Open Access4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State
Author(s) -
Wollmann BM,
Syversen SW,
Lie E,
Gjestad C,
Mehus LL,
Olsen IC,
Molden E
Publication year - 2017
Publication title -
clinical and translational science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 44
eISSN - 1752-8062
pISSN - 1752-8054
DOI - 10.1111/cts.12431
Subject(s) - rheumatoid arthritis , medicine , erythrocyte sedimentation rate , cyp3a4 , inflammation , arthritis , metabolite , etanercept , immunology , gastroenterology , pharmacology , cytochrome p450 , metabolism
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.