4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State
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...
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| Veröffentlicht in: | Clinical and translational science 2017-01, Vol.10 (1), p.42-49 |
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| creator | Wollmann, B M Syversen, S W Lie, E Gjestad, C Mehus, L L Olsen, I C Molden, E |
| description | 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. |
| doi_str_mv | 10.1111/cts.12431 |
| format | Article |
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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.</description><identifier>ISSN: 1752-8054</identifier><identifier>EISSN: 1752-8062</identifier><identifier>DOI: 10.1111/cts.12431</identifier><language>eng</language><publisher>Hoboken: John Wiley & Sons, Inc</publisher><subject>Biomarkers ; Cytokines ; Disease ; Drug dosages ; Enzymes ; Erythrocyte sedimentation rate ; Erythrocytes ; Genotype & phenotype ; Glycoproteins ; Inflammation ; Inflammatory diseases ; Inhibitors ; Lymphocytes B ; Medical treatment ; Metabolism ; Metabolites ; Phenotypes ; Rheumatoid arthritis ; Studies ; Tumor necrosis factor-α</subject><ispartof>Clinical and translational science, 2017-01, Vol.10 (1), p.42-49</ispartof><rights>2017. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1353-11d7114dbad97b7d752f412264107d066e215694959b4daaeb1f38c865cfb5543</citedby><cites>FETCH-LOGICAL-c1353-11d7114dbad97b7d752f412264107d066e215694959b4daaeb1f38c865cfb5543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,862,27907,27908</link.rule.ids></links><search><creatorcontrib>Wollmann, B M</creatorcontrib><creatorcontrib>Syversen, S W</creatorcontrib><creatorcontrib>Lie, E</creatorcontrib><creatorcontrib>Gjestad, C</creatorcontrib><creatorcontrib>Mehus, L L</creatorcontrib><creatorcontrib>Olsen, I C</creatorcontrib><creatorcontrib>Molden, E</creatorcontrib><title>4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State</title><title>Clinical and translational science</title><description>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.</description><subject>Biomarkers</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Drug dosages</subject><subject>Enzymes</subject><subject>Erythrocyte sedimentation rate</subject><subject>Erythrocytes</subject><subject>Genotype & phenotype</subject><subject>Glycoproteins</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Inhibitors</subject><subject>Lymphocytes B</subject><subject>Medical treatment</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Phenotypes</subject><subject>Rheumatoid arthritis</subject><subject>Studies</subject><subject>Tumor necrosis factor-α</subject><issn>1752-8054</issn><issn>1752-8062</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdUUtOwzAQjRBIlMKCG4zEBhYtGcd2kmVp-VQqAvERy8iJbTVVGoPtVnTHEdhwEQ7CITgJhiIWzGZGM-89zdOLon2M-xjquPKuj4QmuBF1MGWkl8WcbP7NjG5HO87N4pgnPGOd6I3Cxzt8vrxerKQ1z6tqahrlvLKmgYlaqgbqFq6Fr1XrHTzUfgo3U7WYC29qCQPrp7b2tYMTpY1VsHR9GOhAh3Eb9oFnWjAaytHl4GbkQLQShsZa1axPP4LjVjdi_i1pV3DrhVe70ZYWjVN7v70b3Z-d3g0vepOr8_FwMOlVmLCkhyhTRCpLIfO0TGXwqCkSwinGqYw5VwQZz2nO8pJKIVSJOsmqjLNKl4zRpBsdrnUfrXlaBN_FvHaVahrRKrNwBWYspzxHngTowT_ozCxsG74rCMnyjOYkzgLqaI2qrHHOKl082nou7KrAuPgOqAgBFT8BJV_K3IUa</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Wollmann, B M</creator><creator>Syversen, S W</creator><creator>Lie, E</creator><creator>Gjestad, C</creator><creator>Mehus, L L</creator><creator>Olsen, I C</creator><creator>Molden, E</creator><general>John Wiley & Sons, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7QO</scope></search><sort><creationdate>20170101</creationdate><title>4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State</title><author>Wollmann, B M ; Syversen, S W ; Lie, E ; Gjestad, C ; Mehus, L L ; Olsen, I C ; Molden, E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1353-11d7114dbad97b7d752f412264107d066e215694959b4daaeb1f38c865cfb5543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Biomarkers</topic><topic>Cytokines</topic><topic>Disease</topic><topic>Drug dosages</topic><topic>Enzymes</topic><topic>Erythrocyte sedimentation rate</topic><topic>Erythrocytes</topic><topic>Genotype & phenotype</topic><topic>Glycoproteins</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Inhibitors</topic><topic>Lymphocytes B</topic><topic>Medical treatment</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Phenotypes</topic><topic>Rheumatoid arthritis</topic><topic>Studies</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wollmann, B M</creatorcontrib><creatorcontrib>Syversen, S W</creatorcontrib><creatorcontrib>Lie, E</creatorcontrib><creatorcontrib>Gjestad, C</creatorcontrib><creatorcontrib>Mehus, L L</creatorcontrib><creatorcontrib>Olsen, I C</creatorcontrib><creatorcontrib>Molden, E</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>Biotechnology Research Abstracts</collection><jtitle>Clinical and translational science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wollmann, B M</au><au>Syversen, S W</au><au>Lie, E</au><au>Gjestad, C</au><au>Mehus, L L</au><au>Olsen, I C</au><au>Molden, E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State</atitle><jtitle>Clinical and translational science</jtitle><date>2017-01-01</date><risdate>2017</risdate><volume>10</volume><issue>1</issue><spage>42</spage><epage>49</epage><pages>42-49</pages><issn>1752-8054</issn><eissn>1752-8062</eissn><abstract>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.</abstract><cop>Hoboken</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1111/cts.12431</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical and translational science, 2017-01, Vol.10 (1), p.42-49 |
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| language | eng |
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| source | DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Online Library Open Access; PubMed Central |
| subjects | Biomarkers Cytokines Disease Drug dosages Enzymes Erythrocyte sedimentation rate Erythrocytes Genotype & phenotype Glycoproteins Inflammation Inflammatory diseases Inhibitors Lymphocytes B Medical treatment Metabolism Metabolites Phenotypes Rheumatoid arthritis Studies Tumor necrosis factor-α |
| title | 4 β ‐Hydroxycholesterol Level in Patients With Rheumatoid Arthritis Before vs. After Initiation of bDMARDs and Correlation With Inflammatory State |
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