced side effects, and 7 of them had to discontinue the treatment due to these effects.

While most patients initially required additional treatments, HCQ monotherapy effectively maintained a partial or complete response in thrombocytopenia for over 4 years in approximately 1 in 5 cSLE patients.

[1.] Khellaf M. Am J Hematol 2014;89:194-8.

The study focused on patients diagnosed with probable or definite JDM as per the Bohan and Peter criteria, followed at the Hospital for Sick Children during the years January 2000 to September 2025, who developed calcinosis based on physical examination or previous imaging studies. Eligible patients who have undergone at least 2 serial non-contrast, ultralow-dose whole-body CT scans during their follow-up were included in the study. Imaging data analysis was conducted to detect the regional distribution and volume of calcinosis, assess changes over time, and compare serial CT scans performed for each included patient.

Out of the 256 patients with JDM, 54 (21%) developed calcinosis during follow-up. Among these, 3 patients with a median age of 7.8 years (IQR 7.2-9.9) at JDM diagnosis underwent 2 serial non-contrast, ultralow-dose whole-body CT scans each to assess their calcinosis during their follow-up. Two of the cases were positive for anti-NXP2, while case 2 had negative myositis-specific antibody serology. The median duration of disease at the development of calcinosis was 17 months (IQR 8.5-22). The median duration between the first and second CT scans was 12 months (IQR 9.5-13). In all 3 cases, follow-up CT scans revealed an increase in the size and distribution of previously observed deposits, along with the appearance of new calcification clusters (Figure 1). Furthermore, the 3D reconstruction of confluent calcinosis revealed a distinct structure and distribution of certain densities compared to earlier evaluations conducted through X-ray and physical examination. This resulted in an intensification of treatment in each of the 3 cases. The median effective dose for a low-dose CT scan used was significantly lower than the standard protocol, about 10 times less than in adults.

An ultra-low-dose protocol for whole-body CT can serve as a safe and objective, valuable tool for monitoring changes in calcinosis, thereby contributing to improved patient care and outcomes.

[1.] Yi BY. Pediatr Rheumatol Online J 2025;23:44.

We analyzed data from the Gladman-Krembil cohort that included patients with PsA followed from January 2016 to April 2025 ("clinical cohort"). Patients in this cohort are followed at 3-12-month intervals with standardized collection of medication use, PsA disease activity measures, patient-reported outcomes, and laboratory tests. The following measures of disease activity were assessed: Disease Activity measures included disease activity in Psoriatic Arthritis (DAPSA), clinical DAPSA (cDAPSA), Minimal Disease Activity (MDA), tender and swollen joint count (TJC, SJC), Psoriasis Area and Severity Index (PASI), enthesitis and dactylitis counts, patient pain, global assessment, and function, classifying patients as remission/low (DAPSA < 14) or moderate/high disease activity (≥14). HsCRP levels were measured using standardized high-sensitivity assays. A smaller subset underwent a comprehensive ultrasound of their joints/entheses before and 3 months following initiation of advanced therapy ("US cohort"). Total inflammatory sonographic scores, including synovitis, paratenonitis, tenosynovitis, and enthesitis, were calculated. Associations between hsCRP and clinical and sonographic measures of disease activity were analyzed using GEE multivariable regression models, which were adjusted for age, sex, and body mass index (BMI).

A total of 1263 patients (10568 visits) from the clinical cohort and 144 patients (222 visits) from the US cohort were analyzed. Baseline mean hsCRP levels were 6.3±15.1mg/L and 8±12.4 mg/L in the clinical and US cohorts, respectively. Higher hsCRP was independently associated with higher DAPSA, TJC, SJC, dactylitis count, PASI (clinical cohort), and with patient-reported outcomes such as pain, global assessment of disease activity, and physical dyfunction (Table 1). Higher hsCRP levels were also significantly associated with reduced odds of achieving DAPSA-LDA, cDAPSA-LDA, and MDA. HsCRP was associated with SPARCC enthesitis score in the US cohort but not in the clinical cohort and with synovitis, paratenonitis, and tenosynovitis scores. HsCRP was associated with sonographic enthesitis count but not with the total enthesitis score. Table 1:

The association between hsCRP and measures of PsA disease activity - GEE regression models

HsCRP is associated with both clinical and sonographic measures of inflammation in PsA. These findings support its utility as a simple, objective biomarker for monitoring both clinical and subclinical disease activity in PsA.

Using a protocol prospectively registered on PROSPERO, systematic review of MEDLINE, EMBASE, Web of Science, Scopus, CENTRAL, and Google Scholar was performed according to PRISMA guidelines. Studies reporting outcomes comparing patients with RA who did and did not receive TNFi during pregnancy were included. Collected outcomes included: 3rd trimester DAS28-CRP, congenital anomalies, pregnancy loss, small for gestation age (SGA), preterm birth, and serious maternal and neonatal infections. Using RevMan version 5.4 with fixed effects modeling if I2 <25%, binary outcomes were analyzed using Mantel-Haenszel risk ratio and continuous outcomes were calculated using inverse variance method as mean difference.

Outcome data from 9 patient populations were included. There were no significant differences between patients who did and did not use TNFi with regard to congenital anomalies (RR = 1.13; 95% CI 0.62-2.08, p = 0.69), SGA (RR = 0.89; 95% CI 0.56-1.41, p = 0.61), and preterm birth (RR = 0.99; 95% CI 0.76-1.31, p = 0.97) (Figure 1). Among outcomes with 3 or fewer studies reporting, there were no significant differences in 3rd trimester DAS28-CRP scores (mean difference = 0.08; 95% CI -0.11-0.26, p = 0.41), pregnancy loss (RR = 1.03; 95% CI 0.26-4.19 p = 0.96), serious maternal infection (RR = 0.94; 95% CI 0.32-2.76, p = 0.91), and serious neonatal/infant infection (RR = 1.02; 95% CI 0.35-3.00, p = 0.97). Figure 1.

Forest plots comparing congenital anomalies (A), small for gestational age (B), and preterm birth (C) among pregnant patients with rheumatoid arthritis who did and did not receive TNFi during prenatal period. Data are depicted by using risk ratios with 95% confidence intervals. CI, confidence interval; TNFi, tumour necrosis factor inhibitor; M-H, Mantel-Haenszel.

To our knowledge, this is the first meta-analysis evaluating outcomes in pregnant women with RA only, treated with or without anti-TNF inhibitors. Among patients with RA, TNFi use in pregnancy does not appear to be associated with congenital anomalies, SGA, or preterm birth. This could help inform patient counselling around the continuation of TNFi in the prenatal period in this particular patient population. Additional original research is required to determine whether the similarities in disease activity are confounded by low sample size, selection bias, additional medication use, and timing of TNFi discontinuation.

[1.] Lv J. BMC Pregnancy Childbirth 2023;23:724. [2.] Sammaritano L. Arthritis Care Res (Hoboken) 2020;72:461-88.

This retrospective case series included 98 patients with confirmed RA-ILD followed in Hamilton, Ontario. Demographics, including sex, smoking history, autoantibody titers, inflammatory biomarkers, and pulmonary function test (PFT) results were abstracted from clinical records. Clinically meaningful progression was defined as ≥10% absolute decline in forced vital capacity (FVC %) or diffusing capacity for carbon monoxide (DLCO %) predicted. Patients with ≥2 PFTs within 2 years of ILD diagnosis (n = 54) were assessed, of whom 14 (26%) exhibited >10% functional change.

Of 98 patients, 82 had pulmonary data and 54 had serial PFTs within 2 years; 14 (25.9%) demonstrated >10% change in FVC and/or DLCO, indicating progression. Of the progressors, 9 were male (64%), suggesting greater susceptibility to functional decline among men. Compared with the broader cohort, the progression group showed higher autoantibody titers (mean RF 280 IU/mL vs 164 IU/mL; anti-CCP 147 vs 131 U/mL) and greater smoking exposure (mean 48.4 vs 38.3 pack-years). Despite greater physiologic decline, they exhibited lower inflammatory markers (CRP 11.5 vs 15.6 mg/L; ESR 21.4 vs 31.8 mm/hr), necessitating further analysis to determine whether decline occurs independently of systemic inflammation. Functionally, the progression group had higher FVC (82.9% vs 75.9%) but lower DLCO (46.9% vs 50.7%), potentially suggesting disproportionate impairment in gas transfer and early fibrotic or microvascular injury. Radiographically, 11 of 16 patients with available HRCT follow-up demonstrated disease progression, 8 of whom exhibited a usual interstitial pneumonia (UIP) pattern, consistent with previously described aggressive fibrosing phenotypes.[2] The rate and pattern of progression are comparable to those reported in previous RA-ILD studies,[3] reinforcing the established link between seropositivity, smoking, and pulmonary decline.[1]

Approximately 1 in 4 RA-ILD patients experienced clinically significant pulmonary function decline within 2 years of diagnosis. Progression occurred predominantly among male patients, who were highly seropositive, heavily smoking-exposed, and more likely to exhibit a UIP pattern with reduced DLCO, even in the absence of elevated systemic inflammation. These findings delineate a distinct high-risk RA-ILD phenotype that warrants early, proactive monitoring and timely therapeutic intervention, including consideration of antifibrotic or immunomodulatory strategies, to prevent irreversible pulmonary decline and respiratory failure.[1-3]

[1.] Assayag D. Respir Med 2014;108:857-64. [2.] Kim EJ. Chest 2010;138:1275-83. [3.] Zamora-Legoff JA. Eur Respir J 2017;49:1601796.

Data on disease burden metrics (FM symptoms, pain areas, disease activity, and irreversible damage), medication use (antimalarials, corticosteroids, immunosuppressants, biologics and narcotics), and sociodemographic factors were collected. Linear mixed-effects models evaluated the effect of FM symptoms and other disease burden variables on 5 functional outcomes: fatigue severity (FSS), cognitive dysfunction (PDQ), disability (WHODAS), depression (BDI), and work role functioning (WRF). Moderation models were used to assess if SLE treatments ameliorated the effect of these variables on function, while correcting for multiple testing.

The models established that a higher number of reported fibromyalgia symptoms was the strongest predictor of functional impairment, being significantly associated with increased fatigue (β = 1.06, p < 0.001), cognitive dysfunction (β = 1.21, p < 0.001), and higher disability (β = 0.68, p < 0.001), and depression scores (β = 0.73, p < 0.001). Conversely, irreversible damage scores were uniquely linked to worsened work role functioning (β = –4.41, p = 0.020). Building on these models, moderation analyses revealed that certain treatments lowered the effect of the disease burden metrics on various function metrics (Figure 1). Immunosuppressants moderated the impact of organ damage on disability from β = 2.62 to β = 0.45 (p = 0.022) and perceived deficits from 2.28 to –0.84 (p = 0.041). Corticosteroids attenuated the association between FM symptoms and cognitive dysfunction falling from β = 1.42 to β = 0.14 in users (p = .024). Figure 1.

Simple Slopes of Effects of Immunosuppressants and Corticosteroids

This study demonstrates that the reported number of fibromyalgia symptoms is the dominant factor driving functional burden across nearly all measured domains in SLE, surpassing the impact of disease activity. Most significantly, we provide evidence that certain SLE treatments act as functional shields: corticosteroids protecting cognition from FM effects and immunosuppressants mitigating disability linked to damage. These moderation effects strongly support tailoring treatment not only to disease activity but also to the patient’s functional risk profile, moving clinical practice closer to truly personalized medicine. Supported by a CIORA grant

Electronic medical records of patients referred to University of Alberta Rheumatology for query GCA between January 2022 and January 2024 were retrospectively reviewed. Patients with relapsing GCA, or those whose charts lacked sufficient data to calculate a GCAPS were excluded. Data was extracted from the first rheumatology visit and inputted into the Southend GCAPS Calculator. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of a High, Intermediate or Low risk GCAPS score were calculated using both 1) the clinical diagnosis of GCA at 3 months follow up, and 2) confirmed diagnosis of GCA by testing [either temporal artery biopsy, ultrasound, or PET/CT], as gold standard. Receiver operator characteristic (ROC) curves were plotted using numerical GCAPS scores.

81 referrals for new onset, suspected GCA were identified, of which 62 contained all data to calculate a GCAPS score. Ultimately, GCA was diagnosed in 39 patients (27 patients confirmed by test, 12 diagnosed clinically) and excluded in 23. Of 62 patients, 31 (50%) had a High risk GCAPS, 23 (37.7%) had Intermediate risk and 8 (12.9%) had Low risk GCAPs. See distribution of results (Table 1). Using the clinical diagnosis at 3 months as gold standard, the sensitivity of having either Intermediate/or High risk GCAPS was very high at 97.4%, with specificity of 30%, PPV of 70.4% and NPV 87.5%. The sensitivity of High risk GCAPS alone was lower at 66.7%, but with higher specificity of 78.3%, PPV=83.9%, NPV=58.1%. Using only confirmed diagnosis of GCA as gold standard, the sensitivity of Intermediate/or High risk GCAPs was 100%, with specificity of 30%, PPV of 62.8% and NPV 100%. The GCAPS ROC AUC was good at 0.805 (95% CI 0.697-0.913). At the previously determined optimal cut-point of 9.5, the sensitivity was 97.4% but specificity was low at 34.8% Table 1.

Distribution of GCA diagnoses and GCAPS risk scores.

In our population, an Intermediate or High risk GCAPS score was highly sensitive for the final diagnosis of GCA, suggesting that for those with Low-risk scores, GCA is unlikely and other diagnosis should be strongly considered.

[1.] Laskou F. Clin Exp Rheumatol 2019;37 Suppl 117:104-8.

Specialist providers involved in the diagnosis or treatment of patients with suspected GCA in Edmonton, AB, were invited by email to complete an anonymous survey regarding their experiences requesting and/or performing temporal artery biopsy (TAB), PET/CT, and temporal artery ultrasound (U/S). Descriptive statistics and 1-way ANOVAs were used to analyze the data.

In total, 31 physicians from 5 specialties completed the survey. See physician demographics (Table 1). Of the 3 tests, urgent access to TAB was deemed the most essential for diagnosing GCA (with mean score 4.3 ±0.86 on 1-5 point scale; 1=not important, 5=essential) as compared to U/S (mean score 3.9 ±0.79) and PET/CT (mean score 3.40 +/0.82), p=0.004. TAB was most difficult to access, however (mean score 3.8 ±0.52; 1=easy to access, 5=cannot access) as compared to U/S or PET/CT (mean 2.6 ±1.1 and 3.1 ± 0.91, respectively, p<0.001.) Administrative burden was also greatest for TAB (mean score 4.2 ±0.62) vs U/S (2.95± 1.2) or PET/CT (2.95 ±0.89), p<0.001. Overall, 15/20 (75%) rheumatologists/neurologists reported that they either cannot access or find it very challenging to access TAB urgently, particularly for patients without visual involvement. Among 8 surgeons who completed the survey, 6 performed an average of 6-10 TABs/each last year, and 2 did not perform TABs. Scheduling of urgent biopsies, focused scope of practice/lack of capacity, and lack of exposure to procedure in training were cited as surgical barriers. Nuclear medicine physicians read between 21-30 PET/CT scans/each for query GCA last year. The limited number of PET/CT scanners and inability to flag untreated, suspected GCA cases for urgent booking were identified as nuclear medicine barriers. The main reported barrier to TA U/S was that it is currently offered by a single provider only. Overall, 62% (18/29) of all respondents reported being very/somewhat unsatisfied with the process for diagnosing GCA, and only 4/20 (20%) rheumatologists/neurologists reported feeling very confident about their current ability to diagnose/exclude GCA. Table 1.

Demographics of survey respondents

Providers across multiple specialties were generally unsatisfied with diagnostic testing for GCA, and perceived confidence in ability to accurately diagnose is low (20%.) Increasing the availability of TA U/S may help offset the need for TAB and improve care.

As part of a patient-initiated follow-up model (called Appointments by Choice or ABC),[1] a multi-method, phased approach was utilized to co-develop and evaluate the flare action plan (Figure 1). Following an environmental scan of patient-facing materials for RA flare self-management,[2] the action plan was iteratively co-developed with the research team (including rheumatologist, physiotherapy, and knowledge mobilization expertise), a design team, and patient partners. The evaluation phase was completed post-ABC implementation to ascertain the real-world value of the action plan. This evaluation included Patient Education Materials Assessment Tool (PEMAT)[3] ratings completed by patient partners (n=4) to capture the understandability and actionability of the action plan, and qualitative interviews with ABC patients (n=15). PEMAT scores were analyzed with descriptive statistics and interviews were analyzed using thematic analysis.

The iterative co-development phase included multiple steps: (1) content development with research team expertise, (2) incorporation of patient partner feedback, (3) visual design with a design team, and (4) research team and patient partner feedback on both content and design. During evaluation, averaged patient partner PEMAT scores were 88.3% for understandability and 90% for actionability. Among the 15 participants who were interviewed, the median age was 61 years (IQR = 9) and participants had lived with RA for a median of 11.5 years (IQR = 4.8). 60% identified as female, and 60% identified as White/European. Three key themes emerged from interview data. (1) "This isn’t new... but it’s good to read it again" - participants described how the flare management strategies presented in the action plan were a good reminder for those who have been living with RA for many years, and a valuable resource for newly diagnosed individuals. (2) "It’s inviting" - participants had positive reactions to the design and visual aspects of the action plan, describing clear organization and layout, and inviting colors and visuals. (3) "It’ll be in my corner" - participants described how the action plan could be valuable for future reference.

The flare action plan was developed for people with RA to support evidence-based self-management. It has demonstrated value for patients on the ABC pathway, as shown by PEMAT ratings and qualitative data, and could be targeted toward newly diagnosed individuals. Furthermore, this patient-facing material could be disseminated more broadly across Canada and adapted for other chronic conditions.

[1.] Ester M. BMC Rheumatol 2025;9:31. [2.] Subdar S. J Rheumatol 2024;51:577-86. [3.] Shoemaker SJ. Patient Educ Couns 2024;96:395-403. Supported by a CIORA grant

The 1-arm non-randomized ABC implementation pilot study began in January 2024 at a multipractice rheumatology clinic in Alberta. People with (1) established RA, (2) well-controlled disease, (3) no major medication changes, and (4) no other active complex conditions were invited to participate in ABC1. Primary implementation outcomes, informed by the RE-AIM framework,[2] included reach, adoption, and implementation. Secondary outcomes were safety and effectiveness. Quantitative data from surveys and chart reviews were summarized using descriptive statistics. Qualitative data from weekly meetings and interviews were analyzed using thematic analysis, with mapping to CFIR,[3] domains within each RE-AIM category (Table 1). Table 1:

Summary of major themes mapped using CFIR across RE-AIM categories

Reach: Over 18 months, 76/140 (54.3%) of eligible individuals consented to participate in ABC. The most common reason for declining was a "preference for usual care" (14/64, 21.9%). Participant altruistic motivation to free-up physician time for those in-need was a facilitator, whereas lack of physician time to discuss ABC was a barrier. Adoption: 5/7 rheumatologists approached participated in ABC, representing over 1/3 of the clinic. The phased rollout of ABC and tension for change were adoption facilitators. Meanwhile, limited early leadership support was a barrier. Implementation: Facilitators included adapting recruitment workflows to rheumatologist preferences, improved integration of ABC processes in the EMR, and clear contact lists for clinical and research teams. Barriers included limited ABC understanding among clinic staff, incomplete transfer of care communication, and participant confusion about ABC due to inconsistent information provided at baseline. Safety/Effectiveness: 68/76 (89.5%) ABC participants remained on ABC, with 2 withdrawing and 6 returning to usual care due to flares, infection and medication change. 31 participants contacted the flare clinic (0.4 calls/week) for support with flares, lab tests, imaging results, and other minor concerns. Overall, 1,520 minutes of rheumatologist time was saved due to reduced appointment frequency, equivalent to 38 new patient consults. Safety and effectiveness facilitators included limited flares and positive participant experiences with flare clinic support. Barriers were mixed rheumatologist perspectives on the value of ABC and limited usefulness of the self-report flare questionnaire.

Early insights show promise of ABC for improving the efficiency and patient-centeredness in rheumatology care. For expanded implementation, adaptations are required to address barriers faced during our pilot study.

[1.] Ester M. BMC Rheumatol 2025;9:31. [2.] Glasgow RE. Front Public Health 2019;7:64. [3.] Damschroder LJ. Implement Sci 2022;17:75. Supported by a CIORA grant

A Markov model simulated disease progression over 5 years using monthly cycles from a U.S. payer perspective. Transition probabilities, EQ-5D utilities, and healthcare resource utilization were derived from a targeted literature review. Patients began in a pre-treatment state and transitioned monthly among 4 health states following DMARD initiation: complete response (sustained MDA), partial response (non-sustained MDA), non-response (did not meet MDA), or death. Modeled therapies included methotrexate (csDMARD), tofacitinib or apremilast (tsDMARDs), and biologic DMARDs (bDMARDs). Early initiation was defined as ≤1 year after PsA diagnosis and delayed initiation occurred >1 year after diagnosis. The mean time from diagnosis to DMARD initiation was 0.2 years in the early group and 8.6 years in the delayed group. Cost differences between exposure groups were modeled using a regression equation linking Health Assessment Questionnaire Disability Index (HAQ-DI) scores to direct medical costs, where higher HAQ-DI scores were associated with higher costs.[3]

Early DMARD initiation resulted in a gain of 0.33 QALYs and a cost savings of USD$7,473.52 per patient relative to delayed initiation, producing a dominant incremental cost-effectiveness ratio of –USD$22,479.24/QALY (Figure 1). The model was most sensitive to changes in direct medical costs (range: –USD$206,875.18/QALY to USD$161,915.70/QALY) and MDA rates (range: –USD$437,673.70/QALY to –USD$14,947.59/QALY).

This study demonstrates that early DMARD initiation in DMARD-naïve patients with PsA provides superior clinical and economic outcomes compared to delayed initiation, making it the dominant strategy. The substantial economic value of early initiation is largely driven by achieving early disease control, preventing irreversible joint damage, and improving long-term functional outcomes. These benefits translate into reduced healthcare costs and greater patient outcomes, reinforcing the importance of early therapeutic intervention and advocating for the reconsideration of reimbursement frameworks to allow timely access to effective treatment.

[1.] Ciliento M. Int J Mol Sci 2023;24:5006. [2.] Mease P. ACR Open Rheumatol 2025;7:e70019. [3.] Ogdie A. J Manag Care Spec Pharm 2022;28:997-1007.

We pooled patient-level data from 4 phase III belimumab trials in adults with active SLE (n=1065). Patients were stratified into 4 previously defined disease trajectory classes according to baseline disease activity (high vs moderate) and treatment response (responder vs non-responder). [2] PROs included Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F), 36-Item Short Form physical (PCS) and mental (MCS) component summaries, EuroQol 5-Dimension (EQ-5D), and EuroQoL Visual Analog Scale (EQ-VAS). Responsiveness was assessed with standardized response means (SRMs) across timepoints and classes. Correlations with SLEDAI-2K, BILAG, and Physician’s Global Assessment (PGA) were examined using Spearman’s coefficients and compared with Steiger’s Z (α=0.05). Sensitivity analyses were performed using complete-case datasets at each timepoint.

FACIT-F and SF-36 PCS were the most responsive PROs and showed the strongest correlations with clinical indices (Table 1). FACIT-F was most responsive early (up to week 20), particularly among non-responders and moderately active responders, while SF-36 PCS was most responsive later (weeks 20-52), especially among responders. EQ-5D consistently demonstrated the lowest responsiveness (peak SRM 0.54) and weakest correlations. PGA correlated most strongly with PRO changes; SLEDAI-2K correlations were weak and inconsistent. Data completeness declined modestly from 95% at baseline to 82% at week 52. Analyses restricted to patients with complete 52-week follow-up yielded results consistent with the main findings, with FACIT-F and SF-36 PCS remaining the most responsive instruments and EQ-5D showing minimal change detection. Table 1.

Correlation of patient-reported outcome measures with physician-assessed disease activity indices at weeks 24 and 52, stratified by disease trajectory class.

This is the first study to longitudinally evaluate PRO performance by disease trajectory in SLE using pooled patient-level data from belimumab trials. We show that PRO performance is dynamic, trajectory-dependent, and domain-specific. FACIT-F and SF-36 PCS consistently outperformed EQ-5D in capturing clinically meaningful change and aligning with physician assessments. The consistently poor responsiveness of EQ-5D underscore limitations of generic preference-based measures in SLE. These findings emphasize the importance of selecting sensitive, patient-centered instruments in clinical trials, routine care, and health technology assessments. Failure to do so risks underestimating the true value of therapies in a complex, symptom-driven disease such as SLE.

[1.] Cornet A. Autoimmun Rev 2025;24:103838. [2.] Parodis I. Rheumatology (Oxford) 2025;64:2697-2705.

Patients enrolled in the ABC pilot were invited via email to participate in semi-structured qualitative interviews. Patients were selected from 2 different time points: mid-study (6 months) and end-of-study (12 months), post-enrollment. Demographic information was collected at study enrollment through an online survey hosted on Qualtrics. Interviews were conducted using Zoom Videoconferencing and were 1 hour in length. Interview transcripts were independently analyzed thematically and in duplicate using the Consolidated Framework for Implementation Research (CFIR) to identify barriers and facilitators to ABC participation.[1] Coders met regularly to address additional themes as they emerged from the transcripts, to discuss and modify codes, and reconcile differences. Interviews ceased once saturation was met. Ten CFIR codes representing key domains (Implementation process, individual, inner setting, innovation, and innovation outcomes) were applied deductively, and 5 additional codes were introduced inductively to capture emergent themes.

Ten participants (5 mid-study, 5 end-of-study) were interviewed. The median age was 61 years (IQR = 13.75), and participants had lived with RA for a median of 11.5 years (IQR = 13). Four out of the 10 participants identified as White/European, and 6 out of the 10 participants identified as female. Reported barriers included uncertainty about whom to contact in the event of a flare or other rheumatologic concern, and challenges maintaining regular lab testing when in-person follow-up reminders were absent. Other barriers included missing the physician/patient relationship and the social visit aspect of the rheumatology clinic appointment. Facilitators included shared decision-making with rheumatologists, the availability of a flare action plan promoting self-management,[2] and the use of a self-reported flare questionnaire,[3] as ongoing "check-ins". Patients valued the flexibility of the ABC model, particularly those living at a distance, and highlighted the responsiveness of the flare clinic and pharmacist support in medication adjustments. An unexpected facilitator was patients’ altruistic motivation, awareness of clinic workload and willingness to defer appointments to allow others with greater needs to be seen sooner. Select domains and patient quotes are displayed (Table 1). Table 1.

Selected Barriers and Facilitators to ABC Participation (as Highlighted in Abstract), with Representative Quotes Mapped to CFIR Domains

People with RA described ABC as a feasible and acceptable model of care, with minimal barriers identified. Addressing clarity around flare management and lab testing will improve patient experience and willingness to participate in this patient-initiated follow-up model.

[1.] Damschroder LJ. Implement Sci 2022;17:75. [2.] Ester M. BMC Rheumatol 2025;9:31. [3.] Bartlett SJ. J Rheumatol 2017;44:1536-43. Supported by a CIORA grant

Parents and their children (10-16 years) with JIA were recruited from clinics at McMaster and Alberta Children’s Hospitals. At enrollment, we measured child mental health using the parent-reported Emotional Behavioral Scales (EBS), and the child-reported EBS (CEBS). Parent psychological distress was measured using the Kessler 6 (K6), and Parent Stress Scale (PSS). Disease activity was measured by self-perceived impact of JIA based on a single question within the Patient Global Assessment (PtGA). Descriptive statistics were determined for all variables of interest. Multiple regression analyses using product-term interactions estimated whether parent psychological distress moderated the association between child mental health, categorized as internalizing and externalizing psychopathology and disease activity. Covariates included parent and child age and sex, household income, and parent education.

Baseline characteristics for parent-youth dyads (n=132) are shown (Table 1). There were significant (p<.05) moderating effects of both measures of parent psychological distress (PSS and K6 modeled independently) on the association between disease activity and internalizing psychopathology. Significant interaction effects were observed for child-reported internalizing x PSS (β=–.248, p=.005) and x K6 (β=–.753, p<.05), as well as parent-reported internalizing x PSS (β=–.218, p=.005), and x K6 (β=–.671, p<.05). No moderating effects were found for the association between externalizing psychopathology and disease activity. Table 1:

Baseline characteristics of children living with JIA and their parents (n = 132 parent–youth dyads).

Overall, parent stress/distress was a significant moderator of the relationship between child mental health and disease activity, with more distress associated with worse disease activity. This study will continue to assess child mental health outcomes for up to 18 months. Findings will inform early prevention of parental stress and subsequent mental health problems in children with JIA. Understanding the psychosocial impact of JIA will support the development of individualized mental health services and support.

[1.] Gowda N. Clin Rheumatol 2024;43:2009-19.

Three out of 5 Rheumatology clinics at the Kingston Health Sciences Centre employ phone call appointment reminders, a fourth clinic employed phone call or email reminders, while the fifth clinic did not employ any reminders. Our primary outcome measure was the non-attendance rate in the reminder group (clinics 1-4) compared to the no reminder group (clinic 5). Secondary outcomes of interest included the correlation between confirmation of attendance and non-attendance rate across clinics, and whether email reminders were comparable to phone call reminders in reducing the non-attendance rate.

The non-attendance rate was lower in clinics utilizing any appointment reminder method (6.9% 95% CI:6.0-7.8) as compared to no reminders (10.0% 95% CI:8.1-12.0) (Chi-square (1,N=3917) 9.73, p=.002). The administrative time cost was the balancing measure for the study and ranged from 28 to 50 hours of administrative time over a 6-month period in the clinics that performed appointment reminders. Appointment confirmation rate correlated with lower non-attendance rate (Pearson r(2) = –0.91, p =.04) at a cost of administrative time if reminders were given by phone call. However, email reminders were a method of increasing confirmation rate with less added time cost and had comparable beneficial influence on non-attendance rate to phone call reminders 5.9% vs 6.9% respectively, (Chi-square (1,N=3346) 0.45, p=.83).

Appointment reminders significantly lowered the non-attendance rate for outpatient rheumatology clinics. This was at a cost of 28 to 50 hours of administrative work over a 6-month period. Confirming appointments at the time of reminders also lowered the non-attendance rate but required extra time to do so if done by telephone. Both reminder calls and reminder emails were comparably effective, and email reminders with the added function of confirming appointments could be a method of improving the confirmation rate at a time savings. Utilizing email reminders for those patients who are able to adopt it may be the more efficient method overall.

[1.] Hwang AS. J Gen Intern Med 2015;30:1426-33. [2.] Liu Q. Cochrane Database Syst Rev 2014;2014(11):CD006594.

Prospective cohort study of pregnant adults aged ≥18 years with positive anti-Ro/SSA antibodies, with or without a systemic autoimmune or rheumatic disease (SARD), who were followed in the Obstetrical Rheumatology Clinic at The Ottawa Hospital until 3 months postpartum. Clinical data was extracted independently by 2 reviewers through standardized chart review. The relationship between maternal HCQ use and neonatal outcomes was analyzed descriptively.

31 pregnant women with anti-Ro/SSA positivity were included. Mean age was 34 ± 5. The majority (61.3%) had a SARD, while 38.7% had no diagnosis. 35.5% had isolated anti-Ro60/SSA antibodies, 19.4% had dual positivity, and 38.7% had triple antibody positivity. 74.2% were treated with HCQ, with 78.2% started pre-conception or first trimester and until delivery. Dose of 400mg (39.1%) or 5mg/kg/day (43.5%). NLE occurred in 3 cases overall (10%), each treated with HCQ, and none reported in the non-HCQ group. 2 NLE cases presented with cutaneous NLE and CHB (8.7%), while the other was limited to cutaneous NLE (4.3%). One case of CHB was treated since pre-conception (type 1) and the other (type III) treated only in third trimester. Both diagnosed between 18-24 weeks gestation, with 87.1% screened for CHB between 16-26 weeks. Each case of NLE occurred with triple positive high titer anti-Ro60, anti-Ro52, and anti-La (Figure 1), with high titer anti-LA/SSB showing a statistically significant difference (p=0.004). Only 10% of patients had anti-La/SSB >1,375, yet this accounted for 66.7% of NLE cases.

This is the first study to evaluate the rates of NLE in neonates of anti-Ro/SSA positive mothers treated with HCQ. The results are skewed by a patient with type III CHB prior to starting HCQ late in pregnancy. Accounting for this, rates of NLE with HCQ (8.6%) compared to without (12.5%) are more aligned with prior data. Additionally, the few cases of NLE in this study occurred only with triple positive high titer Ro/La antibodies. This may suggest that patients with low titer antibodies do not require the same rigorous screening, or that treatment with HCQ is more effective in this subset of patients in preventing NLE.

[1.] Clowse M. Ann Rheum Dis 2021;80:817-23.

Case 1 involves a 46-year-old man with newly diagnosed idiopathic inflammatory myositis who was treated with MMF 500mg daily along with glucocorticoids and IVIG. Within 3 days he developed neutropenia with neutrophils nadiring at 0.4 x 10^9/L on day 6 after MMF initiation. His neutropenia resolved with cessation of MMF and administration of filgastrin. However, re-challenge with MMF at 250mg daily led to recurrence of neutropenia within 1 day so MMF was permanently discontinued, after which his neutrophil count quickly rebounded. Case 2 involves a 73-year-old woman with a new diagnosis of limited cutaneous systemic sclerosis and scleroderma renal crisis, who was initiated on MMF 500mg twice daily. Within 4 days her neutrophils dropped from 11.1 x 10^9/L to 2.4 x 10^9/L. Accordingly, the MMF was held for a day, after which her neutrophil count normalized, so MMF was re-initiated at a lower dose of 500mg daily. Within 4 days neutropenia had recurred, so MMF was discontinued and the neutropenia resolved within 2 days.

Bone marrow suppression is a well-established side-effect of MMF, with leukopenia and neutropenia occurring in as many as 25% of patients.[1] Onset, however, is generally subacute, occurring >100 days after initiation of MMF.[1,2] Prior to our cases, we found no reports of neutropenia or leukopenia developing within a matter of several days of MMF initiation without other obvious causal factors. A complex array of enzymes is responsible for metabolism and defects of any of these can lead to supratherapeutic drug or metabolite levels. Pharmacokinetic studies of MRP2/ABCC2 variants in renal transplant patients have identified both high expressor and low expressor phenotypes that can lead to either sub therapeutic or supratherapeutic MMF levels at standard dosing.[3] However, there is not yet a body of study investigating whether the pharmacokinetic differences seen in MRP2/ABCC2 variants translate into adverse events such as MMF-related neutropenia. The confirmation of such a link would offer a potential target for genetic screening, which could help to prevent hypersensitivity events in patients treated with MMF.

[1.] Varnell CD. Pediatr Transplant 2017;21:10.1111/petr.13033. [2.] Zafrani L. Am J Transplant 2009;9:1816-25. [3.] Brazeau D. J Clin Pharm 2021;61:1592-605.

Single-center cross-sectional study including children ≤18 years, diagnosed with CNO, acute infectious osteomyelitis (AOM) and bone malignancy from June 1, 2018, to May 31, 2024. Patients with other mimicking conditions, immunodeficiency, sickle cell disease, or those previously included in the original development cohort were excluded. Patients were divided into 2 groups: a CNO group and a non-CNO group (AOM and bone malignancy), from the latter a representative, random, sample was selected (www.random.org). Demographic, clinical, laboratory, imaging and pathology data were collected at disease onset. EULAR/ACR criteria were retrospectively applied to the entire cohort, independently from the initial diagnosis. Patients with an aggregate score ≥ 55 points were classified as having CNO. A secondary analysis was conducted excluding patients with missing data. Classification results using the new criteria were compared with the final clinical diagnosis based on physician assessment (criterion standard). The same analysis was applied to Jansson and Bristol criteria. Sensitivity and specificity, positive likelihood ratio (LR+) and post-test probability (PTP) (pre-test probability: 20%, based on CNO prevalence in our center) were calculated.

Of 164 children included, 82 had CNO, 41 were randomly selected from 274 cases of AOM, and 41 from 849 cases of bone malignancy. The median age was 10 years (IQR 3-16), with 62% girls and 37% boys, 33% had a bone biopsy. Overall, 40% scored ≥ 55 and 60% did not, with 19 false positive and 3 false negative. The EULAR/ACR criteria demonstrated 77% sensitivity and 96% specificity, with a LR+ of 19.25 and PTP of 83%. In our secondary analysis excluding patients with incomplete data, results remained consistent (sensitivity 79%, specificity 96%, LR+ 19.75, PTP 83.2%). In comparison, the Jansson criteria showed 78% sensitivity, 67% specificity, LR+ of 2.36, and PTP of 37%. The Bristol criteria yielded 89% sensitivity, 70% specificity, LR+ of 2.97, and PTP of 43%.

Based on its favorable sensitivity and specificity, especially in comparison to existing criteria, the new EULAR/ACR criteria appeared to be more effective in distinguishing CNO from AOM and bone malignancy at disease onset, results consistent with findings from the original validation cohort. Best Abstract by a Rheumatology Post- Graduate Research Trainee Award

Baseline MBI was completed by pediatric rheumatology fellows as a screen of burnout symptoms. All fellows were enrolled in 2023-2024 academic year. The MBI reports scores in 3 categories: emotional exhaustion (EE), depersonalization (DP), and personal accomplishment (PA), with higher scores equating to higher risk of burnout. A stakeholder group was formed, including 8 pediatric rheumatology fellows, and engaged colleagues including allied health team members and staff physicians within the Division of Rheumatology. The workgroup identified key and modifiable contributors to burnout within the workplace. Processes were implemented and modified using multiple plans, do, study, act (PDSA) cycles. Wellness sessions were run by the study leads (fellows and faculty) and implemented with attendance and post-session feedback obtained as process measures to guide subsequent PDSA cycles. The MBI was followed at the 0, 3-, and 6-month mark to assess success of these strategies.

A baseline MBI was completed by 3/12 pediatric rheumatology fellows as an audit. Average scores were EE = 15.7/36 (moderate), DP = 10.0/20 (moderate), and PA = 13.0/32 (low). Each wellness session represented a new PDSA cycle. Five PDSA cycles were completed from January to June 2024. The initial cycle highlighted that there was no process in place to address symptoms of burnout. Implementation strategies included "Treats and Talks" focused sessions during protected educational time, social events among fellows and external events that included the fellows’ families. Eight fellows completed the 6-month follow-up MBI. Six-month MBI scores showed improvement in all MBI domains with EE = 10.8/36 (low), DP = 4.6/12 (low), and PA = 8.8/32 (low), a decrease of 31%, 54%, and 32% respectively. Average session attendance was 7/12 fellows, and average benefit score was 6.1/10.

Our study has revealed a baseline risk of burnout among pediatric rheumatology fellows at our tertiary academic hospital. With a quality improvement-based approach we have implemented change strategies that show reduced risk of burnout, as measured by the MBI at 6 months. Ongoing change ideas will be focused on the sustainability of these changes.

In this cross-sectional study, consecutive SLE patients fulfilling the 2019 EULAR/ACR classification criteria were recruited with informed consent under institutional ethics approval. Demographics, social determinants of health, and LupusQoL scores were collected via standardized questionnaires. Clinical data, including SLEDAI-2K, ACR Damage Index, healthcare utilization, and medication use, were abstracted from medical records. Low QoL was defined as a score below the 50th percentile. Between-group comparisons were performed using t-tests, chi-square, or Mann-Whitney U tests.

Among 207 patients (mean age 53.1 ± 14.2 years; 88.4% female), 39 (18.8%) had low HRQoL and 168 (81.2%) had high HRQoL. Across all 8 LupusQoL domains, patients with high HRQoL scored significantly better (all p < 0.001). The greatest differences were observed in the Physical, Planning and Burden domains. The low HRQoL group had higher ACR Damage Index scores (1.89 ± 1.87 vs 1.21 ± 1.75; p = 0.022), while mean SLEDAI-2K scores were similar (2.12 ± 2.66 vs 2.00 ± 2.31; p = 0.777). Depression/anxiety was more prevalent among patients with low HRQoL (48.0% vs 25.2%; ² = 8.6, p = 0.004). Fibromyalgia was more frequent among patients with low HRQoL compared to those with high HRQoL (21% vs 5.5%; ² = 10.2, p = 0.001), indicating a strong association between comorbid fibromyalgia and impaired quality of life. Prednisone use was also associated with lower HRQoL scores (41% vs 26%; ² = 3.8, p = 0.05). No statistically significant differences were observed in age, ethnicity, marital status, income, or primary care access.

In this SLE cohort depression, anxiety, fibromyalgia, corticosteroid use, and greater cumulative organ damage were the strongest predictors of poor HRQoL, outweighing demographic or disease activity measures. Marked impairments across physical, planning, and burden domains highlight the multifactorial nature of HRQoL in SLE and underscore the need for integrated mental health care, steroid-sparing strategies, and prevention of organ damage to enhance quality of life.

This study was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). A comprehensive search was conducted in Ovid MEDLINE, Embase, Cochrane Library and Scopus from inception to July 14th, 2025. The search strategy used keywords and Medical Subject Headings for "systemic lupus erythematosus" and "frailty." Included articles were English language full-length original research articles of any study design that described the use of a frailty measure/tool in patients with SLE. Data were extracted using a standardized form by 2 independent reviewers. Risk of bias assessment was done using the NHLBI Quality Assessment Tool for Observational Cohorts and Cross-Sectional Studies.

The search yielded 797 articles for title/abstract screening, of which 83 underwent full text review. Twenty-four articles were included (14 cohort studies, 10 cross-sectional studies). All included studies received an overall rating of "fair" or "good" in the risk of bias assessment. Frailty was assessed using 6 different measures. One specifically constructed for use in SLE, the Systemic Lupus International Collaborating Clinics Frailty Index (SLICC-FI), was the most frequently used (15 studies), followed by the Fried phenotype (5 studies) and FRAIL scale (5 studies) (Table 1). The prevalence of frailty was reported by all 24 studies, ranging from 6.2% to 80.9%. Older age was positively associated with frailty in 8 of 13 studies. In univariable analyses, regardless of the measure used, frailty was associated with an increased risk of adverse outcomes during follow-up, including damage accrual, hospitalizations, and mortality, as well as worsening disability, quality of life and cognitive impairment. Table 1.

Measures Used to Characterise Frailty in SLE Patients in the Identified Studies

Several different tools are used to measure frailty among people living with SLE. Regardless of whether it is measured using the phenotypic approach or the deficit accumulation approach, frailty is consistently associated with an increased risk of adverse health outcomes in SLE. The optimal approach for measuring frailty in this population may vary across different clinical and research contexts.

A 36-year-old Hispanic female presented with a 1-year history of progressive bilateral small and large joint arthralgias involving the MCPs, PIPs, wrists, and knees. Laboratory investigations revealed negative rheumatoid factor, anti-cyclic citrullinated peptide antibody, antinuclear antibody, and HLA-B27. C-reactive protein was mildly elevated (11 mg/L), and baseline imaging was normal. The patient received sequential therapy with methotrexate, leflunomide, and biologics agents including adalimumab and JAK inhibitors (tofacitinib, upadacitinib, baricitinib) with only partial or transient responses. Over a 6-year disease course, the patient developed new erosions on serial hand radiographs and violaceous periungual macules with nodular lesions over the digits. Infectious causes were excluded. An urgent dermatology consultation was requested. Skin biopsy revealed multinucleated histiocytes and giant cells with eosinophilic, ground-glass cytoplasm—findings diagnostic of multicentric reticulohistiocytosis.[1] Given persistent disease activity, intravenous tocilizumab was initiated alongside a tapering course of prednisone, resulting in stabilization of joint symptoms and improvement in skin lesions.

Multicentric reticulohistiocytosis is a rare systemic granulomatous disorder that may mimic seronegative erosive arthritis, often leading to diagnostic delay. Recognition of characteristic cutaneous findings and histopathologic confirmation are essential for diagnosis.[2] Reported treatments include corticosteroids, methotrexate, cyclophosphamide, and TNF inhibitors with variable benefit. Although data remain limited, biologic therapies—particularly IL-6 inhibition—appear promising for refractory disease.[3] Early dermatologic collaboration and multidisciplinary management are key to optimizing outcomes.

[1.] Sanchez-Alvarez C. Rheumatology 2020;59:1898-1905. [2.] Tariq S. Springerplus 2016;5:180. [3.] Pacheco-Tena C. J Clin Rheumatol 2013;19:272-6.

We conducted a longitudinal retrospective-cohort (Jan 1, 1997-Dec 31, 2023) using BC administrative health data (capturing all provincially funded services including outpatient and hospital visits, dispensed medications, and demographics). We identified all adults with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) who started HCQ after diagnosis and remained on HCQ for ≥1 year. We followed this cohort for HCQ-R screening from HCQ initiation assessing for baseline and subsequent annual screenings until HCQ discontinuation, loss-to-follow-up, death or administrative end of study. Outcome: A valid screening (guideline-concordant): (1) ICD-9 code (362.XX or V67.51) by an ophthalmologist/optometrist and (2) an optical coherence tomography (OCT) (22067) or/and visual-field (02043) fee item billed by an ophthalmologist/optometrist. We defined "no screening" as the absence of both retinal-exam ICD9-code and OCT/visual-field fee-items. Statistical analyses: We estimated the rates of valid screening at baseline and annually among those remaining on HCQ (risk set). Multivariable generalized-estimating-equations assessed association of valid annual screening with predictors including physician-care pattern (continuous-rheumatologist-care (Rheum-care), family-physician-only-care (FP-only), intermittent rheumatologist-care with gaps of family-physician-only-care (Int-Rheum-FP-only) or started by rheumatologist-care then hands-off to family-physician-only-care (Start-Rheum-then-FP-only)), regional healthcare authority, baseline screening, years since HCQ initiation, demographics, and comorbidity.

Among 22,572 HCQ initiators (75.26% female; mean age 53.64±15.06 years; SLE 8.52%; mean HCQ-exposure 6.40±5.34 years), only 4,400 (19.5%) had a valid baseline screening and 11,676 (51.7%) had no screening. From year 2 to 25, risk set decreased from 21,634 to 809 with valid annual screening ranged from 17.9% to 22.5%. Rates of no screening remained almost constant (~63%). Relative to Rheum-care, odds of having valid annual screening (adjusted-OR, 95% CI) were lower (P-value<0.0001) for FP-only (0.67, 0.62-0.72), Int-Rheum-FP-only (0.71, 0.68-0.75), and Start-Rheum-then-FP-only (0.64, 0.58-0.71). Compared to Vancouver-Coastal health, odds were lower (P-value<0.0001) in Interior (0.84, 0.79-0.90), Fraser (0.76, 0.71-0.81), Northern (0.71, 0.66-0.76), and Island (0.34, 0.31-0.39) health authorities. Table 1 presents adjusted-ORs for valid baseline screening, years since HCQ initiation, and patient-level predictors (Table 1). Table 1.

Patient-Level Predictors Associated with Valid (Guideline-Concordant) Annual HCQ-related Retinopathy (HCQ-R) Screening

In this real-world longitudinal study, about 50% of HCQ initiators and 63% of long-term HCQ users did not receive guideline-concordant HCQ-R screenings. Baseline screening and continuous rheumatologist care had strong association with ongoing guideline-concordant annual screenings. Strengthening guideline-oriented practices and addressing regional gaps may improve screening and reduce preventable vision loss.

[1.] Marmor MF. Ophthalmology 2016;123:1386-94.

We conducted a prospective cohort study in BC, using a standardized retina-screening protocol for HCQ-R through a network of 20 ophthalmologic/retina clinics all-over BC, starting in October 2022. Sample: we included patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) who were on HCQ at enrollment and have been using it for ≥5 years. Over 40 rheumatology practices in BC were engaged to identify eligible participants through their electronic medical record (EMR) system, which were flagged in EMRs. Then, informed consent by their rheumatologist was obtained to be referred to an ophthalmologic/retina clinic closer to them for annual HCQ-R screening using macular Spectral-Domain Optical Coherence Tomography (SD-OCT). Normal scans were booked for the next year’s annual screening. Outcome: We assessed HCQ-R events defined as equivocal or abnormal scans based on the eye specialist diagnosis, which then were uploaded to a secure cloud platform for independent, masked review and staging by 2 retina specialists, with discrepancies resolved through consensus. For quality control, 30% of normal scans were also randomly selected for review. Statistical analyses: We estimated risk of HCQ-R using the cumulative incidence function (CIF), accounting for right censoring and competing risk of death.

There were about 3,000 eligible participants detected and flagged in the EMRs of BC rheumatologists. From October 1, 2022, to September 31, 2025, 1,300 referrals (~40% of flagged) were received; 952 participants completed a first visit, 254 a second, and 54 a third. Participants were predominantly female (84.3%) with mean age of 58.2±15.0 years, and 43.5% had SLE (Table 1). Sixteen HCQ-R events (early or moderate) were confirmed; 13 equivocal cases remain under review pending confirmatory testing. CIF estimates (risk (95% CI) at X years since HCQ initiation) were as following: 0 at 5 years; 0.36% (0.10-1.00) at 10 years; 0.72% (0.07-1.60) at 15 years; 1.25% (0.53-2.55) at 20 years; 4.23% (2.04-7.65) at 25 years; and 6.54% (3.17-11.58) at 30 years. There was no adequate risk set to estimate CIF beyond 30 years. Table 1-

Characteristics of the 952 enrolled participants in the INTACT study who completed their 1st (or 2^nd/3^rd) HCQ-R screening visit (01-10-2022 to 31-09-2025)

In this interim analysis of the INTACT study, we identified that cumulative risk of pre-clinical HCQ-R detected through screening using SD-OCT roughly doubled across 5-year intervals from 10-20 years, then tripled from 20-25 years. Next, we will expand enrollment and link pharmacy claims to capture time-varying dose for dose-stratified risk estimates.

A systematic search of PubMed, Scopus, Ovid, Embase, and WHO databases (inception-December 31, 2024) identified observational studies meeting: (1) adults with rheumatic diseases on HCQ ≥1 year; (2) SD-OCT for HCQ-R screening; (3) reported or data to calculate HCQ-R prevalence or cumulative incidence; (4) risk factors reported as hazard ratios (HRs) or odds ratios (ORs) with 95% CIs or calculable data; and (5) English full-text. Study quality was assessed using Newcastle-Ottawa Scale. Random-effects meta-analysis estimated pooled prevalence, cumulative incidence, and risk-factor associations. We assessed heterogeneity with the Q-test and I², then explored sources of variability via subgroup analyses across cohort type, study quality, publication year, and follow-up length. To address confounding effects, we fit multivariate meta-regression on logit-transformed prevalence/cumulative-incidence to quantify each factor’s independent contribution to between-study heterogeneity. Publication bias was assessed with funnel plots and Egger’s test.

We screened 775 records; 19 met inclusion criteria (18 cohort, 1 case-control). Pooled HCQ-R prevalence (2008-2023) was 5.1% (95% CI: 3.9-6.5) (Figure 1). Pooled HCQ-R cumulative incidence was 0.1% (0.0-0.5) at 5 years, 2.6% (1.6-4.1) at 10 years, and 5.6% (3.2-9.6) at 15 years. Risk factors (HR, 95% CI) were daily dose >5 mg/kg of actual body weight (4.32, 2.80-6.65); chronic kidney disease (CKD) (1.94,1.27-2.96); female sex (3.78, 1.90-7.48) and Asian vs White ethnicity (1.67, 1.07-2.62). There was substantial heterogeneity between studies that reported period prevalence (Q=197.44, p<0.0001; I²=94.4%). Subgroup analysis revealed cohort type (retrospective vs prospective) as the only variable which explained part of heterogeneity (p<0.001) (Figure 1). In multivariable meta-regression, retrospective cohorts still showed higher prevalence after adjustment for follow-up length (β=1.72, 95% CI 1.04-2.40; p<0.001) or publication year (β=1.69, 95% CI 0.52-2.85; p<0.01). Heterogeneity among cumulative incidence studies was non-significant (≤5 years (Q=6.47), 5-10 years (Q=6.85), and 10-15 years (Q=3.94); p>0.05). Prevalence studies showed mild small-study funnel asymmetry, but Egger’s test was non-significant (p>0.05). Cumulative-incidence studies showed a symmetric funnel with non-significant Egger’s test.

Pooled prevalence of 5.1% reflects the overall burden of HCQ-R from 2008 to 2023. HCQ-R risk increases with duration of HCQ use and is dose-dependent, reaching 5.5% by 15 years. Findings support dose optimization with intensified screening for higher-risk patients including CKD, female and Asian patients.

This scoping review followed Joanna Briggs Institute methodology and adhered to the PRISMA-ScR checklist. We searched MEDLINE, EMBASE, Web of Science, Cochrane CENTRAL, and CINAHL from inception to May 2024. We included peer-reviewed studies that evaluated outpatient team-based rheumatology care involving at least 1 rheumatologist and 1 IHP, compared with any other outpatient care model. Terminology describing care models was examined in relation to reported team composition, and outcomes were mapped to the Quintuple Aim targets.

The search identified 6,139 unique records, of which 76 reports representing 67 studies met inclusion criteria. Most included studies were published within the past 15 years, indicating a recent surge in research on team-based rheumatology care (Figure 1). A wide range of team-based care models was evaluated across different rheumatic diseases and clinical contexts, ranging from smaller teams comprising a rheumatologist and 1 IHP to large, comprehensive care teams involving multiple health professionals and physicians from other specialties. Terminology used to describe care models was inconsistent, with terms (eg, multidisciplinary/interdisciplinary) often used interchangeably. In addition, most studies lacked sufficient description of the care model to enable replication. Population/patient health was the most frequently examined Quintuple Aim domain (n = 52, 78%), with outcomes largely centered on disease activity, physical function, and quality of life. Thirty-nine studies (58%) assessed patient experience outcomes (eg, satisfaction, self-efficacy). Cost outcomes were evaluated in 15 studies (22%), and provider-focused outcomes in 8 studies (12%). Equity was addressed in only 1 study, and none investigated the impact of team-based care on provider mental health or burnout. Most evaluations showed positive impacts, but were short-term, with observation periods limited to ≤12 months.

This review highlights a rapidly expanding yet heterogeneous evidence base on team-based care models in rheumatology. Most studies focused on short-term evaluations of health outcomes and patient experience, with few addressing cost-effectiveness, provider well-being, and equity. Future research should adopt standardized terminology, improve reporting of team structures and processes, and include longer-term evaluations to capture impacts across the full Quintuple Aim.

A modified e-Delphi process was utilized to build consensus on the preventability and importance of various hospitalization diagnoses occurring in persons living with RA identified from a systematic literature review. Clinical panelists were Canadian and US healthcare providers (rheumatologists, internists, pharmacists, occupational therapists, and physiotherapists) with expertise in the care of persons with RA. Consumer panelists were Canadians living with physician-diagnosed RA. Clinical panelists completed 2 rounds of anonymous voting, with an asynchronous discussion board hosted between rounds. Consumer panelists completed the same process considering the remaining candidate items where consensus had not yet been reached. An interactive webinar preceded a final combined panel round of voting. Consensus criteria were guided by the RAND/UCLA Appropriateness Method.[2,3]

Twenty-two clinical and 8 consumer panelists provided expert opinion. There were 46 initial conditions for consideration with 1 condition added by the clinical panel and 2 by the consumer panel. At the conclusion of the 5 voting rounds, 12 conditions were identified as RA-specific ACSCs: those specific to RA disease activity (RA disease flare, vasculitis), RA-related associations and complications (osteoarthritis, osteoporotic fracture, cervical spine instability, anemia/pancytopenia) and acute (upper respiratory infection, septic arthritis) and opportunistic (pneumonia/pneumocystis jirovecii, herpes zoster, tuberculosis reactivation, and other general opportunistic) infections.

This study identified 12 potential RA-specific ACSCs. Next steps include monitoring these conditions in a health context to understand their performance as possible RA-specific ACSCs.

[1.] Rocha JVM. Health Policy Open 2021;2:100030. [2.] Fitch K. The RAND/UCLA appropriateness method user’s manual 2021. RAND Corporation. [3.] Jones J. BMJ 1995;311:376-80.

A cross-sectional study was conducted in individuals 16 years or older with SSc, who were employed or had been employed in the last 5 years. Demographics, disease manifestations including patient reported outcomes, frequency of disease flares, specific limitations at work, and the need, availability and use of various workplace supports were collected. Regression models were used to evaluate the unadjusted and adjusted relationship between unmet accommodation needs and workplace outcomes (absenteeism, job disruption and presenteeism; respectively) between participants with and without SSc-associated GI involvement. A p-value of <0.05 was considered statistically significant.

We report 217 participants (175 (80.6%) women, 42 (19.4%) men) where 129 (59.4%) had gastrointestinal symptoms and 88 (40.6%) did not have any GI symptoms related to SSc. Those with GI involvement scored lower on self-related health outcomes (p<0.0001), have greater amounts of pain (p<0.0003) and fatigue (p<0.0001), have worse patient-reported health overall (p<0.0001), more health variability (p<0.0001), and more disease flares (p<0.0004). Participants with SSc-associated GI symptoms needed more workplace accommodations than those without GI symptoms, including flexible hours or flex time (65.9% vs 46.6%), extended health benefits (84.1% vs 68.2%), breaks and rest periods (58.7% vs 33.3%), special equipment (62.1% vs 44.8%), modified job duties (48.8% vs 26.1%), altered work schedule (54.9% vs 33.3%), and the need to work from home on occasion (56.4% vs 37.4%) (Table 1). Participants with SSc-GI manifestations were 3.68 times more likely to have unmet workplace accommodations than those without GI manifestations; this did not change when the subjects disclosed their diagnosis to their supervisors. Those with GI involvement had higher job disruption scores (on average, 1.2 scores higher) and reported greater disease-related impairment in job productivity (on average, 2.3 scores higher) than those without GI involvement; this is also true when adjusted for biological sex and age. Table 1.

Unadjusted relationship of GI involvement and needed workplace accommodations

The presence of GI symptoms poses a significant burden on productive employment in individuals with SSc. This study lays the groundwork for where SSc- specific efforts in workplace policies and practices should be directed.

The study population included all singleton pregnancies with ≥22 weeks of gestation, between July 2008 and December 2024 in Alberta, Canada. Previously validated algorithms based on ICD-10 codes were used to identify women with SLE and no IMID. We compared maternal characteristics, comorbidities and neonatal outcomes between no IMID and SLE groups. Dispensation of SLE-related medications was evaluated in 2 time periods (2008-2016; 2017-2024). Proportion of days covered (PDC) during pregnancy for each medication was calculated to estimate adherence. Logistic regression was used to calculate the odds of developing preterm labor when exposed to SLE-related medications after adjusting for maternal factors.

Among 787,346 pregnancies of 474,197 women, 994 pregnancies were by women with SLE and 786,352 had no IMID. Pregnant women with SLE were more likely to have renal disease (No IMID 5% vs SLE 10.4%), pre-existing hypertension (No IMID 7.6% vs SLE 23.5%), pre-eclampsia/eclampsia (No IMID 4% vs SLE 9.9%) while neonates in mothers with SLE had more congenital anomalies (No IMID 9.8% vs SLE 13%), were smaller for gestational age (No IMID 12.5% vs SLE 16.1%) and had more NICU admissions (No IMID 9.6% vs SLE 20.2%). SLE prescription dispensations included corticosteroids 21%, NSAIDs 5.5%, antimalarials 46.6%, and pregnancy safe DMARDs 9.5%. Mean PDC for anti-malarials increased from 60.6 (SD 30.3) to 72.2 (SD 27.4) between 2008-2016 and 2017-2024. Preterm delivery was more common in women with SLE (17.4%) vs no IMID (7.0%). In multivariable models, factors that were significantly associated with higher risk of preterm delivery in women with SLE included: low PDC (< 40%) of anti-malarials (compared to high PDC (> 80%)); high PDC of corticosteroids (compared to no use); active disease, being married and pre-eclampsia/eclampsia (Table 1). Table 1.

Associations between preterm delivery for Albertan women with SLE, level of adherence to corticosteroids and anti-malarials, and maternal characteristics

Pregnancy-safe medication use has increased over time but peripartum outcomes remain poor for SLE women. Despite use in SLE flares, corticosteroid use may increase risk of preterm labor. Adherence to anti-malarial use during pregnancy may improve outcomes through reduction of flares. Further patient education and close disease monitoring in the peripartum period is recommended. Supported by a CIORA grant

We used administrative data from British Columbia (BC), including all outpatient and hospital visits, all dispensed medications, vital statistics, demographics, and cancer registry. We assembled a population-based retrospective cohort of GCA with incident glucocorticoid use. Sample: all newly diagnosed GCA patients receiving healthcare between January 1997-December 2023 with no glucocorticoid exposure and no CVD events prior to GCA onset. GCA was defined by ≥1 code for GCA by a rheumatologist or hospital (ICD-9-CM 446.5; ICD-10 M31.5), or 2 ICD-9-CM codes for GCA between ≥2 months-2 years apart by a non-rheumatologist physician. Exposure: glucocorticoid dosing was calculated using Pharmanet data. Exposure was categorized as current use (Yes/No), current dose (mg/day), total past cumulative dose (grams), and total cumulative duration of use(months). Outcomes: We identified CVD outcomes using inpatient and outpatient ICD-9 billing codes, including myocardial infarction (MI) (ICD-9 410), stroke (434), and venous thromboembolism (VTE: DVT and PE) (453, 415.1, 673.2, 639.6). Associations between glucocorticoid exposure and CVD were estimated using a Cox proportional hazard model, adjusted for relevant confounders as in our previous studies.

4,681 patients with newly diagnosed GCA were identified with incident glucocorticoid use and no prevalent CVD (mean age 70.4, 68.9% female), with a mean Charlson comorbidity score of 0.94 (SD 1.58). During follow-up, we identified 969 CVD events (439 MI, 645 stroke, 134 VTE). Compared to non-users, glucocorticoid use was associated with a 113% increase in risk of CVD (Table 1). Moreover, current daily dose (15% per each 5 mg) and cumulative glucocorticoid dose (78% per each gram accumulated in the past) were associated with an increased risk of CVD. Cumulative duration of glucocorticoid use was also associated with a 23% increased risk of CVD per each month of use. Table 1.

Increased Risk of Cardiovascular Disease from Glucocorticoid Exposure: Unadjusted and Adjusted Cox Proportional Hazard Models

Among patients with GCA, glucocorticoid use, daily dose, cumulative dose, and cumulative duration were significantly associated with increased risk of CVD. New strategies with newer therapies should target minimizing glucocorticoid use in patients with GCA.

[1.] Aviña-Zubieta JA. Ann Rheum Dis 2016;75:148-54. [2.] Pujades-Rodriguez M. PLoS Med 2020;17:e1003432.

We assembled a retrospective cohort study using administrative data from British Columbia (BC). Our data includes outpatient and hospital visits, all dispensed medications, vital statistics, demographics, and cancer registry. Sample: We identified all patients <50 years of age with an initial MI (ICD-9 410), stroke (434), DVT (453), PE (415.1, 673.2, 639.6), stillbirth (779.9), or preeclampsia (642) between January 1997-December 2023. Outcomes: We identified all outpatient aPL testing ordered for this cohort during the study period for these patients using fee codes (LAC (90377), aCL IgG and IgM antibodies (91145, 91146), aβ2GP1 (90046, 90047)). We report the rates and mean time to outpatient testing for aPL after initial event.

Among 112,622 patients who developed the outcomes of interest, we report 25,010 TEs, 77,725 stillbirths, and 9,847 cases of pre-eclampsia in patients <50. Of these, a minority of patients - 4.4% of MI, 28.9% of stroke, 34.2% of DVT, 36.8% of PE, 4.3% of stillbirths, and 9.6% of preeclampsia - were tested for ≥1 aPL, with median time elapsed between the event and first testing described in Table 1. Among those tested for ≥1 aPL, 21.1% of MI, 12.9% of stroke, 13.0% of DVT, 12.0% of PE, 17.7% of stillbirth, and 14.7% of preeclampsia cases were diagnosed with a systemic autoimmune rheumatic disease within ±90 days of testing; repeat TEs and OEs were also common (Table 1). Table 1:

Thrombotic and Obstetric Event Incidence and Antiphospholipid Antibody Testing in BC Patients Between January 1997-December 2023

We found low levels (<10%) and delays in aPL testing following initial thrombotic/obstetric events. A late APS diagnosis may fail to prevent subsequent recurrences of APS-associated events.

[1.] Sciascia S. Ann Rheum Dis 2015;74:2028-33 [2.] Devreese K. J Thromb Haemost 2020;18:2828-39. [3.] Barbhaiya M. Ann Rheum Dis 2023;82:1258-70.

Patients at 2 specialized Canadian clinics for pregnancy in rheumatic diseases were recruited to the Canadian Pregnancy and Rheumatic Diseases registry (CaPRIS) between July 2020-October 2025. Participants were 18 or older, pregnant or planning pregnancy, and had 1 or more rheumatic diseases. Preeclampsia risk was assessed and ASA was started by the treating rheumatologist or obstetrical provider, either 81mg or 162mg daily starting before 14 weeks gestational age (GA) until 36 weeks GA. Baseline characteristics and pregnancy outcomes were compared with Fisher’s exact test and Student’s t-test.

We included 110 pregnancies and their baseline characteristics and outcomes (Table 1). Seventy-five patients (68%) received ASA; 35 patients (32%) did not. Patients on ASA were more likely to have SLE (p <0.01); 4 of 21 patients (19%) with SLE in our cohort developed pre-eclampsia. Patients not treated with ASA were more likely to have axial spondyloarthritis (p <0.01). Ten patients (13%) on ASA developed preterm PE while 3 patients (9%) not on ASA developed preterm PE (p=0.55). There was no difference in GA at delivery or fetal weight between the groups. Table 1.

Baseline Characteristics and Pre-eclampsia (PE) Outcomes by Acetylsalicylic Acid (ASA) Use in Women with Rheumatic Disease

Guidelines recommend low-dose ASA for prevention of preeclampsia in pregnant patients at increased risk. 68% of patients with rheumatic diseases in our clinics met these criteria. Rates of PE and preterm PE were higher in this cohort than national averages. However, we did not observe a significant difference in rate of preterm PE for high-risk patients treated with ASA compared to low-risk patients. These data suggest that ASA is effective in mitigating risk of preterm PE in high-risk patients with rheumatic diseases and should be considered routinely in such patients.

[1.] Dzakpasu S. CMAJ 2024;196:E897-904. [2.] Clowse ME. Am J Obstet Gynecol 2008;199:127. [3.] Rolnik DL. N Engl J Med 2017;377:613-22.

Records of all patients with AAV were abstracted from 2015-2025 from the electronic medical record at a single tertiary care center. Demographic data, including ethnicity by self-report, diagnostic setting, ANCA subtype (granulomatosis with polyangiitis [GPA], microscopic polyangiitis [MPA], and eosinophilic granulomatosis with polyangiitis [eGPA]), and vital status at last follow-up were included. Descriptive statistics were used to characterize the cohort and compare patients from different ethnic backgrounds and ANCA subtypes. Survival was compared using Cox proportional hazard models.

A total of 334 patients were identified; 192 (58%) were female. Mean age at diagnosis was 53 years ±18; mean disease duration was 10 years ±7. 61% (n=202) of patients were White, 30% (n=101) Indigenous, 8% (n=26) Asian, and 1.5% other (n=5). 49% of patients were diagnosed in a hospital ward, 36% in ambulatory care, 9% in intensive care and unknown in 6%. GPA was diagnosed in 50% (n=167), MPA in 38% (n=128), and EGPA in 11 %. Males were more frequently diagnosed with EGPA (61%, 39% in females; p=0.12) and were older at diagnosis (56±17 years, females 51±19 years; p-0.011). Sixty-two patients (19%) died during the study period. Mean age at death was 61 ±19 years. Indigenous patients were younger at diagnosis (46±18 years; White = 56±18 years; Asian = 55±18 years; p<0.001). Indigenous patients were more often diagnosed with MPA (50%), compared to 34% of white patients and 30% of Asian patients (p = 0.029). More Indigenous patients had died by the end of the follow-up period (28%; White 14%, Asian 19%; p=0.028). Adjusted hazard ratio for mortality was 4.5 (95% CI 2.5-8.3, p<0.001) for Indigenous patients compared to White patients (Figure 1). Figure 1.

Adjusted Survival from Disease Onset by Ethnic Group (p <0.001)

On initial exploratory analysis of a large single center cohort, AAV appears to affect all ethnicities proportionally. We found differences in onset age and AAV subtype between ethnicities, with Indigenous patients diagnosed at a younger age and more often with MPA. Mortality was overall high at 19% during the follow-up period, with adjusted mortality particularly high in Indigenous patients. More studies are needed to determine factors contributing to poor outcomes and differences between ethnic groups.

[1.] Henderson BA. Arthritis Care Res 2025;77:873-80. [2.] Mohammed AJ. Rheumatology 2020;59:iii42-50.

A qualitative study using directed content analysis guided by the Theoretical Domains Framework (TDF),[3] was conducted. Semi-structured Zoom interviews (30-60 minutes) were completed with 13 physiotherapists purposively sampled after delivering OEP+ to community-dwelling older adults for 12 months. OEP+ combined OEP with BAP, a structured approach to support self-management which involves goal setting, action planning, and feedback, plus a Fitbit-compatible app. Interviews were audio-recorded, transcribed verbatim, and analyzed using the TDF, which integrates constructs from behavior change theories to identify factors influencing implementation. Three researchers (CP, ST, EW) independently coded transcripts and reached consensus.

Thirteen physiotherapists participated (7 private, 6 public), aged 20-64 years (31% aged 20-34, 54% aged 35-49, 15% aged 50-64), with a median of 15 years of experience (IQR=6-22). Two had prior exposure to using OEP in practice, and 7 had home-care experience. Facilitators and barriers to delivery were categorized using the TDF (Table 1). Facilitators included prior knowledge of OEP components, structured session planning, use of BAP support materials, context-sensitive application of BAP, ability to adapt exercises for home environments, and prior home care experience. External support (eg, patient family involvement, app-based cues) reinforced program delivery, while minimal equipment needs enhanced accessibility. Barriers included time gaps between training and delivery, rigidity of BAP structure, difficulty recalling exercise progressions, scripted follow-up calls limiting conversation flow, unclear communication about time expectations, scheduling and workload challenges, time-intensive home visits, and technical app issues. Some physiotherapists reported low confidence delivering follow-up phone visits and frustration with scheduling delays, though several planned to continue applying BAP skills in future practice. These factors collectively influenced physiotherapists’ ability to integrate OEP+ effectively into community practice. Table 1.

Summary of Facilitators and Barriers by Theoretical Domains Framework

Modifiable factors, including practical supports and program design, shape physiotherapists’ ability to deliver OEP+ effectively in community falls prevention. Findings can support development of theory-informed strategies to enhance uptake, engagement, and sustainability of community falls prevention.

[1.] Stanmore EK. Arthritis Care Res 2013;65:1251-8. [2.] Robertson MC. J Am Geriatr Soc 2002;50:905-11. [3.] Cane J. Implement Sci 2012;7:37.

We analyzed data from the Community-Based Research Centre’s Our Health 2022 Canada-wide survey. This cross-sectional, multilingual (English, French, Spanish) survey was conducted April-September 2022 and recruited 2S/LGBTQIA+ participants aged ≥15 years through social media, community agencies, and paid advertisements. Respondents self-completed an anonymous online questionnaire capturing sociodemographics, healthcare use, access gaps, and sources of support. Those who self-reported a formal diagnosis of ≥1 rheumatic condition(s) were included. Descriptive statistics summarized outcomes.

Among 4,037 respondents, 497 (12%) reported ≥1 rheumatic conditions. Reported diagnosed conditions included fibromyalgia (n=169), osteoarthritis (n=152), psoriasis or psoriatic arthritis (n=105), Raynaud’s syndrome (n=88), rheumatoid arthritis (n=55), gout (n=36), ankylosing spondylitis (n=32), lupus (n=11), and Sjögren’s syndrome (n=8). Median age was 40 years; 66% were assigned female at birth, 36% identified as trans, 27% as non-binary, and 2% as intersex. Indigenous participants comprised 9% of the sample, of whom 66% identified as Two-Spirit. Among those who reported needing specific health services to manage their chronic health condition(s), unmet need was most frequent for personal home support (68%), foot care (60%), gender-affirming surgery (48%), home nursing (44%), alternative therapies (40%), gender-affirming care (38%), and physical therapy (34%) (Table 1). Common barriers included wait times (75%), difficulty obtaining appointments (70%), referral challenges (46%), service unavailability (45%), cost (40%), transportation (32%), and lack of gender- or sexuality-affirming providers (15%). Nearly half (49%) stopped, reduced, or delayed filling medications because they could not afford them, and 39% reported experiencing discrimination in healthcare. Despite these challenges, participants described drawing strength and support from friends, family/chosen family, pets, partners, social media communities and, among Indigenous respondents, Elders or Knowledge Keepers. Participants also reported positive impacts of living with a chronic condition, including building community connections, finding pride in their identity/experience, and engaging in activism. Table 1.

Healthcare reported as needed and accessed during the COVID-19 pandemic.

Reported challenges reflect entrenched inequities in healthcare that disproportionately affect 2S/LGBTQIA+ communities. Addressing these inequities requires structural change, integrating affirming, inclusive, and community-informed approaches into clinical practice and service delivery. Centering health justice principles in models of care can help ensure 2S/LGBTQIA+ communities receive equitable and affirming rheumatology care.

[1.] Ward BW. Prev Chronic Dis 2015;12:E192. [2.] Pinnamaneni M. Prev Med Rep 2022;28:101881. [3.] Mathias K. Curr Opin Rheumatol 2023;35:117-27.

In the first half of 2025, a survey on patient perceptions about patient support programs was made available in the waiting room at 3 rheumatology centers in Edmonton, Alberta, and was also electronically shared with those using a patient portal at 1 center. A portion of the survey focused on how patients dispose of their syringe/autoinjector, and their interest in recycling their device if that option were available to them.

Of 580 respondents, 265 currently using an injecting device provided responses about their preferences on this topic. 172 dispose of their device in a sharp’s container, 66 return it to their pharmacy, and 27 dispose in their garbage at home. Men more often than women disposed of their devices in the garbage at home, with no differences noted based on age, income, or whether they lived in an urban or rural community. 332 responded with their preferences to recycle their device: 17% definitely would, 27% probably would, 21% might, 27% probably would not, and 8% definitely would not. Patients older than 65 were less likely to be in favor of recycling compared to those younger than 65. How individuals disposed of their devices was not statistically associated with their opinions on recycling.

The majority of rheumatology patients using an advanced therapy are disposing of their injecting device appropriately, although there appears to be room for improved education for some. As a majority of those surveyed would be interested in recycling their device as an alternative option, this may present a unique opportunity for the healthcare industry to invest in this service for patients, simultaneously lessening the environmental impact of these devices.

A Markov model was developed to simulate disease progression over 5 years with monthly cycles from the U.S. payer perspective. Costs included drug acquisition, hospitalizations, outpatient care, and emergency visits, updated to 2024 USD. Transition probabilities, Euro-QoL-5D utility values, and healthcare resource utilization were derived from a targeted literature review. Patients began in a pre-treatment state and transitioned monthly between 4 health states: complete response (assessed by SLE Responder Index-4; SRI-4), partial response, non-response (did not meet SRI-4 and experienced a flare or treatment-emergent adverse event), and death. Patients in the early group had higher disease activity (3-point higher SLEDAI-2K) and higher glucocorticoid use (10mg/day more prednisone) at baseline relative to the delayed group. Early belimumab was defined as initiation within 2 years of diagnosis and delayed initiation followed failure of standard immunosuppressants.

Early belimumab initiation provided an additional 0.09 QALYs at a cost savings of USD$8,639.48 per patient relative to delayed belimumab, yielding a favorable incremental cost-effectiveness ratio (ICER) of –USD$93,092.98/QALY, making it the dominant strategy. Sensitivity analyses identified utility values, flare rates, and SRI-4 response rates as key drivers (Figure 1). Early belimumab retained dominance across most parameter variations, though cost-effectiveness was attenuated in parameter extremes favoring delayed initiation.

Early initiation of belimumab in biologic-naïve adults with clinically active SLE is both clinically and economically advantageous, offering greater health benefits at a lower cost compared to delayed initiation. These findings support timely adoption of belimumab in appropriate patients and highlight the need to reform reimbursement policies that delay access. As mounting evidence across immune-mediated diseases supports early biologic intervention as disease-modifying, frameworks must evolve to recognize treatment timing as a critical driver of long-term outcomes.[3] This model highlights the potential of early belimumab to reduce morbidity, mitigate irreversible organ damage, and generate sustained value for patients and health systems.

[1.] Urowitz M. Arthritis Care Res (Hoboken) 2022;74:1822-8. [2.] Zhao Y. Rheumatology (Oxford) 2025;64:106-16. [3.] Mease P. ACR Open Rheumatol 2025;7:e70019.

We conducted a modified Delphi study with Canadian rheumatologists and interdisciplinary health professionals (IHPs) with experience working in interdisciplinary rheumatology care teams. We developed an initial list of implementation strategies from a case study evaluation,[1] aligned with the Expert Recommendations for Implementing Change taxonomy.[2] In Round 1, participants rated 33 implementation strategies for their usefulness in optimally implementing interdisciplinary team-based rheumatology care (from 1 [not at all useful] to 9 [extremely useful]), nominated additional strategies, and provided feedback on wording. Consensus was achieved for "useful" strategies when ≥70% of participants in both groups rated the implementation strategy as 7-9 after Round 1. Round 2 (ongoing) involves re-rating statements not achieving consensus (after reviewing group medians and quartiles) and rating strategies added. Analyses were completed overall and stratified by rheumatologists and IHPs.

Fifty-five rheumatology health professionals (26 rheumatologists, 29 IHPs) participated in Round 1. Rheumatologists were from Ontario (65%), the Prairies (19%), British Columbia (8%), Quebec (4%), and the Atlantic (4%); most practiced for 10-19 years (39%) in a fee-for-service model (55%). IHPs consisted of physiotherapists, occupational therapists, nurses, pharmacists, physician assistants, and chiropractors from Ontario (76%), the Prairies (14%), the Atlantic (7%), and British Columbia (4%); most practiced for ≥20 years (59%) and were salaried (90%). After Round 1, consensus was achieved for 25 implementation strategies (76%) (Table 1), with 5 additional strategies proposed by participants for subsequent rating. The highest rated implementation strategies reaching consensus were in the categories: support clinicians (constructing IHP roles, shared communication mechanisms, identifying champions), clinic space (shared electronic medical record), external needs (funding for implementation and sustainment), and training (by rheumatologists, mentorship). Table 1.

Preliminary list of implementation strategies for optimal team-based models of rheumatology care from an initial around of consensus of Canadian rheumatology health professionals*

Twenty-five implementation strategies reached consensus after Round 1. Canadian rheumatology health professionals agreed that support and training for clinicians, shared team communication mechanisms, and access to sustainable funding were the most useful implementation strategies for optimal team-based rheumatology care. Results of this study will be used in a future co-design study with patients, clinicians, researchers, and organization/policy representatives to operationalize core and adaptable implementation strategies, including feasibility and contextual considerations, to develop an overall implementation approach.

[1.] King L. J Rheum 2025;52 Suppl 2:101. [2.] Powell B. Implement Sci 2015;10:1-14.

RRAC was established at St. Michael’s Hospital (SMH) in September 2022 to provide care for patients with semi-urgent conditions referred from the SMH Emergency Department, family practice units and subspecialty clinics. Referral criteria included patients with inflammatory arthritis (acute mono/polyarthritis, crystalline arthropathies), systemic autoimmune rheumatic diseases, vasculitis, polymyalgia rheumatica, and acute non-inflammatory conditions. Long-term rheumatology care was not provided in the RRAC. A retrospective chart review was conducted for all new patient referrals to the RRAC from September 2022 through October 2024. Extracted data included demographics, referral source, diagnosis, time from referral to consultation date provided, number of RRAC follow-up visits, and final patient disposition. Descriptive statistics summarized patient characteristics.

The RRAC database included 334 patient referrals, of which 305 (92%) were seen in consultation and 26 (8%) who did not attend. The mean age of patients seen was 57 years (range 20-98) with 56% being female (184). The most common referral sources were family health teams (31.1%), specialty clinics (22.8%), and the emergency department (20.1%). Median wait time from referral to consultation date was 10.2 days (mean 7.5), with 33 patients (11.1%) seen on the same day. Inflammatory conditions were diagnosed in 61% of referred patients, with detailed diagnostic outcomes summarized (Table 1). Follow-up in the RRAC was deemed necessary for 180 patients (59%), with a mean of 1.54 visits per patient. Final disposition included referral to long-term rheumatology care (43%), discharge to family health teams (27%), referral to specialty care (16%), and inpatient admission (0.99%).

Table 1

Implementation of the RRAC at SMH improved timely access for semi-urgent patients, with wait times to consultation date well below Canadian Rheumatology Association benchmarks.[3] The RRAC successfully prioritized patients with inflammatory conditions, ensuring early diagnosis and treatment initiation. By focusing on triage, assessment, and short-term follow-up, the clinic preserved long-term rheumatology capacity. These findings support RRACs as a scalable strategy to address access gaps in rheumatology care. Future studies should evaluate patient-reported outcomes and cost-effectiveness to inform integration of RRACs into broader healthcare frameworks.

[1.] Nene S. World J Gastroenterol 2020;26:759-69. [2.] Fox D. Rural Remote Health 2023;23:8098. [3.] Widdifield J. Healthc Policy 2021;16:119-34.

MEDLINE, EMBASE, CINAHL, Scopus, and Cochrane Library were searched from inception through February 29, 2024. Full text longitudinal studies were included if they: described a minimum of 2 patients with active LV-GCA on baseline PET, and the results of follow up PET scan done ≥ 3 months after escalating immunosuppression, along with an assessment of clinical disease activity. Two reviewers independently performed screening, full text review and data collection, and assessment of study quality using the Quality Assessment of Diagnostic Studies-2 (QUADAS-2).[1]

3131 unique references were screened, of which 25 studies were included (7 prospective, 18 retrospective), describing 377 patients with GCA. Mean patient age was 70.2 years (±5.4 yrs) and 72% were women. In 24 (96%) studies, patients received glucocorticoids, and in 10 studies (40%) tocilizumab was added. Patients underwent an average of 2.3 PET scans, at mean 9.2 ±5 months apart. An assessment of both clinical disease activity and follow up PET in comparison to baseline results (improved/not improved) was available for 158 LV-GCA patients. Overall, vascular FDG uptake improved on follow up PET in 122/149 (82%) patients who clinically improved with treatment. In the 62 patients who received TCZ, follow up PET improved in 100%. In the 9 patients without clinical improvement, none (0%) had radiographic improvement on repeat PET. In 283 patients with LV-GCA, baseline and follow up PET scans were reported as either still active or inactive. Ultimately, follow up PET became inactive in 119 of 254 patients (47%) who entered clinical remission on treatment. Among the 29 patients who remained clinically active, PET became inactive in 3 (10%). In the TCZ-treated patients, follow up PET became inactive in 76/112 patients (68%) in clinical remission, and remained radiographically active in 6/6 (100%) who remained clinically active.

Vascular FDG uptake on follow up PET improved in most (>80%) patients with LV- GCA patients who clinically improved on treatment but ultimately became radiographically- inactive in fewer than half (47%.) Follow up scans improved (100%) and became inactive (68%) more often in TCZ-treated patients.

[1.] Whiting PF. Ann Intern Med 2011;155:529-36.

This was a population-based longitudinal study following an inception cohort of children/adolescents with JIA diagnosed between 2010 and 2018, and followed until January 2024. JIA patients were defined as those with at least 3 diagnosis codes for inflammatory arthritis (ICD 714, 720, 721) over 2 years, with at least 1 by a pediatric rheumatologist before their 16th birthday. Patients were followed from their first pediatric rheumatologist visit until the earliest of their first adult rheumatologist visit, 23rd birthday, death, out-migration or study end date. For each follow-up year, we classified patients as engaged in care (at least 1 pediatric rheumatologist visit), out of care (no visits that year), lost to follow-up (after 3-year gap), re-engaged in care (after gap year(s)), or transferred to adult rheumatology care, and assessed for longitudinal transitions between care states. For JIA patients transitioning to adult rheumatology care, we described the interval between their last pediatric rheumatologist visit prior to their first adult rheumatologist visit.

Among 2,919 patients with JIA, the median (IQR) age at diagnosis was 11 (6-14) years and 63% were female. By 5 years of follow-up, only 42% of patients were engaged in pediatric rheumatology care, with 31% lost to follow-up (Figure). Among 923 patients who successfully transitioned to adult rheumatologists, 601 (65%) where seen by adult rheumatology within 6 months of their last pediatric rheumatology visit (throughout the entire study period), and the mean (SD) interval between the last pediatric and first adult visit decreased from 584 (891) days at the start of the observation period to 150 (289) by end of the study period. Figure.

Sankey diagram representing JIA patient flow between states over 5-years.

This study found that nearly half of JIA patients do not remain continuously engaged in pediatric rheumatology care through to transition to adult rheumatology care. However, transition times from pediatric to adult rheumatology care improved over calendar time. Given the limitations of health administrative data with few diagnosis codes to identify all JIA subtypes (some of whom do not require transition), further research requires more detailed clinical data to identify which JIA patients are experiencing gaps in care and further strengthen retention and successful transitions to adult care.

Discussions and needs assessment were conducted prior to establishing the clinic to determine its aims, patient population, capacity, infrastructure, workforce planning, location, and feasibility. The clinic was modeled after the Young Adult with Rheumatic Diseases clinic at BC Children’s Hospital as a shared-care clinic with pediatric and adult providers. To evaluate the clinic’s impact, a registry was created to collect data on attendees’ engagement and health outcomes. The registry was developed in collaboration with pediatric and adult teams.

The Women’s College Hospital Young Adult Clinic opened in 2019, staffed by a pediatric and adult rheumatologist and an advanced-practice physiotherapy practitioner. From 2019-2025, the clinic has followed 225 patients. The JIA Young Adult Clinic Helping Transition (JIA YACHT) registry was created and modeled after the Canadian Arthritis Network Disease Impact and Outcomes (CANDIO) registry at The Hospital for Sick Children. Recruitment began in May 2025, and since inception, 65 participants have been enrolled. Of these, 52/65 (80%) were female, 63/65 (97%) were on medications, with a median swollen joint count of 0 (range: 0-14), median physician global assessment score of 3 (range: 1-8), median patient global assessment score of 2 (range: 1-8), and median pain score of 3 (range: 1-9). The median time from referral to first clinic visit for registry participants was 134 days. The registry has proven to be an effective tool for monitoring important health outcomes post transfer such as uveitis status.

The creation of a dedicated transition clinic and registry has provided a strategic approach to transferring young adults with JIA from pediatric to adult care. This first-in-Canada transition registry enables standardized, systematic monitoring and evaluation of post-transfer care processes, identification of practice gaps, and tracking of patient outcomes. These insights will inform best practices and support ongoing improvements in transitional care.

Participants aged 12-18 years with a JSpA diagnosis and their caregivers were recruited in person through the JSpA Clinic at The Hospital for Sick Children using purposive sampling prioritizing those screening positive for anxiety and/or depression. Nine semi-structured interviews were completed with youth living with JSpA (n=4) and their caregivers (n=6). Youth participants included 3 males and 1 female, with a mean age of 17 years. Caregiver participants included 2 fathers and 4 mothers, with 1 interview completed jointly by both parents. Interviews were virtually conducted by a social worker experienced in qualitative mental health research, audio-recorded, transcribed verbatim, de-identified, and imported into Dedoose Software for qualitative analysis. Data was analyzed using Braun and Clarke’s thematic analysis.

Preliminary analysis identified 5 interconnected themes illustrating the mental health impact in youth with JSpA. (1) Families were the primary source of emotional and practical support, as youth commonly relied on parents for reassurance, encouragement and help coping with symptoms. (2) Youth demonstrated resilience by maintaining a positive outlook, focusing on tasks they could still participate in and showing determination to continue meaningful activities despite pain, fatigue, or fear of treatment procedures. (3) They described varied coping strategies to manage emotional and physical challenges, including engaging in sports and hobbies when able, resting during pain flares or low-energy periods, and seeking comfort through enjoyable activities and family. (4) Symptom burden significantly disrupted school, social life, and recreation, particularly before effective disease management. Although improved control of arthritis enhanced daily functioning for many youths, ongoing pain and fatigue continued to limit participation and require adaptations, demonstrating that challenges persist even with inactive disease. (5) Symptoms and aspects of medical care often trigger distressing emotions, including frustration when symptoms persisted, worry about future flares, and stress or fear associated with procedures such as MRIs and injections.

Youth with JSpA experience disruptions to daily life and emotional distress, particularly early in their disease course, and some continue to face challenges despite disease management and inactive disease. Although many show resilience and benefit from strong family support and adaptive coping strategies, these findings underscore the need for integrated mental health resources within pediatric rheumatology to better support youth wellbeing and reduce stress on families.

In the first half of 2025, a survey on patient perceptions about PSPs was made available in the waiting room at 3 rheumatology centers in Edmonton, Alberta, while also electronically shared with those using ATs with access to a patient portal at 1 center. The survey asked patients about their experiences with PSPs, perceived value, and understanding of the programs.

580 individuals started the survey, with 63% completing it in its entirety. Respondents reported using 36 ATs (17 biosimilars); 43% were on their first AT and 23% had used 3+, with 66% having been on treatment for 4+ years. Only 43.1% knew they were enrolled in a PSP, while 27.4% were not sure. More than 45% of these respondents did not know the name of their PSP, 57% did not know the name of their PSP contact, and 60% did not know where their PSP was located. One-third of patients did not recall the last time they were contacted by their PSP, while another third indicated it was annually or less. At least 36% indicated they had experienced challenges with their PSP. 36.2% of respondents were not told or unsure if their rheumatologist told them they would be enrolled in a PSP, and 49% did not know PSPs were funded by pharmaceutical companies. Those with less education and rural living were more likely to be unaware of this funding model, while those with higher incomes were more likely to be aware. Over 50% were unsure or did not think it was right that PSPs are funded by pharmaceutical companies. Despite this, 73.3% of patients were generally satisfied with PSP support, with just under 80% felt there was at least some value to PSPs, and 63.3% felt it likely improved their overall treatment experience.

While it appears, most patients have some appreciation of PSPs, improved communication from healthcare providers and PSPs is likely necessary for patients to better understand basic information about their PSP, including how PSPs are funded. Further data about patients perceived program values and challenges would likely help to further improve the structure of these programs.

In the first half of 2025, a survey on patient perceptions about PSPs was made available in the waiting room at 3 rheumatology centers in Edmonton, Alberta; the survey was also electronically shared with all patients using b/tsDMARDs signed up to a patient portal at 1 site. A portion of the survey focused on, in addition to collecting demographic data, where patients fill their b/tsDMARD, and how important it was to them to fill the prescription at their home pharmacy. Data were analyzed descriptively.

Of 580 respondents, 244 provided responses about which pharmacy dispenses their advanced therapy. While 51% are able to access their b/tsDMARD at their home pharmacy, 23% use a pharmacy as instructed by their PSP, and 15% receive it delivered to their home. 56% of all patients preferred to fill prescriptions at their home pharmacy, 35% indicated it did not matter, while 9% were not sure. Of those who fill at their own pharmacy, 84% preferred this option, 10% indicated it did not matter, while 6% were not sure. Of those who did not fill at their home pharmacy, 32% would prefer to use their home pharmacy. There was no difference in patient preferences based on age, gender, income, education, type(s) of insurance, or if they lived in an urban vs rural community.

Individuals on advanced therapies generally prefer to fill their prescriptions at their home pharmacy. In order to best accommodate patient preferences, as well optimize overall patient outcomes and safety, patient support programs should be encouraged to transparently work with their clients to ensure their medications are filled in a manner that is most preferred by them.

H-CARE was developed using the OSCARPro EMR and launched on January 27, 2025. It is staffed by 2 part-time administrative coordinators, an Advanced Clinician Practitioner in Arthritis Care (ACPAC), and staff rheumatologists who review referrals on a rotating weekly basis. Standard operating procedures were established to standardize referral intake, urgency categorization, and assignment to appropriate physicians. H-CARE operates under a CT Quality Improvement Subcommittee comprising senior rheumatologist investigators, a rheumatology fellow primary investigator, methodologists, and CT administrators. A cross-sectional descriptive analysis was conducted for the first 6 months. Metrics analyzed included the number of referrals per week, distribution by differential diagnosis, urgency category, proportion of redirected or rejected referrals, and time required for triaging.

In the first 6 months, a total of 1,095 referrals were processed, with 229 direct referrals to specific providers (Table 1). The most common referral diagnoses were inflammatory arthritis (IA) (226, 21%), rheumatoid arthritis (RA) (129, 12%), osteoporosis (OP) (88, 8%), vasculitis (67, 6%), and polymyalgia rheumatica (58, 5%). IA, RA, and OP accounted for over 40% of all referrals. Wait-time distribution showed 72% of referrals were triaged and booked to be seen within 3 months, with 4.7% booked within 1 week, 6.9% within 2 weeks, and 23.5% within 1 month. With H-CARE, 100% of referrals sent to individual rheumatologist’s office were booked within the time frame recommended on triage. Additionally, 100% of referrals were acknowledged within the 14-day period mandated by the College of Physicians and Surgeons of Ontario (CPSO. A total of 60 (5.5%) referrals were rejected and 144 (13.2%) were redirected to another service such as neurology, physiatry, or pain specialists. Table 1.

Distribution of Rheumatology Referrals by Triage Diagnosis and Wait-Time Category

H-CARE has been a successful pilot, generating valuable data to inform rheumatology service demand. All referrals were assigned to rheumatologists with availability and booking within triage-designated time frames. By centralizing referral intake, H-CARE provides a scalable foundation for innovations such as integrating ACPACs and future consideration of artificial intelligence (AI)-assisted triaging within rheumatology across the region.

[1.] Widdifield J. CMAJ Open 2016;4:E205-12.

We conducted a mixed methods feasibility study in 2 outpatient settings. Following 3 months of usual care, clinicians completed an online questionnaire to capture baseline QI adherence.[2] With help from "clinical champions," we introduced the QUICK toolkit and 6 weeks later the EQUIP toolkit. After a 3-month transition phase, the clinics entered a maintenance phase with continued access to toolkit resources (video, checklist, infographic, QUICK guides). We collected QI adherence data continuously over 9 months (chart audits and patient questionnaires) and pre-post study (clinician questionnaires). We performed descriptive analyses for participant demographics and QI adherence. For effectiveness data (HOOS/KOOS-4 subscales), we explored relationships between QI adherence, outcomes and experience using SAS (V9.4, Cary, NC).

We consented 46 THR/TKR patients: mean age 71.7 (7.2) years, mostly female (63%), retired (76%), living with ≥1 family member (79%) and ≥1 comorbidity (50%). All agreed to have their charts audited using a standardized REDCap form and 31 complete questionnaires. Fifteen physiotherapists and 1 rehabilitation assistant gave consent and 14 completed pre/post QI questionnaires. Clinicians were 50% female, and 63% were ≥40 years and had >10 years THR/TKR treatment experience. Mean (SD) baseline QI adherence was THR 12% (8.4%) and TKR 8.1% (11.1%) (chart audit) and 55.0% (12.9%) and 42.9% (27.3%) (patient questionnaire) (Figure 1). During the maintenance phase, mean QI adherence was not significantly different for THR and TKR by either data source. Mean clinician-reported pre/post QI data was THR 17.3% (12.8%) and 28.2% (24.8%) (p=0.06) and TKR 18.0% (13.2%) and 26.7% (25.7%) (p=0.09). In univariate analyses, there were no notable differences in HOOS/KOOS subscale values between baseline and maintenances phases. Overall, 73% of patients rated their rehabilitation experience as excellent and 47% were very satisfied with their outcomes. Patient reported QI adherence was strongly associated with overall satisfaction (p=0.004) and positively associated with overall experience (p=0.10). Figure 1

Comparing QI adherence for THR and TKR by data source and study phase

Overall, adherence to 10 THR/TKR rehabilitation QIs was low, regardless of data source, with minimal improvement after introduction of QI toolkits and resources. Positive associations between QI adherence and patient experience and satisfaction are promising. Implementation issues need to be addressed before conducting a definitive implementation trial.

[1.] Westby MD. Osteoarthritis Cartilage 2018;26:370-82. [2.] Westby MD. Physiother Can 2025;77:28-41.

We conducted a 9-month mixed methods, pragmatic feasibility study at 2 outpatient settings. Following 3 months of providing usual rehabilitation care, we led site-specific focus groups with clinicians to identify barriers and facilitators to QI implementation. With help of clinical champions, we then provided a 45-minute training webinar, introduced the clinician toolkit (QUICK-TJR) and 6 weeks later, the patient toolkit (EQUIP-TJR). This transition phase was followed by a 3-month maintenance phase with ongoing toolkit access. Clinical champions identified potentially eligible patients at time of discharge and provided contact information to a research coordinator. After confirming eligibility, we asked consenting patients to complete a REDCap online questionnaire and audited their chart using a standardized form. We collected QI adherence data continuously (chart audits, patient questionnaires) and prepost study (clinician questionnaire). We analyzed feasibility data descriptively.

Sixteen clinicians (100%) at a private clinic and hospital outpatient department consented; 14(88%) participated in baseline focus groups/interviews; 100% completed the initial clinician QI questionnaire and 15(94%) participated in or viewed the webinar. Post-webinar, 93% said they intended to access the toolkit within the next week and 100% agreed the resources would positively impact their care of THR/TKR patients. Initially, 14 accessed the online toolkit; this decreased to 7/14(50%) in the maintenance phase. Clinician retention was good with 88% completing the final questionnaire and 100% end of study discussions. In total, 46 patients following primary THR (n=10) or TKR (n=36) participated; well below anticipated levels during the Mar.-Nov. 2024 study period. There were 66 patients deemed eligible by clinicians; we screened 59(89%) and 7(11%) did not respond to calls; 49(83%) were confirmed eligible and 46(94%) provided consent. All had their chart audited and 31(67%) completed the QI questionnaire. Of the 22 patients who had access to the EQUIP toolkit in the later phases, 5(23%) accessed it and 4(80%) agreed it helped them engage in their own care.

Study feasibility was confirmed with the high rates of recruitment, consent and retention by both clinicians and patients. Despite good initial clinician engagement, there was limited uptake of QI resources among clinicians and patients overall. This will be addressed prior to the planned trial.

[1.] Westby MD. Osteoarthritis Cartilage 2018;26:370-82.

Physiotherapists working in the Greater Vancouver Area were randomly assigned to receive OEP training either alone (OEP group) or with Brief Action Planning (BAP) training and use of an exercise tracking app (OEP+ group; NCT04851405). BAP is a structured coaching approach involving goal setting, action planning, and monitoring/feedback. Following training, physiotherapists were matched with older adults with a recent history of falls recruited through the Vancouver Falls Prevention Clinic. They delivered the program through 5 home visits over 6 months, followed by monthly phone calls for 6 months. Older adults were instructed to perform lower-body exercises (>3x/week) and short walks (2x/week). OEP adherence (primary outcome) was self-reported by monthly calendar over 12 months. Secondary outcomes included prospective fall count, Short Physical Performance Battery (SPPB), daily step count, and EuroQol-5D-5L assessed at baseline, 6 months, and 12 months. Exercise and walking adherence were calculated separately as: (sessions completed/sessions expected) x 100. Analyses followed an intention-to-treat approach using Generalized Linear Mixed-effect Models for longitudinal outcomes adjusting for age and sex. Fall counts were analyzed using quasi-Poisson regressions with robust sandwich standard errors to address potential overdispersion. Missing data was handled using multiple imputations.

Thirty-five physiotherapists visited 128 older adults (OEP+: n=58, 81.0% female; OEP: n=70, 68.6% female). Both groups were similar in age [OEP+: 80.9 years (SD 6.1); OEP: 82.0 years (SD 6.8)]. 61.7% reported arthritis and 37.5% participated during the COVID-19 pandemic. The adjusted mean difference in exercise adherence was 11.4% (95% CI 0.4, 22.4), favoring OEP+ (Table 1). Multiple imputation analyses showed a similar magnitude of difference in exercise adherence; 8.0% (95% CI 1.6%, 14.3%). Walking adherence was similar between groups. The adjusted mean difference from baseline to 12 months for SPPB was 0.83 (95% CI 0.14, 1.52). Fall rates were lower in OEP+ (incident rate ratio: 0.63; 95% CI 0.48-0.82). Table 1:

Older Adult Participant Outcomes

Delivery of the OEP by physiotherapists trained in BAP and supported by an exercise tracking app improved exercise adherence, physical performance, and fall counts over 12 months in older adults at risk of falls. This research may inform the delivery of fall prevention interventions among older adults with arthritis.

A 2-page decision aid was designed to compare treatment efficacy data for patient switching therapies after TNF-IR. Relative treatment effects for ACR50 response for second-line biologic and targeted synthetic DMARDs were derived from an NMA of clinical trials.[1] These effects were converted into real-world outcome probabilities using data from a Canadian observational study of outcomes after TNF-IR.[2] We explored various data presentation formats to understand preferences among patients and rheumatologists, testing variation in how treatment benefits were scaled, grouped, and displayed.[3] Feedback was collected through semi-structured interviews with patients and a survey of the Canadian Rheumatology Association Guidelines panels.

Six semi-structured interviews with patients living with RA provided multiple diverse perspectives on treatment decision-making. Thematic analysis highlighted a strong need for more comprehensive and accessible information than what patients typically receive from health care providers. Patients explained the emotional and cognitive challenges of switching treatment and expressed that more comprehensive information could reduce uncertainty. They value resources that improve understanding and confidence in choosing treatments. They also valued time to review treatment options before appointments, allowing them to prepare questions and engage more confidently with their rheumatologist. A key theme was information gaps; this caused an increase in patients’ reliance on clinicians. Many patients explained how limited knowledge and confidence led them to defer to their rheumatologist’s judgment when making decisions. Patients responded positively to the prototype decision aid, appreciating its clarity, relevance, and inclusion of Canadian scaled data. Percentages were preferred over point estimates, and responders valued content reflecting real-world clinical experiences. Physician survey responses (n=7) reinforced the value of decision aids in clinical care and overall aligned with patient feedback (Table 1). (Table 1).

Physician survey responses from Guidelines panels evaluating decision aid for second-line RA treatments (n=7).

Implementing a patient-centered decision aid that provides accessible, localized information can enhance understanding, confidence, and engagement in treatment planning for patients with RA. Improving how data are presented supports informed treatment choices and strengthens shared decision making in RA care and beyond. By bridging the gap between complex evidence and patient experience, this approach supports evidence-informed and value-based care. This could be used to implement similar tools across chronic disease contexts and strengthen shared decision making overall.

[1.] MAGIC Evidence Ecosystem Foundation. https://www.magicevidence.org/match-it [2.] Bessette L. J Rheumatol 2024;51:145-54. [3.] Nota I. Arthritis Care Res (Hoboken) 2022;74:875-8.

Forty-two vasculitis patients consented to participate, 21 completed screening using the Patient Health Questionnaire-2 and -9 (PHQ-2, PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), Multidimensional Fatigue Inventory (MFI), Pittsburgh Sleep Quality Index (PSQI), Herth Hope Index (HHI), AAV-PRO, SF-36 and Alcohol Use Disorders Identification Test-Consumption (AUD-C). Disease severity was measured using the Birmingham Vasculitis Activity Score (BVAS) and Vasculitis Damage Index (VDI). Three voluntary sessions with a clinical psychologist were offered. Patient-reported outcomes were assessed at baseline and post-psychologist sessions.

Thirteen patients (62%) attended psychology sessions. Five attended 3 sessions, 1 attended 2, and 7 attended 1. Post-sessions, the AAV-PRO indicated improvements in systemic symptoms (mean 38.0 to 26.9), treatment side effects (33.1 to 22.3), social/emotional impact (28.2 to 21.1), and future concerns (30.7 to 22.7). SF-36 scores improved in energy/fatigue (38% to 50%) and sleep quality (PSQI 7.8 to 6.6). PHQ-9 and GAD-7 scores showed minor improvements (PHQ-9: 5.8 to 5.5; GAD-7: 4.15 to 4.38). AUD-C scores decreased from 3.0 to 2.38. Overall, 54% reported improved well-being, 70% perceived mental health benefits and satisfaction with care (mean 9.15/10).

Integrating mental health screening and referral is feasible and may improve patient-outcomes. Future research should refine and validate a comprehensive screening tool with interpretation guidance and establish clear referral guidelines.

[1.] Robson JC. Patient Relat Outcome Meas 2018;9:17-34.

Adults (≥18 years) with low back pain >3 months duration, onset age <45 years were referred by their primary care provider, specialist (eg, ophthalmologist, gastroenterologist) or provincial low back pain program (https://lowbackrac.ca) for axSpA screening. Screeners performed standard of care assessment (ie, history, physical exam, imaging and laboratory investigations). Screened patients were reviewed by the attending rheumatologist with expertise in spondyloarthritis. Screeners indicated risk of axSpA on a 11-point scale (–5, high confidence not axSpA to +5, high confidence axSpA). Risk assignment was dichotomized to negative or positive risk of axSpA. The rheumatologist provided final diagnosis for all patients. Prevalence of axSpA was calculated as the number of axSpA diagnoses/total number of patients screened. Sensitivity and specificity were calculated for the screener’s assignment of risk against the rheumatologist’s diagnosis (gold standard). Number needed to screen was calculated as 1/ (prevalence of axSpA in the screening model * sensitivity of the screener).

In total, 269 patients completed the screening process: mean (SD) age of 39.6 (10.5) years; 38% were male; mean (SD) duration of back pain was 11.5 (11.1) years. Referral sources varied by site. 36 patients were diagnosed with axSpA, for a prevalence of 13.4%. Overall sensitivity and specificity of the screener’s assignment of axSpA risk were 91.7% (95% CI 87.4% to 95.9%) and 75.0% (95% CI 68.3% to 81.7%), respectively, with 100% sensitivity at Thunder Bay and Toronto sites. NNS was 9 people with chronic back pain to identify 1 patient with axSpA and ranged from 5 to 19, depending on site (see Table 1). Table 1:

Number needed to screen across all, and by, FASTRAX site.

The FASTRAX model for axSpA screening demonstrates the NNS for 1 patient diagnosed with axSpA is 9, ranging from 5 to 19 depending on screening site in Ontario. This is far fewer NNS based on current population prevalence estimates and demonstrates a valid and efficient pathway to identify patients with axSpA.

[1.] Reveille JD. Arthritis Care Res (Hoboken) 2012;64:905-10.

We present the case of a 15-year-old Haitian girl with no significant past medical history who presented with a 6-month history of progressive fatigue, arthralgias and myalgias. Clinical examination was notable for polyarthritis, painful subcutaneous nodules on the upper and lower extremities, hemorrhagic bullous lesions on the toes and absence of muscle weakness. Investigations revealed bicytopenia (Hb 68 g/L; lymphocytes 0.8x10^9/L), elevated inflammatory markers (C protein reactive 45 mg/L and serum erythrocyte sedimentation rate 60 mm/h), low levels of complement C3 (0.39 g/L) and C4 (0.06 g/L), elevated serum immunoglobulin G (23.57 g/L), normal muscular enzyme levels (CK 68 U/L), proteinuria (urine protein/creatinine ratio 0.39 g/mmol) and mild microscopic hematuria. Autoantibodies tests were significantly positive for anti-nuclear (1/640 homogenous pattern), anti-double-stranded DNA (139.9 UI/mL, normal < 100 UI/mL) but negative for anti-extractable nuclear antigen. While awaiting specific autoantibody results, 18F-FDG PET/CT was performed to better understand the underlying process and help in the differential diagnoses. The study demonstrated increased FDG uptake/avidity in (a) fascias of bilateral upper and lower extremities (Figure 1), a feature that, to our knowledge, has not previously been reported in SLE; (b) the muscles predominantly in the upper limbs; (c) the basal ganglia; (d) both kidneys and (e) multiple lymph nodes. Renal biopsy revealed a diffuse segmental lupus nephritis (class IV-S). The patient was started on immunomodulatory therapy (intravenous steroids pulses, intravenous belimumab, mycophenolate mofetil and hydroxychloroquine), resulting in progressive symptoms resolution including relief from upper and lower limb pain, which were not only related to myositis but also to inflammatory fasciitis. Figure 1:

¹⁸F-FDG PET/CT demonstrated increased FDG uptake/avidity in fascias of bilateral upper and lower extremities

This is the first SLE patient reported with extensive fascia uptake on 18F-FDG PET/CT. In patients with SLE, typical 18F-FDG PET/CT findings include cerebral metabolism modifications and increased metabolic activity in lymph nodes, the spleen and bone marrow.[1] This unique case highlights the importance of recognizing SLE in patients presenting with inflammatory fasciitis or when extensive fascia uptake is seen on 18F-FDG PET/CT.

[1.] Curiel R. Ann N Y Acad Sci 2011;1228:71-80.

A 9-year-old girl was referred to our Tertiary Center for painless unilateral swollen upper eyelids, progressing for 5 months. Personal history was negative. Imagery confirmed a well-defined heterogeneous mass of the upper orbit. Initial workup showed elevated inflammatory markers, normal IgG4, absence of antinuclear and slightly positive p-ANCA antibodies (MPO). Histopathological examination of the orbital biopsy revealed IgG4-positive plasma cell infiltration, confirming the diagnosis of IgG4-RD. Remission was rapidly achieved with oral steroids (initially 1 mg/kg/day) with a 5 month-tapering. Few months later, the patient presented with subcutaneous asymptomatic lesions on her left thigh, initially diagnosed as post-traumatic hematoma. Persistence and the emergence of a second lesion on the thorax raise the suspicion of infiltrative tumor. On 18F-FDG PET/CT, 2 other lesions on the right thigh and the right buttock were revealed. Skin biopsy confirmed IgG4-RD relapse. Complementary workup showed serological positivity of IgG4 (3.15 g/L). Rituximab was started with initial remission during the first year. Relapses occurred with recurrent skin infiltration following each viral episode, even with a second cure of rituximab. Given the lack of response to rituximab, treatment was switched to MMF (2000 mg/m²/day) with a complete remission (and negative PET/CT).

This case highlights the importance of considering atypical forms of IgG4-RD, especially in pediatric populations, which can lead to misdiagnosis. As far as we know, this case is the fifth one describing cutaneous involvement in pediatric patients. The treatment remains challenging. Corticosteroids and B cell-targeted therapies are the cornerstones of treatment.[1] Rituximab has been considered a first-line therapy in IgG4-RD, particularly for patients with severe or refractory disease. However, for some patients, alternative therapies are sometimes needed.[2] MMF is an alternative effective steroid sparing agent with more positive evidence for the latter.[3]

[1.] Stone J. Rheumatology 2025;64:i24-i27. [2.] Sapountzi E. Children 2025;12:213. [3.] Karim F. Pediatric Rheumatology 2016;14:18.

100 SSc patients and 100 HV were studied from the Cardiovascular Imaging Registry of Calgary. All patients underwent CMR imaging inclusive of cine and late gadolinium enhancement (LGE). Conventional analyses were performed using cvi42 software. A comparison of conventional CMR markers between SSc patients and HV were utilized to identify SSc patients with a cardiomyopathy, defined as an abnormal left ventricular ejection fraction [LVEF] < 55% or LGE presence. SSc cardiomyopathic individuals were processed using 4Deep and age- and sex-matched compared against HV to characterize SSc cardiomyopathy phenotype. 4Deep is a locally developed deep learning-based 4D modeling pipeline which automatically segments cines to deliver spatially registered bi-layer 4D LV meshes, providing regional 3D wall thickness, mass, and principal strain. Patients were followed for a composite outcome of death, heart failure admission, or sustained ventricular tachycardia.

Clinical and CMR characteristics of the SSc (median age 57 years old, 67% female) and HV patients (median age of 46 years old, 54% female) are summarized (Table 1). Conventional CMR analysis revealed 30% of SSc patients with a cardiomyopathy (21% abnormal LVEF, 18% abnormal LGE) and 20% with an abnormal right ventricular (RV) EF. 4Deep analysis of 24 age- and sex-matched SSc patients with LV cardiomyopathy to HV revealed SSc patients experienced significant reductions of 14.7% LVEF, 18.8% mean max. principal strain, and increases of 1.3 mm in LV wall thickness and 3.1% mean min. principal strain in comparison to HV. SSc patients with a cardiomyopathy experienced significantly reduced minimum principal strain deformation in septal and apical segments of the heart. Over a median follow-up of 4.1 years, 32% of SSc patients developed a composite primary outcome. In the full cohort, a multivariable model including age, sex, LVEF, LGE fibrosis burden, and RVEF showed RVEF as the only independent predictor (HR 0.95 [0.91-0.99], p=0.006). Table 1.

Systemic Sclerosis Patient Cohort Characteristics

In this large cohort of SSc patients referred for CMR, one-third demonstrated LV cardiomyopathy with 38% showing LV or RV abnormality. LV disease localized to the septal and apical segments. Larger studies are needed to determine the incremental prognostic value of these features beyond RVEF.

A 57-year-old man with rheumatoid arthritis was in remission on methotrexate and a TNFi when he was diagnosed with metastatic renal cell carcinoma (RCC) and both immunosuppressives were discontinued. After failing 3 lines of therapy, he was initiated on ICI (nivolumab). Following 3 cycles of ICI he experienced a P-IA flare, which failed to respond to intraarticular glucocorticoids and methotrexate. Given the significant impact on his quality of life (QOL), a TNFi was re-initiated, his P-IA went into remission and no further irAEs developed. After a total of 78 cycles (6.5 years) of nivolumab, and palliative radiation to the bone, the patient had progression of his RCC, and the decision was made to discontinue ICI.

This case outlines a man with metastatic RCC and P-IA who received concurrent treatment with an ICI and TNFi for over 6-years with control of his and P-IA and no other irAEs. Current guidelines for management of P-IA prior to ICI initiation recommend reducing immunosuppression to the lowest required amount or stopping it completely.[2] The optimal management of P-IA flares during ICI is less clear. Despite attempts to minimize immunosuppression, some patients will require treatment with a bDMARD to facilitate ongoing ICI and maximize QOL. A recent phase 1 clinical trial suggested that concomitant use of a TNFi and ICI may increase ICI efficacy while also preventing irAEs.[3] We hypothesize that use of the TNFi in our patients may have ameliorated the risk of developing other irAEs. Further research is needed into the safety of long-term bDMARDs use in patients receiving ICI.

[1.] Lopez-Olivo M. Eur J Cancer 2024;207:114148. [2.] Ye C. J Rheumatol 2025;52:1207-17. [3.] Montfort A. Clin Can Res 2021;27:1037-47.

PsABIOnd (NCT05049798) is a global observational study in PsA patients starting GUS or IL17i as 1st-to-4th line of biologic therapy per standard of care.[1] Here, the full population of the PsABIOnd study was analyzed over the first 6 months of follow-up. Work productivity and activity impairment were assessed via the Work Productivity and Activity Impairment Questionnaire (WPAI; 0-100).[2] Patient-reported disease impact was assessed using the PsA Impact of Disease-12 (PsAID12; 0-10),[3] including the mean total score and proportions of pts achieving minimal clinically important improvement (MCII); improvement by ≥1.4; among pts with BL PsAID-12 score ≥1.4). All analyses were performed according to initial treatment group allocation, and treatment comparison was based on 95% confidence intervals (CI).

1134 patients were analyzed; 555 and 579 received GUS or IL-17i, respectively, as their initial treatment. Mean age (53.2/53.5 yrs), sex (60.4%/59.2% female), and prior exposure to a targeted drug (63.4%/62.3%) were comparable for GUS/IL-17i. Mean overall baseline work productivity loss (42.3%/44.5% for GUS/IL17i groups), absenteeism (14.3%/12.9%), presenteeism (39.2%/42.1%), activity impairment (48.5%/50.6%), and mean baseline PsAID-12 total score (5.1/5.1) were also similar between groups. At the 6-month visit, comparable improvements were observed in all WPAI outcomes with GUS and IL-17i. Mean (95% CI) improvements in GUS/IL-17i were: overall work productivity loss (–13.1 [–16.5, –9.7]/–13.8 [–17.5, –10.1]%), absenteeism (–6.4 [–10.4, –2.4]/–2.5 [–5.1, 0.2]%), presenteeism (–12.5 [–15.7, –9.3]/–14.0 [–17.5, –10.5]%), activity impairment (–13.1 [–15.4, –10.8]/–15.7 [–18.2, –13.1]%); (Figure 1). Mean PsAID-12 total scores also improved significantly (–1.6 [–1.7, –1.4]/–1.8 [–2.0, –1.6]) reaching levels (3.5/3.3) indicative of symptom impact below the patient acceptable symptom state threshold (≤ 4.0) in both groups. Rates of pts achieving PsAID-12 MCII at 6 months were also comparable (54.7%/55.9%).

By 6 months of treatment in real-world, improvements in work productivity and ability to perform daily activities were observed with both GUS and IL-17i, paralleled with clinically meaningful improvements in patient-reported multidomain disease impact. Based on overlapping CIs, improvements in PROs were comparable between the 2 classes. These results may be useful for reimbursement decisions and healthcare provider/patient shared treatment decision-making.

[1.] Siebert S. Rheumatol Ther 2023;10:489. [2.] Teilly MC. Parmacoeconomics. 1993;4:353. [3.] Gossec L. Ann Rheum Dis 2014;73:1012.

PsABIOnd (NCT05049798) is a global observational study in patients with PsA starting GUS or IL17i as 1st-to-4th line of biologic therapy per their standard of care.[2] The full population of the PsABIOnd study over 6 months of follow up was analyzed. Analyses were performed according to initial treatment group allocation in the overall population and in specific subgroups defined by baseline (BL) age, sex, BMI categories, and prior biologic use. Persistence on treatment (ie, no stop/switch) over 6 months was assessed via the Kaplan-Meier estimator function. Propensity score (PS) analysis was used to evaluate hazard ratio (HR) of GUS vs IL-17i stop/switch prior to the 6-month visit, adjusting for BL variable imbalances across cohorts. Effectiveness was descriptively assessed using rates and means at BL and 6 months of the following measures: swollen and tender joint counts, clinical Disease Activity Index for PsA -based low disease activity /remission, the Leeds Enthesitis Index, psoriasis body surface area, Dermatology Life Quality Index and number of nails affected by psoriatic disease. Dactylitis was not assessed due to the low prevalence of dactylitis at BL.

Of the 1134 pts analyzed, 555 and 579 pts received GUS or IL-17i, respectively, as their initial treatment. At BL, the GUS/IL-17i cohorts were generally well balanced across subgroups of interest: 83.4%/81.3% were <65 years of age; 60.4%/59.2% were female; 48.0%/43.4% had BMI≥30 kg/m2; and 63.4%/62.3% had previously received ≥1 targeted therapy. Persistence on treatment was high in both cohorts, with 526/555 (94.8%) GUS and 539/579 (93.1%) IL-17i pts remaining on their initial treatment at the 6-month visit (PS-adjusted HR of GUS vs IL-17i stop/switch [95% confidence interval]: 0.93 [0.75-1.16]); (Figure 1). Across patient subgroups of interest, similar improvements in joint symptoms enthesitis skin involvement, and psoriatic nail disease were observed with GUS and IL-17i at the 6-month visit.

Treatment with GUS or IL-17i resulted in comparable treatment persistence and effectiveness, regardless of age, sex, BMI, or treatment history, through 6 months. These results support the real-world effectiveness of GUS and IL-17i across PsA subpopulations.

[1.] Haddad A. Semin Arthritis Rheum 2025;152737. [2.] Siebert S. Rheumatol Ther 2023;10:489.

APEX enrolled adults with active PsA (≥3 tender, ≥3 swollen joints; CRP ≥0.3 mg/dL) and ≥2 erosive joints on radiographs of hands/feet, despite previous non-biologic therapy. The modified full analysis set comprised 1020 randomized pts (273 GUS 100mg Q4W; 371 GUS 100mg at W0/W4 then Q8W; 376 PBO-to-GUS Q4W at W24). Key endpoints through W48 included ACR20/ACR50 rates and least squares mean (LSM) change in PsA-modified van der Heijde-Sharp (vdH-S) score per reading session 2 (W0/24/48 radiographs). Exposure-adjusted incidence rates of adverse events (AEs) per 100 pt-years (100PY) [95% CI] are reported through W48.

GUS Q4W/Q8W ACR20 rates increased from W24 (67%/68% vs 47% PBO; both p<0.001) to W48 (71%/74%). GUS ACR50 rates increased from W24 (41%/42% vs 20% PBO; both nominal-p<0.001) to W48 (51%/56%). At W48, 71% and 48% of PBO-to-GUS Q4W pts achieved ACR20 and ACR50, respectively. Reading session 2 results indicated continued suppression of radiographic progression with GUS Q4W/Q8W from W0-24 (LSM changes in PsA-modified vdH-S score: 0.36/0.46) throughout W24-48 (0.24/0.32). Radiographic progression in the PBO group from W0-24 (0.96) was curtailed by GUS W24-48 (0.41). Through W24, AE incidence rates with GUS Q4W/Q8W (168[146-191]/163[145-183]) and PBO (174[155-195]) were similar. Incidence rates did not increase with continued GUS (W0-48: 147 [132-163]/148 [136-162]), or after PBO-to-GUS transition (W24-48: 156 [138-176]).

In biologic-naïve adults with active and erosive PsA, inhibition of radiographic progression and joint disease activity improvements with GUS were durable through W48 without increased AE incidence, further substantiating GUS benefit for preserving joint health.

We conducted a retrospective analysis using data from the Newfoundland and Labrador Centre for Health Information (NLCHI) spanning 2009 to 2019. Patients diagnosed with PsD were identified using the ICD-9 code 696 and matched with 75,500 controls without PsD. From this cohort of approximately 100,000 patients, individuals with IBD were identified using ICD-9 codes 555 for Crohn’s disease (CD) and 556 for ulcerative colitis (UC). The study recorded the sequence of IMID occurrences, mortality rates, and total hospitalization costs.

The analysis identified 15,100 patients with PsD and 2,800 with IBD. Among these, 14,368 had only PsD, 2,068 had only IBD, and 732 had both conditions, indicating that 4.8% of PsD patients also had IBD, including 525 with CD and 207 with UC. Notably, 65% of patients with both PsD and IBD were diagnosed with IBD first (Figure 1). This trend was consistent for both CD and UC, where 65% of patients developed CD or UC prior to PsD. For those diagnosed with PsD first, CD appeared an average of 7.58 years later, while PsD developed 9.76 years later when CD was diagnosed first (p = 0.004). In the case of UC, it followed PsD by 6.88 years, whereas PsD followed UC by 7.41 years (p = 0.13). The average age at death for patients diagnosed with CD before PsD was 67.6 years, compared to 70.7 years for those diagnosed with PsD first (p = 0.06). For patients diagnosed with UC before PsD, the average age at death was 66.5 years, compared to 78.3 years for those diagnosed with PsD first (p = 0.0001). No significant differences in total hospitalization costs were observed among the groups.

The sequence of diagnosis in patients with multiple IMIDs significantly influences the timing of the onset of the second disease and may have implications for mortality. These findings highlight the necessity for effective management strategies for patients with concurrent IMIDs and underscore the potential impact of the order of diagnosis on patient outcomes.

We searched the Canadian Research Group of Rheumatology in Immuno-Oncology (CanRIO) retrospective and prospective cohorts for cases of de novo ICI-LVV. Cases of pre-existing LVV were excluded. Demographic, clinical and laboratory data were extracted from the study databases.

We identified 13 patients who developed LVV after ICI exposure, most commonly for melanoma (n=5) and non-small cell lung cancer (n=3). Most patients received single agent ICI (69%). The median time from ICI exposure to symptom onset was 4.0 months (IQR 1.5-15). Isolated large vessel (n=5) or isolated cranial involvement (n=5) were the most common presentations. In those with cranial involvement (n=8), headache (n=8), jaw claudication (n=6) and scalp tenderness (n=6) were the most common symptoms. In those with confirmed large vessel involvement, (n=8), the most common radiographic finding was hypermetabolism on PET scan (n=6), often found incidentally without associated symptoms. There was 1 case of stenosis, and no aneurysms identified on imaging. Six patients had temporal artery biopsy and 2 were consistent with LVV, without clear histopathologic differences from idiopathic giant cell arteritis. Eleven patients were treated with glucocorticoids: Two relapsed during taper, 1 required additional immunosuppression (methotrexate and tocilizumab). Two patients with normal inflammatory markers and isolated large vessel involvement (hypermetabolism on PET) had remission without treatment. Only 2 patients continued ICI after ICI-LVV diagnosis, both without vasculitis recurrence/progression. There was no vision loss or death attributable to ICI-LVV.

Isolated cranial or large vessel involvement were the most common presentations of ICI-LVV. Like idiopathic GCA, headache was the most common clinical manifestation in those with cranial involvement. In contrast, isolated large vessel involvement was commonly found on PET, incidentally and without clinical symptoms. Careful clinical correlation is required in cases of isolated large vessel involvement, as not all may require treatment. This has important implications given the potential impact of immunosuppression on ICI and tumor outcomes. Further studies are needed into the clinical presentation, underlying pathological mechanisms and optimal management of ICI-LVV.

[1.] Cottu A. Rheumatology (Oxford) 2025;64:4546-54.

We reviewed the charts of 3 pediatric patients referred for suspected JIA and later diagnosed with Lyme arthritis. We describe the demographics, exposure history, symptoms and physical examination findings, investigations, treatment, and outcomes. Case 1: An 11-year-old boy from rural Norfolk County, Ontario, developed chronic right-knee arthritis with a large Baker’s cyst and significantly limited range of motion. He reported a suspected tick bite 1 year earlier. He was initially thought to have oligoarticular JIA with MRI confirming active synovitis and a larger Baker’s cyst. However, Lyme serology was positive. After 8 weeks of doxycycline and naproxen, he achieved complete clinical resolution of arthritis and Baker’s cyst that has been sustained for the past 4 years. Case 2: A 13-year-old boy from Mount Pleasant, Ontario with subacute left-knee swelling accompanied by fever and highly elevated CRP of 163 was admitted due to suspected septic arthritis. Synovial fluid was markedly neutrophilic but culture-negative, and he later developed contralateral knee and right wrist effusions, prompting consideration of JIA. A detailed history revealed a febrile illness with erythema-migrans-like rash the prior summer. Lyme serology was positive and Lyme PCR in synovial fluid later returned positive. He completed 1 week of IV ceftriaxone, 8 weeks of doxycycline, and a subsequent 4-week course of IV ceftriaxone for persistent mild arthritis with full recovery. There has been no recurrence at 1 year of follow-up. Case 3: A 13-year-old girl from Oakville, Ontario, developed right-knee arthritis and left TMJ pain with visible swelling, tenderness, and limited range of motion. She had been camping extensively in Nova Scotia, PEI, and Maine 8 months earlier. While she was initially suspected to have oligoarticular JIA because of TMJ involvement, Lyme disease was suspected due to the mismatch between arthritis affecting only 2 joints and elevated inflammatory markers (CRP 68, ESR 45). Her Lyme serology was positive. After 8 weeks of doxycycline and naproxen, she was asymptomatic with no recurrence over the past 5 years.

These cases highlight the importance of maintaining a high index of suspicion for Lyme arthritis in children and adolescents with inflammatory joint disease, including presentations that suggest JIA. Recognizing the variable presentations of Lyme arthritis and incorporating appropriate testing can ensure timely, targeted therapy and prevent unnecessary immunosuppression.

[1.] Murison K. PLoS One 2023;18):e0295909. [2.] Huynh N. Curr Opin Rheumatol 2022;34:335-43.

Our research team included patient partners and a wide range of HCPs and researchers with expertise in JIA and shared decision making. We conducted individual virtual consultations with research team members to present recent evidence on approaches to managing JIA-related pain, fatigue, and mental health symptoms. Approaches were identified through a scoping review. For each approach, we presented evidence from clinical practice guidelines (CPGs), systematic reviews and clinical trials, along with assessments of their methodological quality. Team members were asked whether each approach should be added to the JIA Option Map, and to rate the level of recommendation based on evidence and expert recommendations (ie, usually, sometimes or not recommended).

Thirteen team members participated in the consultations (5 patient partners and 8 HCPs), during which we presented evidence on 7 approaches. Most team members agreed that the approaches should be added to the JIA Option Map, with most rated as "sometimes" or "usually" recommended. These included massage for youth and parent anxiety and youth stress, and self-management programs for parent stress and child self-esteem. Three members did not agree to add the following approaches until more information on safety and accessibility was gathered: laser therapy for fatigue and pain, Watsu (Water-Shiatsu) for pain, and video game-based task-oriented activity for pain. Both HCPs and patient partners indicated that they based their decisions primarily on CPG recommendations, personal experience, and evidence on effectiveness, safety and accessibility.

Overall, most HCPs and patient partners supported adding the proposed approaches to the JIA Option Map based on available evidence. They considered similar factors when making decisions and found accessibility of some approaches to be a limiting factor. Next steps will include gathering additional information on certain approaches to reach consensus on their inclusion and recommendation levels. These findings provide insight into the decision-making process for integrating symptom management approaches into a complex patient decision aid. Supported by a CIORA grant

We searched MEDLINE, Embase, PsycINFO, CINAHL, and CENTRAL from inception to September 2024. We included randomized controlled trials (RCTs), systematic reviews (SRs) and clinical practice guidelines (CPGs) evaluating approaches to manage mental health symptoms compared to any control group in children and youth 0-21 years with JIA. Two reviewers independently screened studies, extracted data, and assessed risk of bias using Cochrane RoB 2.0 (RCTs), AMSTAR 2 (SRs with meta-analyses) and AGREE II (CPGs). Certainty of evidence was appraised using GRADE. Findings were summarized descriptively, and standardized mean differences or risk ratios were calculated where applicable. Reporting followed PRISMA guidelines.

We included 11 RCTs, 1 SR and 2 CPGs. The RCTs evaluated educational and self-management programs, cognitive behavioral therapy, exercises, massage and relaxation. One SR on eHealth and mHealth interventions reported on the RCTs already included without conducting a meta-analysis. One CPG recommended Pilates, and another recommended early psychological care. Overall, RCTs were rated as having moderate to high risk of bias, resulting in low to moderate certainty of evidence. Most studies did not show statistically significant effects on mental health outcomes, except for 4 RCTs that showed positive results. One showed, with moderate certainty, that Pilates improved psychosocial health-related quality of life compared with conventional exercises. Another showed, with moderate certainty, that healthy sleep improved youth mood compared with restricted sleep. Another showed, with low certainty, that a web-based self-management program for parents reduced parent stress and improved child self-esteem compared with usual care. The last showed, with low certainty, that parent-delivered massage reduced youth and parent anxiety and youth stress compared with relaxation. No adverse events were reported in these trials.

Few studies have evaluated approaches to managing mental health symptoms in JIA. Pilates, healthy sleep, parent web-based self-management programs and massage may be beneficial, but the certainty of evidence is limited, and adverse events were often not reported. These findings may assist patients’ and providers’ decision making and will inform updates to the JIA Option Map. Supported by a CIORA grant

We conducted a comprehensive search of 5 major databases (MEDLINE, Embase, PsycINFO, CINAHL, and CENTRAL) from inception to September 2024. We included randomized controlled trials (RCTs), SRs and clinical practice guidelines (CPGs) evaluating approaches to manage fatigue compared to any control group in children and youth 0-21 years with JIA. Two reviewers independently screened studies, extracted data, and assessed risk of bias using Cochrane RoB 2.0 (for RCTs), AMSTAR 2 (for SRs with a meta-analysis) and AGREE II (for CPGs). Certainty of evidence was appraised using GRADE. Evidence was summarized descriptively, and standardized mean differences and risk ratios were calculated where applicable. Reporting follows PRISMA guidelines.

We included 4 RCTs and 2 SRs. The RCTs assessed laser therapy, exercises and self-management strategies. The SRs summarized existing evidence on physical activity and self-management approaches but did not conduct meta-analyses. No CPGs were included in this SR as they did not report recommendations specific to fatigue. Overall, RCTs were rated as having moderate to high risk of bias, resulting in low to moderate certainty of evidence. RCTs did not demonstrate statistically significant effects, except for 1 RCT, which showed with moderate certainty that adding low-level laser therapy to an exercise program reduced fatigue compared with exercise alone. No adverse events were reported.

We included 4 RCTs and 2 SRs. The RCTs assessed laser therapy, exercises and self-management strategies. The SRs summarized existing evidence on physical activity and self-management approaches but did not conduct meta-analyses. No CPGs were included in this SR as they did not report recommendations specific to fatigue. Overall, RCTs were rated as having moderate to high risk of bias, resulting in low to moderate certainty of evidence. RCTs did not demonstrate statistically significant effects, except for 1 RCT, which showed with moderate certainty that adding low-level laser therapy to an exercise program reduced fatigue compared with exercise alone. No adverse events were reported. This SR highlights the limited number of studies assessing interventions to manage fatigue in JIA. A low-level laser added to an exercise program RCT may improve fatigue; however, the certainty of the evidence was suboptimal, and adverse events were not reported. These findings will inform updates to the JIA Option Map to help support families’ and clinicians’ decision-making and will orient future research priorities. Supported by a CIORA grant.

Patients 14-17 years with JIA or jSLE were recruited from the multidisciplinary McMaster Rheumatology Transition Clinic and asked to complete the 14-item Transition-Q (max 100) at each visit to assess transition readiness. After each patient completed the Transition-Q, a member of the healthcare team would discuss their responses with them and set goals for the next appointment. Descriptive statistics summarized patient demographics. Generalized estimating equations examined the predictive value of sex, number of visits, age at enrollment and age at diagnosis on changes in transition readiness while accounting for time.

Analyses included 384 observations from 94 participants. Number of clinic visits per participant ranged from 1 to 8, with varying time between visits. Age at diagnosis was not a significant predictor of changes in Transition-Q score (p=0.551). More visits (β=8.02, p=<0.001), female sex (β=6.87, p=0.031), and older age at enrollment (β=3.94, p<0.001) were significant positive predictors of improvements in Transition-Q score (Figure.). There was no significant interaction between sex and number of visits (p=0.17) indicating that the association between visit number and Transition-Q score did not differ meaningfully between males and females.

Our study demonstrated improvements in transition readiness with females, older age and longer follow-up predicting larger improvements. This suggests that males and those who are younger may require additional supports to optimize transition readiness prior to the transfer to adult care. It also suggests that these males and those who had fewer visits in pediatric care prior to the transfer may require more supports upon arrival in adult care.

Since March 2020, a nurse trained in hypnosis has offered this technique to children undergoing IAS injections. To evaluate its impact, children provided feedback using visual analog scales (VAS) and personal reflections.[3] Procedure difficulty score was rated from 0 (no difficulty) to 10 (maximum difficulty), and perceived benefit score from 0 (no benefit) to 10 (maximum benefit). During the same period, children receiving IAS injections with other supportive strategies completed the same scales and shared reflections. Feedback was collected post-procedure by the same nurse who supported each child using their chosen method.

Data was collected on 80 procedures in 62 children: 55 procedures with hypnosis, 25 using other strategies (phone distraction (7), music (4), conversation (4), midazolam (2), breathing techniques (4) or no specific intervention (4)). Groups were comparable for age, gender and joint injected (Table 1). All children successfully completed the procedure. Children in the hypnosis group reported lower procedure difficulty and higher perceived benefit compared to those with other methods. Overall, children voiced that hypnosis helped them focus on their chosen experience and not on the procedure, while children using other methods expressed more physical sensations. Clinicians observed a calming effect with hypnosis contributing to better procedural tolerance. Table 1:

Characteristics of the cohort

Children consistently report hypnosis as helpful. Hypnosis provides a compassionate way to accompany children in a challenging moment. It helps them stay engaged, feel capable, and actively participate in their own care.

[1.] Geagea D. Pain Med 2022;24:661-702. [2.] Tran L. Front Pediatr 2021;9:719626. [3.] Gift A. Nurs Res 1989;38:286-7.

A 16-year-old male, diagnosed with sJIA at age 13, initially presented with quotidian fever, evanescent rash, hepatosplenomegaly and polyarthritis, with no MAS... Initial treatment included prednisone, naproxen and tocilizumab. Due to persistent rash and arthritis, his therapy was changed to anakinra 100mg daily. One year later, he developed pharyngitis and fevers, progressing over 2 weeks into fulminant MAS with unremitting fevers, and supportive labs (Figure 1). His hepatic enzymes remained normal throughout. He stabilized with pulsed methylprednisolone and increasing anakinra to 200mg (3mg/kg). One month later, he developed significant liver injury, with transaminitis and mildly elevated unconjugated bilirubin. Workup revealed no concurrent infection, fever/sJIA flare, or other etiology. His presentation was most consistent with drug-induced liver injury, and anakinra was discontinued. Canakinumab started at 300 mg every 4 weeks. This allowed for prednisone tapering to 10mg over 3 months. However, a progressive transaminitis recurred, spiking 2-3 weeks following each canakinumab administration. During treatment, the patient had no symptoms of sJIA with normal CRP and cell counts. After 3 doses of canakinumab, he developed jaundice, elevated INR and elevated conjugated bilirubin with a peak ALT of 3000 U/L. Liver biopsy demonstrated features of drug-induced liver injury and hemophagocytosis, suggesting a possible mixed presentation with underlying sJIA disease activity and residual MAS. However, he remained afebrile with no signs of sJIA disease activity. Canakinumab was discontinued and 1 month later he started tofacitinib for breakthrough arthritis while on 10mg of prednisone. Two months later, he remains asymptomatic from sJIA and his liver injury has been resolved. His CRP is only mildly elevated on tofacitinib monotherapy.

This case represents the first detailed description of reversible severe liver injury associated with canakinumab in sJIA complicated with MAS. On tofacitinib, the patient was able to effectively recover from the liver injury and taper off corticosteroid.

[1.] Baldo F. Rheumatology 2025;64:32-44. [2.] Martins FR. Pediatr Rheumatol 2023;21:112. [3.] Ruperto N. Ann Rheum Dis 2018;77:1710-9.

A nonrandomized, prospective, interrupted time series quality improvement project guided by the Model for Improvement framework was initiated in April 2025 and is ongoing. Encounters within scope were in-person visits with established Rheumatology patients aged 2-17 years who had an indication for ROM exercise prescription.

To date, 25 ROM exercise video links have been shared with patients/patient families. Initial PDSA cycles focused on several technical challenges, such as creating a unique URL link of source videos to patients. Subsequent focus has been on promoting access at home and securing feedback from patients/families. Preliminary survey response was 20%; however, informal feedback from >90% of those who did access the videos at home illustrated high satisfaction and self-efficacy (Figure 1). Prescribers found the process easy, though logistical barriers such as password protected access during busy clinics reduced satisfaction.

Preliminary results suggest success in leveraging this novel online platform to prescribe ROM exercise videos to patients with Rheumatological diagnoses in a secure and user-friendly manner. Future directions will center on dissemination of platform access to sites across Canada and entail a large-scale study that closely tracks any technical issues and incentivizes patient/family feedback. We anticipate that successfully and appropriately spreading access to this platform will address the unmet needs of PRCPs, especially those without access to allied health.

[1.] Philpott J. J Paediatr Child Health 2010;15:213-8. [2.] Ramdani S. [Abstract. Poster 91.] J Rheumatol 2019;46:802-3. [3.] Stinson J. Arthritis Care Res 2008;59:65-72.

This 2-phase initiative was conducted at McMaster Children’s Hospital Rheumatology clinic, serving >800 youth with JIA annually. Eligible patients were 12-18 years old attending in-person clinics. We employed driver diagrams, fishbone analysis, and workflow mapping to identify barriers and refine processes. In Phase 1, clinicians administered the Patient Health Questionnaire (PHQ-4) verbally upon arrival, and documented results in the electronic health record (EHR) using standardized templates.[2] During Phase 2, a structured algorithm, co-created by a multidisciplinary team, was implemented to ensure follow-up was tailored to the patient’s score, with options including education and resource provision, referral to allied health professionals, connection to community support, or urgent safety assessment. Follow-up action was recorded in the EHR. Process, outcome, and balancing measures were tracked.

Between May 2024 and February 2025, screening rates increased from 0% to >75% and were sustained (Figure 1). Phase 2, implemented May to August 2025, saw >75% of positive screens have documented follow-up actions in the EHR, consistent with the care algorithm. Of 266 patients screened, 221 (83%) scored in the normal range (0-2), 33 (12%) mild (3-5), 7 (3%) moderate (6-8), and 5 (2%) severe (9-12) on the PHQ-4. Balancing measures indicated that screening was acceptable to both patients and clinicians, as assessed through in-house questionnaires. Across both phases, key enablers included iterative education and reminders to sustain engagement, workflow modifications to address time constraints, and integration of EHR tools and feedback charts to support adherence and provider buy-in. Weekly performance feedback, statistical process control charts, and targeted staff training further facilitated implementation and sustainment. Figure 1.

Control chart of proportion of eligible patients screened using PHQ-4

This QI initiative demonstrates that integrating routine PHQ-4 screening into pediatric rheumatology care is both feasible and sustainable, improving identification of at-risk youth and standardizing follow-up. Lessons learned provide a scalable model for other pediatric subspecialty clinics.

[1.] Fair DC. Open Access Rheumatol 2019;11:237-52. [2.] Kroenke K. Psychosomatics 2009;50:613-21.

We reviewed all provincial formularies and NIHB program to determine bDMAARD/sDMARD coverage for pediatric and adult inflammatory arthritis relative to HC indications and compared our data to previously published findings from 2012.[1] We surveyed and interviewed 1 academic pediatric rheumatologist from each province to determine ease of access to these drugs.

More HC indications exist for bDMARD/sDMARD in adults compared to children. In adults, 9x more drugs are listed for ankylosing spondylitis and 6x more for psoriatic arthritis compared to juvenile idiopathic arthritis (JIA) subtypes (Table 1). There are 2x more drugs with HC indications for rheumatoid arthritis than polyarticular JIA. Even when these drugs have a federally approved pediatric indication, NIHB, intended to promote equitable access for disadvantaged populations, only covers half of them (Table 1). NIHB demonstrated greater accessibility overall, with faster approval times and longer renewal periods compared to the provinces. The total number of distinct adult and pediatric bDMARD/sDMARD for inflammatory arthritis indications covered by NIHB and provincial public plans doubled since 2010. However, significant pediatric interprovincial variability is observed, with 7 bDMARDs in Ontario, and 67% of the remaining provinces funding 4 or less drugs (Table 1). The success observed in Ontario reflects strong advocacy efforts and physician-led submissions. All provincial formularies included anti-IL-6 treatment for systemic JIA whereas the Maritimes and Ontario notably also covered anti-IL-1 drugs. Pediatric rheumatologists reported differences in ease of accessing bDMARDs, with approval times under 1 week in Manitoba and Saskatchewan and 1-4 weeks in all provinces except Quebec, which averaged 3-6 months. Renewal intervals were 3 months in Alberta, 6 months then annually in all provinces except Ontario, which reported 1-3 years. Denials occurred in all provinces because of restrictive formularies and nonstandard indications. Table 1.

Health Canada–Approved Indications and NIHB/Provincial Publicly Funded bDMARDs/sDIMARDs/Other Drugs for Inflammatory Arthritis. NIHB – Non-Insured Health Benefits; AB – Alberta; BC – British Columbia; MB – Manitoba; NL – Newfoundland and Labrador; NS – Nova Scotia; ON – Ontario; PE – Prince Edward Island; QC – Quebec; SK – Saskatchewan. T-cell inhibitor: ABA – Abatacept, TNFa inhibitor: ADA – Adalimumab: ETA – Etanercept; INF – Infliximab: GOL – Golimumab: CER – Certolizumab Pegol. IL-6 inhibitor: TOC – Tocilizumab; SAR – Sarilumab, IL-1 inhibitor: ANA – Anakinra; CAN – Canakinumab, B-cell inhibitor: RIT – Rituximab, IL-17 inhibitor: SEC – Secukinumab; IXE – Ixekizumab, IL-12/23 inhibitor: UST – Ustekinumab; GUS – Guselkumab, JAK inhibitor: TOF – Tofacitinib; BAR – Baricitinib; UPA – Upadacitinib, PDE4 inhibitor: APR – Apremilast. * ≥2 years, ≥4 years, ≥6 years, § ≥40kg

While bDMARDs have significantly improved JIA outcomes,[2] access to these drugs remains limited compared with adults despite advances since 2010. Substantial interprovincial disparities and inequities were reported in the approval and renewal processes.

[1.] Leblanc CMA. J Rheumatol 2012;39:1875-79. [2.] Adrovic A. Arch Rheumatol 2020;36:146-57.

Four scientific literature databases were searched for qualitative studies published in peer-reviewed journals from 2014 to 2024 that explored social or stigma experiences of youth with JIA (aged <25 years). A total of 1471 articles were retrieved from the search. After removing duplicates, 697 unique titles and abstracts were screened for eligibility, leading to 32 articles for full text review. and 18 studies were included for data extraction. Two reviewers conducted a meta-synthesis following the 3-stage method outlined by Thomas and Harden.[2]

Six key themes emerged: (1) Physical Barriers to Social Interaction (absences, limited participation, and pushing beyond limits); (2) Lack of Understanding from Others (lack of factual information, invisible disease, ability to relate, and over/under-estimated); (3) Enacted Stigma (not believes of accused of lying or exaggerating, trivialization, social isolation, verbal harassment or bullying, and discrimination), (4) Anticipated Stigma (anticipation of a negative reaction, anticipation of discrimination, and concealment); (5) Internalized Stigma (wanting to be normal or feeling different, personal identity, perceived burden to others, and social-emotional impact); and (6) Social Strengths and Supports (self-disclosure, supportive others, supportive accommodation, peers with JIA, social media, and positive outlook).

The review findings suggest that increasing public awareness, fostering peer support, enhancing self-advocacy skills, and implementing stigma-reduction strategies better support the social functioning of youth with JIA. Future research should explore the long-term effects of stigma and evaluate targeted interventions to improve social experiences and quality of life for this population.

[1.] Min M. JBI Evidence Synthesis 2022;20:60-120. [2.] Thomas J. BMC Medical Research Methodology 2008;8:45-54.