Abstract
Objective. Rapidly predicting future outcomes based on short-term clinical response would be helpful to optimize rheumatoid arthritis (RA) management in early disease. Our aim was to derive and validate a clinical prediction rule to predict low disease activity (LDA) at 1 year among patients participating in the Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial escalating RA therapy by adding either etanercept or sulfasalazine + hydroxychloroquine [triple therapy (TT)] after 6 months of methotrexate (MTX) therapy.
Methods. Eligible subjects included in the derivation cohort (used for model building, n = 186) were participants with moderate or higher disease activity [Disease Activity Score 28-erythrocyte sedimentation rate (DAS-ESR) > 3.2] despite 24 weeks of MTX monotherapy who added either etanercept or sulfasalazine + hydroxychloroquine. Clinical characteristics measured within the next 12 weeks were used to predict LDA 1 year later using multivariable logistic regression. Validation was performed in the cohort of TEAR patients randomized to initially receive either MTX + etanercept or TT.
Results. The derivation cohort yielded 3 prediction models of varying complexity that included age, DAS28 at various timepoints, body mass index, and ESR (area under the receiver-operator characteristic curve up to 0.83). Accuracy of the prediction models ranged between 80% and 95% in both derivation and validation cohorts, depending on the complexity of the model and the cutpoints chosen for response and nonresponse. About 80% of patients could be predicted to be responders or nonresponders at Week 12.
Conclusion. Clinical data collected early after starting or escalating disease-modifying antirheumatic drug/biologic treatment could accurately predict LDA at 1 year in patients with early RA. For patients predicted to be nonresponders, treatment could be changed at 12 weeks to optimize outcomes.
Footnotes
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Support from Amgen. A US National Institutes of Health (NIH) planning grant from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) supported the initial phases of the TEAR study. Dr. Curtis receives support from the NIH (AR 053351) and the US Agency for Healthcare Research and Quality (R01 HS018517) and has received research grants and/or done consulting for Amgen, Abbott, BMS, Crescendo, CORRONA, Genentech, Janssen, Pfizer, and UCB. Dr. Ranganath also receives support from NIH (NIAMS K23 AR057818) and research grants and/or does consulting for BMS and UCB. Dr. Mikuls has received a research grant from Roche.
- Accepted for publication December 20, 2012.