THU0196 TOFACITINIB IN PATIENTS WITH RHEUMATOID ARTHRITIS AND INDICATIVE OF DEPRESSION AND/OR ANXIETY: A POST HOC ANALYSIS OF PHASE 3 AND PHASE 3B/4 CLINICAL TRIALS

Abstract

Objectives: Depression and anxiety are common in patients with rheumatoid arthritis (RA). The 36‐Item Short Form Health Survey (SF‐36) Mental Component Summary (MCS)≤38 has been used to identify probable major depressive disorder and/or probable generalized anxiety disorder (pMDD/pGAD) in patients with RA.1 Tofacitinib is an oral JAK inhibitor for the treatment of RA. We assessed pMDD/pGAD prevalence by SF‐36 MCS≤38 status in tofacitinib clinical trials for RA, and efficacy by baseline pMDD/pGAD status. Methods: This post hoc analysis pooled data from five Phase 3 trials and one Phase 3b/4 trial, and included patients receiving tofacitinib 5 or 10mg twice daily (BID), adalimumab 40mg every other week (ADA), or placebo, with non‐missing baseline SF‐36 MCS. Demographics/baseline characteristics were reported by baseline pMDD/pGAD status (SF‐36MCS ≤38, presence; >38, absence). At Months (M)3/6/9/12, SF‐36 MCS change from baseline (Δ) was estimated bymodeling pooled data and percentage of patients with pMDD/pGAD reported. Efficacy endpoints (American College of Rheumatology [ACR]20/50/70 response rates; Disease Activity Score in 28 joints, erythrocyte sedimentation rate [DAS28‐4(ESR)]<2.6 rates; ΔHealth Assessment Questionnaire‐ Disability Index [HAQ DI]) were estimated atM3/6/12 by linear models, comparing tofacitinib‐treated patients by baseline pMDD/pGAD status. Results: Baseline pMDD/pGAD were reported in 44.5% (tofacitinib 5mg BID), 39.8% (tofacitinib 10mg BID), 45.4% (ADA), and 39.1% (placebo) of patients. At baseline, higher C‐reactive protein levels and worse disability, fatigue, pain, and sleep were reported in patients with vs without pMDD/pGAD. A numerically, and sometimes significantly, greater increase in SF‐36 MCS was reported with tofacitinib vs placebo/ADA (ADA throughM12). The proportion of patients with baseline pMDD/pGAD who continued to have pMDD/pGAD atM3/6/9/12was generally lower with tofacitinib vs placebo/ADAand had reduced from baseline by 61.9‐63.7% at M12. Efficacy at M3/6/12 was generally similar with tofacitinib 5 and 10mg BID, irrespective of baseline pMDD/pGAD status. Conclusions: Around 40% of patients with RA had baseline pMDD/pGAD identified by SF‐36 MCS≤38. Improvement in SF‐36 MCS was greater in patients receiving tofacitinib vs placebo/ADA. In tofacitinib‐treated patients, the proportion with pMDD/pGAD reduced by 60% at M12. Tofacitinib efficacy was similar in thosewith/without baseline pMDD/pGAD. Future research using a gold‐standard psychiatric interview is required to validate SF‐36 MCS≤38 in the identification of pMDD/pGAD.