文摘
Systemic inflammation has been linked to suppressed CYP3A(4) activity. We determined 4<em>βem>-hydroxycholesterol (4<em>βem>OHC), an endogenous CYP3A4 metabolite, in patients with rheumatoid arthritis (RA) before and after treatment with biological disease-modifying antirheumatic drugs (bDMARDs). The 4<em>βem>OHC was compared in 41 patients before and 2–5 months after initiating TNFα inhibitors (<em>nem> = 31), IL-6 inhibitors (<em>nem> = 5), or B-cell inhibitors (<em>nem> = 5). Correlations between 4<em>βem>OHC and inflammatory markers (C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)) were also tested before and after bDMARDs. 4<em>βem>OHC did not differ following bDMARD treatment (<em>Pem> = 0.6), nor in patients who started with IL-6 inhibitors (median 51.6 vs. 50.6 nmol/L). The 4<em>βem>OHC and CRP/ESR did not correlate before treatment (<em>Pem> > 0.5), but correlated significantly after bDMARDs (CRP = Spearman <em>rem> -0.40; <em>Pem> < 0.01; ESR = <em>rem> -0.34; <em>Pem> = 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.