title: Hepatic steatosis in chronic hepatitis C: baseline host and viral characteristics and influence on response to therapy with peginterferon alpha-2a plus ribavirin.
abstract: Hepatic steatosis is common in hepatitis C virus (HCV)-infected patients and may be associated with the metabolic syndrome. We studied steatosis in patients treated with peginterferonalpha-2a plus ribavirin. Forty-five of 207 patients (22%) had >5% hepatic steatosis at baseline. Significantly more patients with steatosis than without were HCV genotype 3 (51%vs 14%; P < 0.0001) had higher HCV-RNA (P = 0.0045), body weight (P = 0.0176), body mass index (BMI, P = 0.0352) and serum triglycerides (TG) (P = 0.0364), hypertriglyceridaemia (P = 0.0009), elevated blood pressure/history of hypertension (P = 0.0229) and lower cholesterol (P = 0.0009). Significant steatosis predictors were genotype 3 (OR 9.04, 95% CI 3.85-21.21, P < 0.0001), HCV-RNA (OR 2.96, 1.49-5.88, P = 0.0019) and triglycerides (OR 1.06, 1.02-1.11, P = 0.0071). In genotype 3 patients, HCV-RNA was the only significant predictor (OR 11.15, 2.60-47.81, P = 0.0012). In non-genotype 3 patients, hypertriglyceridaemia was the only significant predictor (OR 1.07, 1.02-1.12, P = 0.0041). 134 of 207 patients (65%) achieved an sustained virological response (SVR) with peginterferon alpha-2a plus ribavirin, similar to the overall response rate. In genotype 3 patients with an SVR, steatosis decreased from 48% to 13% (baseline to end-point). No change was seen in the steatosis rate in non-genotype 3 patients with an SVR. This large and comprehensive analysis of a large data base from a multinational trial further adds to the observations that chronic HCV is associated with hepatic steatosis in approximately a fifth of patients. Further, features of the metabolic syndrome are associated with hepatic steatosis in most of these patients. Steatosis is significantly more common in genotype 3 compared with other genotypes, and in these patients, an SVR is associated with steatosis clearance.
authors.affiliation: GI Division, University of Pennsylvania, Philadelphia, PA 19104, USA. rajender.reddy@uphs.upenn.edu
authors.forename: K R
authors.initials: KR
authors.lastname: Reddy
authors.forename: S
authors.initials: S
authors.lastname: Govindarajan
authors.forename: P
authors.initials: P
authors.lastname: Marcellin
authors.forename: D
authors.initials: D
authors.lastname: Bernstein
authors.forename: J L
authors.initials: JL
authors.lastname: Dienstag
authors.forename: H
authors.initials: H
authors.lastname: Bodenheimer
authors.forename: J
authors.initials: J
authors.lastname: Rakela
authors.forename: D
authors.initials: D
authors.lastname: Messinger
authors.forename: G
authors.initials: G
authors.lastname: Schmidt
authors.forename: A
authors.initials: A
authors.lastname: Ackrill
authors.forename: S J
authors.initials: SJ
authors.lastname: Hadziyannis
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D004338:Drug Combinations; D005234:Fatty Liver / Q000209:etiology*; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects* / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology / Q000821:virology; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D011994:Recombinant Proteins; D012189:Retrospective Studies; D012254:Ribavirin / Q000627:therapeutic use*
chemical_list: D000998:Antiviral Agents; D004338:Drug Combinations; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a