title: Do steatosis and steatohepatitis impact on sustained virological response (SVR) rates in patients receiving pegylated interferon and ribavirin for chronic hepatitis C infection?
abstract: The impact of steatosis on treatment response in chronic hepatitis C infection is controversial. The aim of this study was to determine whether steatosis +/- steatohepatitis on pre-treatment liver biopsy influenced sustained virological response (HCV RNA negative 6 months after completing therapy) in patients with chronic hepatitis C infection treated with pegylated interferon-alpha and ribavirin. One hundred and seventy-nine patients, median age 46 years (interquartile range 40-52), treated between 2001 and 2005. Histological evidence of steatosis was present in 93 patients (52%) and steatohepatitis in 33 patients (18%), 31 patients (17.3%) were cirrhotic. There were 106 (59%) responders, who were similar to non-responders in respect to gender, age, and pre-treatment ALT. On univariate analysis, infection with genotype 2 or 3 was associated with sustained virological response (odds ratio 6.5 (95% CI, 3.3-12.5); P < 0.0001), whereas cirrhosis and patient weight were associated with a reduced response (odds ratios 0.23 (95% CI, 0.11-0.48); P < 0.0001, and 0.97 (95% CI, 0.95-0.99); P < 0.01, respectively); steatohepatitis but not steatosis impacted on the likelihood of achieving sustained virological response (odds ratio 0.37 (95% CI, 0.17-0.77); P = 0.009, and P = 0.18, respectively). Multivariate analysis revealed that infection with genotype 1 or 4 (odds ratio 0.09 (95% CI, 0.03-0.32); P < 0.001) and pre-treatment weight (odds ratio 0.94 (95% CI, 0.90-0.98); P = 0.002) were the only variables associated independently with sustained virological response. In chronic hepatitis C infection, although steatosis was associated with steatohepatitis, neither was shown to affect sustained virological response, which was influenced by genotype, patient weight and the presence of cirrhosis.
authors.affiliation: Institute of Liver Studies, King's College Hospital, Denmark Hill, London, United Kingdom.
authors.forename: T J S
authors.initials: TJ
authors.lastname: Cross
authors.forename: A
authors.initials: A
authors.lastname: Quaglia
authors.forename: J
authors.initials: J
authors.lastname: Nolan
authors.forename: S
authors.initials: S
authors.lastname: Hughes
authors.forename: P M
authors.initials: PM
authors.lastname: Harrison
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage*; D001706:Biopsy; D005234:Fatty Liver / Q000473:pathology*; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000473:pathology*; D006651:Histocytochemistry; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage*; D008103:Liver Cirrhosis / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000008:administration & dosage*; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012254:Ribavirin / Q000008:administration & dosage*; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C417083:peginterferon alfa-2b; C100416:peginterferon alfa-2a