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Systemic inflammation has been linked to suppressed CYP3A(4) activity. We determined 4 β ‐hydroxycholesterol (4 β OHC), an endogenous CYP3A4 metabolite, in patients with rheumatoid arthritis (RA) before and after treatment with biological disease‐modifying antirheumatic drugs (bDMARDs). The 4 β OHC was compared in 41 patients before and 2–5 months after initiating TNFα inhibitors ( n  = 31), IL‐6 inhibitors ( n  = 5), or B‐cell inhibitors ( n  = 5). Correlations between 4 β OHC and inflammatory markers (C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR)) were also tested before and after bDMARDs. 4 β OHC did not differ following bDMARD treatment ( P  = 0.6), nor in patients who started with IL‐6 inhibitors (median 51.6 vs. 50.6 nmol/L). The 4 β OHC and CRP/ESR did not correlate before treatment ( P  > 0.5), but correlated significantly after bDMARDs (CRP = Spearman  r  ‐0.40;  P  < 0.01; ESR =  r  ‐0.34;  P  = 0.028) suggesting that mainly non‐CYP3A4‐suppressive cytokines were reduced during treatment. Thus, this study does not support a generally regained CYP3A4 phenotype in patients with RA following initiation of bDMARDs.

4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State