title: Evolution of hepatic steatosis in patients with advanced hepatitis C: results from the hepatitis C antiviral long-term treatment against cirrhosis (HALT-C) trial.
abstract: Hepatic steatosis is a common histologic feature in patients with chronic hepatitis C (CHC) but there are no large longitudinal studies describing the progression of steatosis in CHC. We examined changes in steatosis on serial biopsies among CHC patients participating in the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial. All 1050 patients in the trial had advanced fibrosis at baseline biopsy and were documented not to have had a sustained virological response to peginterferon and ribavirin. Most (94%) patients had genotype 1 infection. At least one protocol follow-up biopsy was read on 892 patients, and 699 had the last biopsy performed 3.5 years after randomization. At enrollment, 39% had cirrhosis and 61% had bridging fibrosis; 18%, 41%, 31%, and 10% had steatosis scores of 0, 1, 2, and 3 or 4, respectively. The mean steatosis score decreased in the follow-up biopsies in both the interferon-treated patients and controls with no effect of treatment assignment (P = 0.66). A decrease in steatosis score by > or =1 point was observed in 30% of patients and was associated with both progression to cirrhosis and continued presence of cirrhosis (P = 0.02). Compared to patients without a decrease in steatosis, those with a decrease in steatosis had worse metabolic parameters at enrollment, and were more likely to have a decrease in alcohol intake, improvement in metabolic parameters, and worsening liver disease (cirrhosis, esophageal varices, and deterioration in liver function).
  
  
  CONCLUSIONS
  Serial biopsies demonstrated that in patients with CHC, steatosis recedes during progression from advanced fibrosis to cirrhosis. Decreased alcohol intake and improved metabolic parameters are associated with a decline in steatosis and may modulate hepatitis C progression.
authors.affiliation: Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI 48109, USA. aslok@med.umich.edu
authors.forename: Anna S
authors.initials: AS
authors.lastname: Lok
authors.forename: James E
authors.initials: JE
authors.lastname: Everhart
authors.forename: Raymond T
authors.initials: RT
authors.lastname: Chung
authors.forename: Hae-Young
authors.initials: HY
authors.lastname: Kim
authors.forename: Gregory T
authors.initials: GT
authors.lastname: Everson
authors.forename: John C
authors.initials: JC
authors.lastname: Hoefs
authors.forename: Joel K
authors.initials: JK
authors.lastname: Greenson
authors.forename: Richard K
authors.initials: RK
authors.lastname: Sterling
authors.forename: Karen L
authors.initials: KL
authors.lastname: Lindsay
authors.forename: William M
authors.initials: WM
authors.lastname: Lee
authors.forename: Adrian M
authors.initials: AM
authors.lastname: Di Bisceglie
authors.forename: Herbert L
authors.initials: HL
authors.lastname: Bonkovsky
authors.forename: Marc G
authors.initials: MG
authors.lastname: Ghany
authors.forename: Chihiro
authors.initials: C
authors.lastname: Morishima
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications* / Q000473:pathology; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a