title: Statin use is associated with a reduced risk of fibrosis progression in chronic hepatitis C.
abstract: OBJECTIVE
  Therapies that slow fibrosis progression in chronic liver disease are needed. Animal models have demonstrated that statins prevent the progression of hepatic fibrosis, but human data is lacking so far. We evaluated the association between statins and fibrosis progression in the HALT-C trial cohort.
  
  
  METHODS
  Subjects with chronic hepatitis C (CHC) and advanced hepatic fibrosis underwent serial liver biopsies over 3.5 years. The primary outcome was a ⩾ 2-point increase in the Ishak fibrosis score on at least one of two serial biopsies. We used complementary log-log regression analysis to assess the association between statins and fibrosis progression among subjects without baseline cirrhosis.
  
  
  RESULTS
  Fibrosis progression occurred in 3/29 (10%) statin users and 145/514 (29%) non-users. The unadjusted hazard ratio (HR) for fibrosis progression among statin users compared to non-users was 0.32 (95% CI 0.10-0.99). This association remained significant after adjusting for established predictors of histological outcome, including body mass index, platelets and hepatic steatosis (adjusted HR 0.31; 95% CI 0.10-0.97). The mean change in Ishak fibrosis score over the 3.5 year study period was -0.34 (SE 0.18) for statin users compared to +0.42 (SE 0.07) for non-users (p = 0.006, after adjustment for baseline fibrosis score).
  
  
  CONCLUSIONS
  Statin use is associated with a reduced risk of fibrosis progression in advanced CHC. Our findings suggest a potential role for statins in preventing liver disease progression.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
authors.forename: Tracey G
authors.initials: TG
authors.lastname: Simon
authors.affiliation: Liver Center, Gastrointestinal Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
authors.forename: Lindsay Y
authors.initials: LY
authors.lastname: King
authors.affiliation: Biostatistics Center, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
authors.forename: Hui
authors.initials: H
authors.lastname: Zheng
authors.affiliation: Liver Center, Gastrointestinal Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: rtchung@partners.org.
authors.forename: Raymond T
authors.initials: RT
authors.lastname: Chung
mesh_terms: D001706:Biopsy; D004279:DNA, Viral / Q000032:analysis; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000175:diagnosis / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008103:Liver Cirrhosis / Q000175:diagnosis / Q000209:etiology / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged
chemical_list: D004279:DNA, Viral; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors
keywords: Cirrhosis; Hepatitis C virus; Lipid lowering agent