title: Sustained virologic response and other potential genotype-specific roles of statins among patients with hepatitis C-related chronic liver diseases.
abstract: BACKGROUND
  While statins have shown antiviral effects in different studies, few data are available about their effect among different HCV genotypes.
  
  
  OBJECTIVE
  To evaluate the effect of concomitant statin use on sustained virologic response (SVR) and other treatment outcomes among patients with HCV genotypes 1-3.
  
  
  METHODS
  Using US Department of Veterans Affairs database, multivariate (MV), propensity score matched (PSM) and repeated measures mixed model analyses were performed on patients who received combination therapy with Peg-IFN and Ribavirin for treatment of HCV genotypes 1-3 between October 2001-December 2011. Concomitant statin users were matched with non-users in each genotype and SVR rates were compared. Changes in serum ALT during treatment was assessed.
  
  
  RESULTS
  Of 37,611 treated patients, 236 genotype 1 (GT1), 78 genotype 2 (GT2) and 23 genotype 3 (GT3) statin users and non-users were used for PSM. SVR among GT1 patients was 22.8% (overall), significantly higher among statin users (26.3% vs. 19.5% P<0.01 from PSM; OR=1.49 CI 1.06-2.08 P=0.02 from MV). No significant impact of statin use was observed among GT2 (overall SVR - 55.8%, statin users vs. non-users - 53.9% vs. 57.7%, P=0.32), and GT3 (overall SVR - 58.7%, statin users vs. non-users - 60.9% vs. 56.2%, P=0.39) patients. Higher baseline LDL was positively associated with SVR while statin use reduced ALT during treatment in GT1 patients.
  
  
  CONCLUSIONS
  In view of additional benefits of statins, and the prohibitive cost of newer HCV therapies, statins could be a potential assist for hard-to-treat GT1 patients especially in resource-poor settings.
authors.affiliation: Kansas City VA Medical Center, Department of Gastroenterology (Hepatology Division), Kansas City, MO, USA; University of Kansas Medical Center, Department of Internal Medicine, Kansas City, KS, USA.
authors.forename: Prashant
authors.initials: P
authors.lastname: Pandya
authors.affiliation: University of Kansas Medical Center, Department of Internal Medicine, Kansas City, KS, USA.
authors.forename: Fadi
authors.initials: F
authors.lastname: Rzouq
authors.affiliation: Kansas City VA Medical Center, Hepatology Research Unit, Kansas City, MO, USA. Electronic address: Olurinde.Oni@va.gov.
authors.forename: Olurinde
authors.initials: O
authors.lastname: Oni
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects* / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D008887:Military Medicine; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use*; D012307:Risk Factors; D016896:Treatment Outcome; D014481:United States; D014728:Veterans
chemical_list: D000998:Antiviral Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a