title: Insulin resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis.
abstract: OBJECTIVE
  Our study was designed to test the association between insulin resistance (IR) and hepatitis C virus (HCV) genotypes, serum HCV RNA level and liver fibrosis stage in a large prospective cohort of chronic hepatitis C (CHC) patients.
  
  
  METHODS
  Six hundred consecutive patients (CHC, n = 500; chronic hepatitis B (CHB), n = 100) were evaluated on the day of liver biopsy. IR (Homeostasis Model for Assessment of Insulin Resistance) and all components of the metabolic syndrome were assessed. By logistic regression, independent factors associated with IR and those associated with significant fibrosis were assessed in nondiabetic and noncirrhotic CHC, respectively. Parameters of IR were compared between hepatitis B and 240 CHC matched by epidemiologic, metabolic, and histologic features.
  
  
  RESULTS
  IR was present in 32.4% of the 462 nondiabetic CHC and associated with the metabolic syndrome, genotypes 1 and 4, significant fibrosis, and severe steatosis. IR was diagnosed in 15% of 145 CHC without metabolic syndrome or significant fibrosis, and associated with genotypes 1 and 4, high serum HCV RNA level, and moderate-severe necroinflammation. Significant fibrosis was present in 51.1% of the 454 noncirrhotic CHC patients and associated with male sex, age >40 years, IR, moderate-severe necroinflammation, and severe steatosis. IR was less frequent in CHB than in matched CHC (5% vs 35%, respectively, P < .001).
  
  
  CONCLUSIONS
  IR is a specific feature of CHC, associated with genotypes 1 and 4 and high serum HCV RNA level. Significant fibrosis is associated with IR independent from steatosis.
authors.affiliation: AP-HP, Hôpital Beaujon, Service d'Hépatologie, Clichy F-92110, France.
authors.forename: Rami
authors.initials: R
authors.lastname: Moucari
authors.forename: Tarik
authors.initials: T
authors.lastname: Asselah
authors.forename: Dominique
authors.initials: D
authors.lastname: Cazals-Hatem
authors.forename: Hélène
authors.initials: H
authors.lastname: Voitot
authors.forename: Nathalie
authors.initials: N
authors.lastname: Boyer
authors.forename: Marie-Pierre
authors.initials: MP
authors.lastname: Ripault
authors.forename: Rodolphe
authors.initials: R
authors.lastname: Sobesky
authors.forename: Michèle
authors.initials: M
authors.lastname: Martinot-Peignoux
authors.forename: Sarah
authors.initials: S
authors.lastname: Maylin
authors.forename: Marie-Hélène
authors.initials: MH
authors.lastname: Nicolas-Chanoine
authors.forename: Valérie
authors.initials: V
authors.lastname: Paradis
authors.forename: Michel
authors.initials: M
authors.lastname: Vidaud
authors.forename: Dominique
authors.initials: D
authors.lastname: Valla
authors.forename: Pierre
authors.initials: P
authors.lastname: Bedossa
authors.forename: Patrick
authors.initials: P
authors.lastname: Marcellin
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D015331:Cohort Studies; D018450:Disease Progression; D005234:Fatty Liver / Q000503:physiopathology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics* / Q000472:pathogenicity; D019698:Hepatitis C, Chronic / Q000503:physiopathology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000503:physiopathology / Q000821:virology*; D016015:Logistic Models; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood*; D012720:Severity of Illness Index
chemical_list: D012367:RNA, Viral