{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T17:20:35Z","timestamp":1781889635667,"version":"3.54.5"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,11,5]],"date-time":"2016-11-05T00:00:00Z","timestamp":1478304000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Translational Sci"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:p>Systemic inflammation has been linked to suppressed CYP3A(4) activity. We determined 4<jats:italic>\u03b2<\/jats:italic>\u2010hydroxycholesterol (4<jats:italic>\u03b2<\/jats:italic>OHC), an endogenous CYP3A4 metabolite, in patients with rheumatoid arthritis (RA) before and after treatment with biological disease\u2010modifying antirheumatic drugs (bDMARDs). The 4<jats:italic>\u03b2<\/jats:italic>OHC was compared in 41 patients before and 2\u20135 months after initiating TNF\u03b1 inhibitors (<jats:italic>n<\/jats:italic> = 31), IL\u20106 inhibitors (<jats:italic>n<\/jats:italic> = 5), or B\u2010cell inhibitors (<jats:italic>n<\/jats:italic> = 5). Correlations between 4<jats:italic>\u03b2<\/jats:italic>OHC and inflammatory markers (C\u2010reactive protein (CRP) and erythrocyte sedimentation rate (ESR)) were also tested before and after bDMARDs. 4<jats:italic>\u03b2<\/jats:italic>OHC did not differ following bDMARD treatment (<jats:italic>P<\/jats:italic> = 0.6), nor in patients who started with IL\u20106 inhibitors (median 51.6 vs. 50.6 nmol\/L). The 4<jats:italic>\u03b2<\/jats:italic>OHC and CRP\/ESR did not correlate before treatment (<jats:italic>P<\/jats:italic> &gt; 0.5), but correlated significantly after bDMARDs (CRP = Spearman <jats:italic>r<\/jats:italic> \u20100.40; <jats:italic>P<\/jats:italic> &lt; 0.01; ESR = <jats:italic>r<\/jats:italic> \u20100.34; <jats:italic>P<\/jats:italic> = 0.028) suggesting that mainly non\u2010CYP3A4\u2010suppressive cytokines were reduced during treatment. Thus, this study does not support a generally regained CYP3A4 phenotype in patients with RA following initiation of bDMARDs.<\/jats:p>","DOI":"10.1111\/cts.12431","type":"journal-article","created":{"date-parts":[[2016,11,6]],"date-time":"2016-11-06T04:12:34Z","timestamp":1478405554000},"page":"42-49","source":"Crossref","is-referenced-by-count":12,"title":["4<i>\u03b2<\/i>\u2010Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State"],"prefix":"10.1111","volume":"10","author":[{"given":"BM","family":"Wollmann","sequence":"first","affiliation":[{"name":"Center for Psychopharmacology Diakonhjemmet Hospital  Oslo Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"SW","family":"Syversen","sequence":"additional","affiliation":[{"name":"Department of Rheumatology Diakonhjemmet Hospital  Oslo 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