This supplement comprises the proceedings of the Second Update on Psoriatic Disease, a conference held at the University Federico II Congress Center, Via Partenope 36, Naples, Italy, July 6–7, 2011.
The ancient university city of Naples (University Federico II, one of the oldest in Europe, dates from the early 13th century) provided a stimulating and attractive conference backdrop.
This conference represented a followup of the first update (Procida Update of Psoriatic Disease) held at the Orphans’ Conservatory of Terra Murata on the island of Procida in the Gulf of Naples, May 22–24, 2008. Proceedings of that conference appeared as a supplement to the Journal of Rheumatology in August 2009 (Volume 36: Supplement 83). And that conference in turn followed a similar conference on psoriatic disease (PsD) held at the University Federico II Congress Center in Naples in 2006; proceedings were published the following year as a supplement to Reumatismo (Volume 59: Supplement 1).
These 3 conferences, with their common thread of PsD, have been pivotal in introducing, expanding, and consolidating the concept of psoriasis as central in a group of associated conditions, in addition to psoriatic arthritis (PsA) itself. Accordingly, PsD is now considered a wider expression of psoriasis and PsA than had been previously realized; albeit still strongly within the spondyloarthropathy (SpA) complex and as an essential member of the group. PsD is thus characterized by overlapping links with other members of the SpA complex, and their spondylitic, ocular, intestinal, and genitourinary features.
A central figure in promoting the PsD concept has been Professor Raffaele Scarpa, head of the Rheumatism Research Unit at the Policlinico, University of Naples. He and his team work across a wide range of rheumatology-orientated specialties. His staff is associated with an Early Psoriatic Arthritis Clinic, a much-needed and forward-looking clinical and research facility.
By way of comparison and contrast, the PsD concept is in some respects like the situation some years ago of rheumatoid arthritis (RA), which in many quarters attracted the label “rheumatoid disease.” This name arose when rheumatoid multisystem expressions, such as arteritis, nodules, anemia, and eye and lung disease, became evident. And the grouping of rheumatoid disease with systemic lupus erythematosus, systemic sclerosis, dermatomyositis, polyarteritis nodosa, and related conditions, as “connective tissue disease,” “collagen disease,” or “collagenosis” draws parallels with the grouping of PsD with other members of the SpA complex. However, this is not to suggest that similarities between RA and PsA extend beyond this, as for some years there has been strong international agreement that PsA and RA are substantially different disorders, across a wide spectrum of tested criteria and with different genotypes.
This latest conference (only 5 years after the first on the PsD theme) and the papers on which it was based take the notion of PsA as part of PsD a significant stage further. This has been made possible by the remarkable and rapidly developing advances in new technologies. Not least among these are the exciting developments in the fields of molecular genetics, immunobiology, and imaging in its many new forms (magnetic resonance imaging, ultrasound, and computed tomography).
The benefits to the patient of this recent research “renaissance” have been highly significant in terms of diagnosis, treatment, and therapeutic assessment. And for the first time, patients with severe, previously intractable, skin and/or rheumatic manifestations can be offered therapy with higher hopes of better control, induction of disease remission, and cessation of tissue damage. And with therapeutic improvements achieving newer heights year by year, a cure now seems more immediately on the horizon. Therefore the term disease-modifying antirheumatic drug (DMARD) has taken on a new meaning since the development of biological therapies (“biologics”). Further, as an extension of this new therapeutic molecular science, it can be imagined that prevention as well as cure could be possible in the not-too-distant future.
The general format of the conference was as follows: After a memorable opening ceremony, the scientific program was divided into 10 sessions. These covered basic science, clinical science (2 sessions), imaging, and therapy (5 sessions).
The meeting was concluded by presentation of a seminal paper entitled Future Trends in Research, and by an overview during closing remarks.
The conference, over 2 days, comprehensively examined recent developments in each of the main categories. And together with valuable and enthusiastic contributions from the audience during the several discussion periods, a fascinating global picture of PsD emerged. Also, much useful clinical and scientific cross-fertilization arose from the different specialties (rheumatology, dermatology, and several related disciplines) and from the different countries represented.
Specific topics among many others within the general themes included recent thoughts on the synovio-entheseal complex; details of the metabolic syndrome associated with psoriasis; the role of biomarkers in PsA; and new insights into the PsD concept.
With regard to the growing interest in the synovio-entheseal complex, and to previous work on the enthesis itself, this topic opens up several proposals concerning the nature of the psoriatic diathesis. Thus, in addition to its interesting and complex anatomical structure, only recently revealed, entheseal science could contribute in other ways. For example, it could explain certain superficial psoriatic clinical expressions (e.g., the relationship between nail disease and terminal phalangeal and distal interphalangeal pathology); it could be relevant to etiological triggering (through microtrauma, as part of a deep Koebner or isomorphic phenomenon); and it could be a component in pathogenesis (through vascular, cellular, and molecular changes, perhaps genetically determined).
Considering the new broader view of the enthesis, with its location at tendon, ligament, and joint capsule insertions, and now with its established links with adjacent synovia, a common factor to explain the polymorphism, asymmetry, and anatomical-site vulnerability of the peripheral and axial manifestations of PsA might be at hand. This would provide yet another significant difference between psoriatic and rheumatoid processes and profiles.
As a further but more tentative speculation for the future, the enthesis concept, with its association with microtrauma, could even be applicable to certain non-musculoskeletal manifestations of PsD in soft-tissue locations genetically primed to respond to overstretched physiological dynamics. For example, the mouth, bowel, genital tract, eye, heart, and great vessels could be targets in this respect. And at these sites, perhaps the physiological stresses (such as friction, turbulence, or stretching) are translated into microtrauma and operate through the Koebner phenomenon to cause tissue damage at these deeper levels.
Therapeutically, 2 main messages were clear about biological therapies, in addition to the usual cautions about any side effects or complications. First, that they exhibit superior efficacy compared with other DMARD; and second, that they have the advantage of controlling the axial arthritis of patients with psoriasis in addition to its peripheral rheumatic manifestations.
Presentations on specific biologics included the now-traditional drugs infliximab, etanercept, and adalimumab, and 2 new biological molecules — ustekinumab and golimumab. Lessons from the treatment of RA were also discussed, and included appraisals of tocilizumab and abatacept.
The conference, and the following articles arising from it, emphasized several important (and optimistic) points. These included increased understanding of PsD causation and pathogenesis; increased realization of the level of morbidity and even mortality associated with PsD; and that improved therapy, through biologics, for both psoriasis and PsA can be expected in the near future.
On a final note, the editorial team wishes to acknowledge the academic support provided by the Chancellor of the University Federico II, Naples, and by the Dean of the Faculty of Medicine. We also thank the bodies providing financial contributions toward the conference and this supplement. And of course we are also most grateful to all those who contributed to the conference program itself: chairpersons, speakers, delegates, and not least, the scientific and organizing secretariats.
Guest Editors’ Note
Dr. Dafna D. Gladman is a Professor of Medicine at the University of Toronto, and Senior Scientist at the Toronto Western Research Institute. She is Deputy Director of the Centre for Prognosis Studies in The Rheumatic Diseases, Director, Psoriatic Arthritis Program, University Health Network, and co-director of the University of Toronto Lupus Clinic at Toronto Western Hospital.
She received her MD degree from the University of Toronto and trained in internal medicine and rheumatology at the same university. She spent some time training in HLA typing with Professor Paul Terasaki in Los Angeles, California, USA and has directed the HLA research laboratory since 1979.
Dr. Gladman’s research has focused on both systemic lupus erythematosus (SLE) and psoriatic arthritis (PsA), with emphasis on database development, prognosis studies, genetic and other biomarkers for disease susceptibility and expression, assessment instruments, quality of life measures, and outcome measures. She has also been involved in clinical trials in these conditions, including design and execution of both company-initiated and investigator-initiated trials.
Dr. Gladman has produced 450 peer-reviewed publications, 177 chapters and invited publications, and 636 published abstracts. Her important contributions to PsA include the recognition that the disease was more severe than previously noted. Dr. Gladman and colleagues demonstrated that PsA progressed over time, and was associated with increased mortality. Moreover, her group identified predictors for disease progression and mortality. On the other hand, they also identified patients who achieved remission. They have also identified genetic and other biomarkers that identify patients with psoriasis destined to develop PsA. Her important contributions in SLE include description of disease features, recognition of disease subsets such as patients who have serologically active but clinically inactive disease, and those who have clinical activity in the face of serological inactivity, prognostic factors for mortality in SLE, atherosclerosis disease in SLE, pregnancy studies, the development of the SLE disease activity index and its modification, the development of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology damage index, and more recently the development of a new responder index for SLE, the SRI-50.
Dr. Gladman’s work has been supported by research grants from The Arthritis Society, the Canadian Institutes of Health Research, and the Krembil Foundation. She received the Distinguished Investigator Award, Canadian Rheumatology Association in 2002, and the Laurentian Conference of Rheumatology, First Jeffrey Shiroky Prize for Major Contributions to Research in Inflammatory Arthritis, in 1998.
Dr. Gladman is immediate past president of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, and is currently President of the Spondyloarthritis Research Consortium Canada.
As the Rheumatology Program Director from 1992–2003 she has trained over 50 residents, in addition to numerous postgraduate fellows.
Dr. Gladman was awarded the Second Verna Wright Prize in 2011 for her work in PsA (Figure 1).