title: Steatosis is an independent predictor of relapse following rapid virologic response in patients with HCV genotype 3.
abstract: OBJECTIVE
  It is recommended that patients with chronic hepatitis C virus (HCV) genotype 3 infections receive 24 weeks of treatment. A rapid virologic response (RVR; at week 4) predicts a sustained virologic response (SVR), although not all patients with an RVR achieve an SVR. We explored the relationships among hepatic steatosis, level of HCV RNA, relapse, and RVR in a phase 3 randomized controlled trial of 932 patients infected with HCV genotype 2 (n = 427) or 3 (n = 505) who received 24 weeks of therapy with interferon-α.
  
  
  METHODS
  In patients with an RVR (HCV RNA <43 IU/mL), the presence of an SVR was modeled using multivariate logistic regression as a function of age, sex, weight, body mass index, insulin resistance, steatosis, and levels of γ-glutamyl transpeptidase, alanine aminotransferase, liver fibrosis, and baseline HCV RNA.
  
  
  RESULTS
  RVR, SVR, and relapse rates among patients with HCV genotype 3 were 79.6%, 79.2%, and 15.6%, respectively; corresponding rates among patients with HCV genotype 2 were 86.7%, 84.3%, and 10.1%. An RVR had high predictive value for an SVR in patients with HCV genotypes 2 (88.9%) and 3 (88.1%). The strongest independent predictors of relapse in patients with genotype 3 and an RVR were steatosis (odds ratio 3.0; P = .003) and HCV RNA ≥400,000 IU/mL (odds ratio 2.5; P = .04). Relapse rates in patients with steatosis were 17.4% and 20.9% for low and high baseline levels of HCV RNA, respectively; corresponding rates in those without steatosis were 2.5% and 8.8%.
  
  
  CONCLUSIONS
  Steatosis was associated with significantly higher rates of relapse, irrespective of viral load, in patients infected with HCV genotype 3 who had an RVR. Further studies are needed to determine if longer treatment durations are effective in patients with an RVR and these risk factors.
authors.affiliation: Department of Gastroenterology, Jaslok Hospital, Mumbai, India.
authors.forename: Samir R
authors.initials: SR
authors.lastname: Shah
authors.forename: Keyur
authors.initials: K
authors.lastname: Patel
authors.forename: Patrick
authors.initials: P
authors.lastname: Marcellin
authors.forename: Graham R
authors.initials: GR
authors.lastname: Foster
authors.forename: Michael
authors.initials: M
authors.lastname: Manns
authors.forename: Shyam
authors.initials: S
authors.lastname: Kottilil
authors.forename: Letha
authors.initials: L
authors.lastname: Healey
authors.forename: Erik
authors.initials: E
authors.lastname: Pulkstenis
authors.forename: G Mani
authors.initials: GM
authors.lastname: Subramanian
authors.forename: John G
authors.initials: JG
authors.lastname: McHutchison
authors.forename: Mark S
authors.initials: MS
authors.lastname: Sulkowski
authors.forename: Stefan
authors.initials: S
authors.lastname: Zeuzem
authors.forename: David R
authors.initials: DR
authors.lastname: Nelson
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000008:administration & dosage*; D005234:Fatty Liver / Q000175:diagnosis*; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D016898:Interferon-alpha / Q000008:administration & dosage*; D008103:Liver Cirrhosis / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012367:RNA, Viral / Q000097:blood; D012008:Recurrence; D017211:Treatment Failure; D019562:Viral Load; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D012367:RNA, Viral; D005723:gamma-Glutamyltransferase; D000410:Alanine Transaminase