%0 Journal Article %A KATHERINE J. DONNITHORNE %A RANDY Q. CRON %A TIMOTHY BEUKELMAN %T Attainment of Inactive Disease Status Following Initiation of TNF-α Inhibitor Therapy for Juvenile Idiopathic Arthritis: Enthesitis-related Arthritis Predicts Persistent Active Disease %D 2011 %R 10.3899/jrheum.110427 %J The Journal of Rheumatology %P 2675-2681 %V 38 %N 12 %X Objective. To analyze the attainment of inactive disease following initiation of tumor necrosis factor-α (TNF-α) inhibitors in a heterogeneous cohort of children with juvenile idiopathic arthritis (JIA). Methods. We performed retrospective chart review of all children with JIA at 1 academic center who had started TNF-α inhibitor therapy. We retrospectively determined inactive disease status according to the 2004 criteria of Wallace, et al. We evaluated inactive disease status at 1 year after initiation of TNF-α inhibitor and attainment of inactive disease at any point during the study period. Predictors of inactive disease were determined using univariate analyses and multivariable logistic regression models. Results. A total of 125 patients started TNF-α inhibitors, and 88 patients had data available for the 1-year followup visit. Many patients (49%) started TNF-α inhibitors within 6 months of the diagnosis of JIA. Diverse JIA phenotypes were represented: at baseline, 29% of all patients had active enthesitis and only 23% had active polyarthritis. At the 1-year followup, 36 of 88 (41%) patients had inactive disease. Overall, 67 of 125 (54%) patients ever attained inactive disease status during the study period. In multivariable models, enthesitis-related arthritis (ERA) and higher Childhood Health Assessment Questionnaire (CHAQ) scores at baseline were independently associated with failure to later attain inactive disease status. Conclusion. Treatment with TNF-α inhibitors appears to be less effective for attaining inactive disease status in patients with ERA or higher baseline CHAQ scores. Further studies are needed regarding the clinical effectiveness of TNF-α inhibitor therapy and the optimal treatment of ERA. %U https://www.jrheum.org/content/jrheum/38/12/2675.full.pdf