title: Insulin resistance is associated with steatosis in nondiabetic patients with genotype 1 chronic hepatitis C.
abstract: Conflicting data exist regarding the relationship between hepatitis C virus genotype 1 and hepatic steatosis as well as the latter's role in the progression of fibrosis and treatment response. We assessed factors associated with hepatic steatosis in genotype 1 chronic hepatitis C and the impact of hepatic fat on fibrosis development and interferon responsiveness. Two hundred ninety-one non-diabetic patients with genotype 1 chronic hepatitis C were examined for the presence of steatosis and its correlation with clinical, virological, and biochemical data, including insulin resistance (IR), evaluated by the homeostasis model assessment (HOMA) score. Steatosis was graded as mild (1%-20% of hepatocytes involved), moderate (21%-40% of hepatocytes involved), and severe (>40% of hepatocytes involved). Steatosis was mild in 110 of 291 (37.8%) and moderate/severe in 55 of 291 (18.9%) subjects. By logistic regression, moderate/severe steatosis was independently associated with the female sex (odds ratio [OR] 2.74; 95% CI 1.40-5.35), high gamma-glutamyltransferase levels (OR 1.52; 95% CI 1.22-1.91), and HOMA-score (OR 1.076; 95% CI 1.001-1.26). By logistic regression, moderate/severe steatosis (OR 2.78; 95% CI 1.21-6.4), and platelet counts (OR 0.97; 95% CI 0.96-0.98) were independent predictors of advanced fibrosis. Patients with moderate/severe steatosis had an OR of 0.52 (95% CI 0.30-0.90) for sustained virological response compared with patients with mild/absent steatosis. In conclusion, in nondiabetic European patients with genotype 1 hepatitis C at low risk for the metabolic syndrome, the prevalence of steatosis was nearly 60%. IR is a risk factor for moderate/severe steatosis, especially in men. Moderate/severe steatosis has clinical relevance, being associated with advanced fibrosis and hyporesponsiveness to antiviral therapy.
authors.affiliation: Unità Operativa di Gastroenterologia, University of Palermo, Italy. camma@ibim.cnr.it
authors.forename: Calogero
authors.initials: C
authors.lastname: Cammà
authors.forename: Savino
authors.initials: S
authors.lastname: Bruno
authors.forename: Vito
authors.initials: V
authors.lastname: Di Marco
authors.forename: Danilo
authors.initials: D
authors.lastname: Di Bona
authors.forename: Mariagrazia
authors.initials: M
authors.lastname: Rumi
authors.forename: Maria
authors.initials: M
authors.lastname: Vinci
authors.forename: Chiara
authors.initials: C
authors.lastname: Rebucci
authors.forename: Agostino
authors.initials: A
authors.lastname: Cividini
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Pizzolanti
authors.forename: Ernesto
authors.initials: E
authors.lastname: Minola
authors.forename: Mario U
authors.initials: MU
authors.lastname: Mondelli
authors.forename: Massimo
authors.initials: M
authors.lastname: Colombo
authors.forename: Giovanbattista
authors.initials: G
authors.lastname: Pinzello
authors.forename: Antonio
authors.initials: A
authors.lastname: Craxì
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D005234:Fatty Liver / Q000209:etiology* / Q000378:metabolism; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification* / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000821:virology; D006801:Humans; D007333:Insulin Resistance; D008103:Liver Cirrhosis / Q000209:etiology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D012737:Sex Factors; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D005723:gamma-Glutamyltransferase