title: Cirrhotic patients are still at risk of developing hepatocellular carcinoma despite Interferon-induced sustained virological response.
abstract: BACKGROUND
  Hepatitis C virus (HCV) infection is a common cause of chronic liver disease and hepatocellular carcinoma (HCC). The prevalence of HCC significantly declines among patients achieving a sustained virological response (SVR) after antiviral therapy with pegylated(PEG)-interferon (IFN) and ribavirin. However, up to 5% of patients with SVR may develop HCC.
  
  
  METHODS
  We investigated the epidemiological, clinical, biochemical and virological characteristics of a small cohort of patients with chronic hepatitis C (CHC) who developed HCC after being successfully treated with PEG-IFN-α and ribavirin.
  
  
  RESULTS
  Between September 2000 and January 2003, 598 patients with CHC underwent a complete course of treatment with PEG-IFN-α and ribavirin; 221 out of 598 (37%) patients obtained a SVR. Throughout the 10-year post-treatment follow up, 13 of 221 ( 5.8% ) SVR patients developed HCC. All 13 patients were male and were affected with Child A liver cirrhosis; in addition, at baseline they were significantly older (p < 0.05) and had higher alpha-fetoprotein levels (p < 0.05) in comparison with those who did not develop HCC. Nine patients (69.3%) developed HCC within the first 3 years after antiviral treatment completion, one patient (7.7%) between 3 and 5 years and 3 subjects (23%) between 5 and 10 years; 12 of 13 had a solitary lesion with a mean diameter of 2.5± 0.5 cm. Eleven cases (84.6%) underwent surgical resection, one (7.7%) received liver transplantation, one (7.7%) received palliative care.
  
  
  CONCLUSIONS
  The risk of developing HCC after achieving SVR persists in patients with HCV-related cirrhosis. As a consequence, these patients should continue to undergo long-term surveillance for HCC, in order to early detect and treat it.
authors.affiliation: Department of Clinical and Molecular Biomedicine, Division of Infectious Diseases, University of Catania, Italy. cacopardobruno@inwind.it.
authors.forename: M R
authors.initials: MR
authors.lastname: Pinzone
authors.forename: A M
authors.initials: AM
authors.lastname: Zanghì
authors.forename: L
authors.initials: L
authors.lastname: Rapisarda
authors.forename: V
authors.initials: V
authors.lastname: D'Agata
authors.forename: F
authors.initials: F
authors.lastname: Benanti
authors.forename: D
authors.initials: D
authors.lastname: Spartà
authors.forename: G
authors.initials: G
authors.lastname: Nunnari
authors.forename: B
authors.initials: B
authors.lastname: Cacopardo
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000517:prevention & control / Q000821:virology*; D015331:Cohort Studies; D004359:Drug Therapy, Combination; D005260:Female; D016174:Hepacivirus / Q000187:drug effects / Q000502:physiology; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000188:drug therapy / Q000378:metabolism / Q000821:virology; D008113:Liver Neoplasms / Q000517:prevention & control / Q000821:virology*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use*; D016896:Treatment Outcome; D000509:alpha-Fetoproteins / Q000378:metabolism
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D000509:alpha-Fetoproteins; D011092:Polyethylene Glycols; D012254:Ribavirin