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Race, insulin resistance and hepatic steatosis in chronic hepatitis C Potential conflict of interest: Dr. Zacks is on the speakers' bureau of Roche. He also received grants from Salix Pharmaceuticals.

dc.contributor.authorConjeevaram, Hari S.en_US
dc.contributor.authorKleiner, David E.en_US
dc.contributor.authorEverhart, Jay E.en_US
dc.contributor.authorHoofnagle, Jay H.en_US
dc.contributor.authorZacks, Stevenen_US
dc.contributor.authorAfdhal, Nezam H.en_US
dc.contributor.authorWahed, Abdus S.en_US
dc.date.accessioned2007-09-20T17:55:22Z
dc.date.available2008-04-03T18:45:01Zen_US
dc.date.issued2007-01en_US
dc.identifier.citationConjeevaram, Hari S.; Kleiner, David E.; Everhart, Jay E.; Hoofnagle, Jay H.; Zacks, Steven; Afdhal, Nezam H.; Wahed, Abdus S. (2007). "Race, insulin resistance and hepatic steatosis in chronic hepatitis C Potential conflict of interest: Dr. Zacks is on the speakers' bureau of Roche. He also received grants from Salix Pharmaceuticals. ." Hepatology 45(1): 80-87. <http://hdl.handle.net/2027.42/55881>en_US
dc.identifier.issn0270-9139en_US
dc.identifier.issn1527-3350en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/55881
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17187406&dopt=citationen_US
dc.description.abstractHepatic steatosis is common in chronic hepatitis C and has been linked to concurrent obesity, insulin resistance, diabetes, disease severity, and poor response to therapy. Racial differences in rates of obesity and diabetes may contribute to racial differences in hepatic steatosis and treatment response. The aim of the present study was to compare hepatic steatosis and its associations between African American (AA) and Caucasian American (CA) patients with chronic hepatitis C, genotype 1, participating in a prospective study of peginterferon and ribavirin therapy. Liver biopsy results were available from 194 AA patients and 205 CA patients. The 2 groups were compared for anthropometric, clinical, and biochemical features and insulin resistance estimated by the homeostasis model assessment index (HOMA-IR). Sixty-one percent of the AA patients and 65% of the CA patients had hepatic steatosis ( P = 0.38). In univariable analysis, steatosis was associated with HOMA-IR, body mass index, waist circumference, serum triglycerides, aminotransferase level, and histological scores for inflammation and fibrosis. After adjusting for these features, AA patients had a lower risk of steatosis than did CA patients (OR 0.54, 95% CI 0.32-0.91, P = 0.02). Insulin resistance but not steatosis was associated with a lower rate of sustained virological response when adjusted for known factors that predict response (relative risk 0.87, 95% CI 0.77-0.99, P = 0.028). Conclusion : After adjusting for the higher prevalence of features associated with hepatic steatosis, AA patients had a lower prevalence of hepatic steatosis than did CA patients with chronic hepatitis C, genotype 1. Insulin resistance but not steatosis was independently associated with lower sustained virological response. (H EPATOLOGY 2006;45:80–87.)en_US
dc.format.extent150621 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherHepatologyen_US
dc.titleRace, insulin resistance and hepatic steatosis in chronic hepatitis C Potential conflict of interest: Dr. Zacks is on the speakers' bureau of Roche. He also received grants from Salix Pharmaceuticals.en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan, Ann Arbor, MI ; fax: (734) 936-7392 ; Division of Gastroenterology, University of Michigan, 3912 Taubman Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0362en_US
dc.contributor.affiliationotherNational Cancer Institute, National Institutes of Health, Bethesda, MDen_US
dc.contributor.affiliationotherNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MDen_US
dc.contributor.affiliationotherNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MDen_US
dc.contributor.affiliationotherUniversity of North Carolina at Chapel Hill, Chapel Hill, NCen_US
dc.contributor.affiliationotherBeth Israel Deaconess Medical Center, Boston, MAen_US
dc.contributor.affiliationotherUniversity of Pittsburgh, Pittsburgh, PAen_US
dc.identifier.pmid17187406en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/55881/1/21455_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/hep.21455en_US
dc.identifier.sourceHepatologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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