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Article: Prevention of hepatocellular carcinoma in hepatitis B virus infection

TitlePrevention of hepatocellular carcinoma in hepatitis B virus infection
Authors
Issue Date2009
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
Journal Of Gastroenterology And Hepatology, 2009, v. 24 n. 8, p. 1352-1357 How to Cite?
AbstractChronic hepatitis B is the main risk factor for hepatocellular carcinoma (HCC) in Asia. The most important preventive strategy's adoption of the universal hepatitis B vaccination program is now in its third decade. There is a clear reduction in both chronic hepatitis B virus (HBV) infection (hepatitis B surface antigen "carriage") but also in childhood HCC in Taiwan. An outstanding concern is variability in vaccine coverage between countries. For patients with chronic hepatitis B, serum HBV DNA levels have emerged as the key risk factor for development of HCC. The initial treatment for chronic hepatitis B was interferon. One randomized control trial, and several case-control or cohort studies have shown benefits for preventing HCC, particularly in cirrhotic patients who responded to therapy. With nucleos(t)ide analogs, the most important study has been the Asian Cirrhosis Lamivudine multicenter randomized controlled trial. This showed that lamivudine can reduce disease progression in HBV-related cirrhosis, including an approximately 50% decrease in HCC incidence. Such efficacy was achieved despite emergence of drug resistance in approximately 50% of cases. Case-control studies have suggested that hepatitis B cases without cirrhosis may also benefit. In conclusion, it is now possible to prevent HBV-related HCC. The most effective method is hepatitis B vaccination, which prevents chronic HBV infection and chronic liver disease resulting therefrom. Interferon therapy appears to confer benefit but the evidence is weaker. First-generation oral antiviral (lamivudine) reduces HCC risk, particularly in cirrhotics. Long-term outcome data with newer, more potent HBV antivirals that have a higher genetic barrier to drug resistance are eagerly awaited.
Persistent Identifierhttp://hdl.handle.net/10722/163267
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLim, SGen_US
dc.contributor.authorMohammed, Ren_US
dc.contributor.authorYuen, MFen_US
dc.contributor.authorKao, JHen_US
dc.date.accessioned2012-09-05T05:29:21Z-
dc.date.available2012-09-05T05:29:21Z-
dc.date.issued2009en_US
dc.identifier.citationJournal Of Gastroenterology And Hepatology, 2009, v. 24 n. 8, p. 1352-1357en_US
dc.identifier.issn0815-9319en_US
dc.identifier.urihttp://hdl.handle.net/10722/163267-
dc.description.abstractChronic hepatitis B is the main risk factor for hepatocellular carcinoma (HCC) in Asia. The most important preventive strategy's adoption of the universal hepatitis B vaccination program is now in its third decade. There is a clear reduction in both chronic hepatitis B virus (HBV) infection (hepatitis B surface antigen "carriage") but also in childhood HCC in Taiwan. An outstanding concern is variability in vaccine coverage between countries. For patients with chronic hepatitis B, serum HBV DNA levels have emerged as the key risk factor for development of HCC. The initial treatment for chronic hepatitis B was interferon. One randomized control trial, and several case-control or cohort studies have shown benefits for preventing HCC, particularly in cirrhotic patients who responded to therapy. With nucleos(t)ide analogs, the most important study has been the Asian Cirrhosis Lamivudine multicenter randomized controlled trial. This showed that lamivudine can reduce disease progression in HBV-related cirrhosis, including an approximately 50% decrease in HCC incidence. Such efficacy was achieved despite emergence of drug resistance in approximately 50% of cases. Case-control studies have suggested that hepatitis B cases without cirrhosis may also benefit. In conclusion, it is now possible to prevent HBV-related HCC. The most effective method is hepatitis B vaccination, which prevents chronic HBV infection and chronic liver disease resulting therefrom. Interferon therapy appears to confer benefit but the evidence is weaker. First-generation oral antiviral (lamivudine) reduces HCC risk, particularly in cirrhotics. Long-term outcome data with newer, more potent HBV antivirals that have a higher genetic barrier to drug resistance are eagerly awaited.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGHen_US
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAntiviral Agents - Therapeutic Useen_US
dc.subject.meshAsiaen_US
dc.subject.meshCarcinoma, Hepatocellular - Prevention & Control - Virologyen_US
dc.subject.meshChilden_US
dc.subject.meshChild, Preschoolen_US
dc.subject.meshDna, Viral - Blooden_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshDrug Resistance, Viralen_US
dc.subject.meshHepatitis B Vaccinesen_US
dc.subject.meshHepatitis B Virus - Genetics - Immunologyen_US
dc.subject.meshHepatitis B, Chronic - Complications - Diagnosis - Drug Therapy - Prevention & Controlen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunization Programsen_US
dc.subject.meshInfanten_US
dc.subject.meshInfant, Newbornen_US
dc.subject.meshInterferons - Therapeutic Useen_US
dc.subject.meshLamivudine - Therapeutic Useen_US
dc.subject.meshLiver Cirrhosis - Prevention & Control - Virologyen_US
dc.subject.meshLiver Neoplasms - Prevention & Control - Virologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTreatment Outcomeen_US
dc.subject.meshViral Loaden_US
dc.subject.meshYoung Adulten_US
dc.titlePrevention of hepatocellular carcinoma in hepatitis B virus infectionen_US
dc.typeArticleen_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1440-1746.2009.05985.xen_US
dc.identifier.pmid19702903-
dc.identifier.scopuseid_2-s2.0-69049092778en_US
dc.identifier.hkuros174517-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-69049092778&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume24en_US
dc.identifier.issue8en_US
dc.identifier.spage1352en_US
dc.identifier.epage1357en_US
dc.identifier.isiWOS:000269057900009-
dc.publisher.placeAustraliaen_US
dc.identifier.scopusauthoridLim, SG=7404081127en_US
dc.identifier.scopusauthoridMohammed, R=7006069283en_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.scopusauthoridKao, JH=7201375585en_US
dc.identifier.citeulike5491930-

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