title: Does antiviral therapy reduce the risk of hepatocellular carcinoma in patients with chronic hepatitis C?
abstract: Infection with the Hepatitis C virus (HCV) affects nearly 200 million people in the world. It is a leading cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC). It is estimated that 25% of HCC worldwide is related to HCV, being the main cause in Western Europe, North America and Japan. HCV can be implicated in the development of HCC in an indirect way through induction of chronic inflammation, or directly by means of viral proteins activating several signaling pathways. For patients with clinically significant hepatic fibrosis there is widespread agreement that antiviral therapy is indicated in order to eliminate the virus. It is generally accepted that sustained virologic response (SVR), i.e. undetectable HCV RNA at 24 weeks after treatment withdrawal, is associated with resolution of liver disease in patients without cirrhosis. In the last decades, results of treatment for chronic hepatitis C have improved substantially. The current standard of care is a combination of pegylated interferon and ribavirin for 24 to 48 weeks, depending on the genotype. In the near future, this standard of care will include addition of directly-acting antivirals. In 2011 two protease inhibitors (boceprevir and telaprevir) have been registered for use in adults with genotype 1 chronic hepatitis C, increasing the SVR rates from less than 50% to about 70% in patients treated with a triple combination. There is limited evidence for the role of interferon-based therapy in primary, secondary and tertiary prophylaxis of HCC in patients with chronic Hepatitis C, as most studies were primarily designed to assess the antiviral effect of treatment and not the long-term impact on the natural history of the disease. Further prospective studies using the more successful emerging treatments of chronic hepatitis C are to be conducted to evaluate the risk of HCC.
authors.affiliation: Division of Gastroenterology and Hepatology, University Hospital, Faculty of Medicine, University of Antwerp, Antwerp, Belgium. peter.michielsen@uza.be
authors.forename: P
authors.initials: P
authors.lastname: Michielsen
authors.forename: E
authors.initials: E
authors.lastname: Ho
authors.forename: S
authors.initials: S
authors.lastname: Francque
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology / Q000517:prevention & control* / Q000821:virology; D004359:Drug Therapy, Combination; D005060:Europe / Q000453:epidemiology; D016174:Hepacivirus / Q000187:drug effects* / Q000472:pathogenicity; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy* / Q000453:epidemiology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D007564:Japan / Q000453:epidemiology; D008113:Liver Neoplasms / Q000453:epidemiology / Q000517:prevention & control* / Q000821:virology; D009656:North America / Q000453:epidemiology; D009842:Oligopeptides / Q000627:therapeutic use; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011392:Proline / Q000031:analogs & derivatives / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use; D018570:Risk Assessment; D016896:Treatment Outcome; D019562:Viral Load / Q000187:drug effects
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D009842:Oligopeptides; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C486464:telaprevir; C512204:N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide; D011392:Proline; C100416:peginterferon alfa-2a