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Prevention of hepatocellular carcinoma in hepatitis B virus infection


  • Seng Gee Lim,

    Corresponding author
    1. Department of Gastroenterology and Hepatology, Department of Medicine, National University Health System, Yong Yoo Lin School of Medicine, National University of Singapore, Singapore;
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  • Rosmawati Mohammed,

    1. Department of Medicine, University of Malaya, Kuala Lumpur, Malaysia;
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  • Man-Fung Yuen,

    1. Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong SAR; and
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  • Jia-Horng Kao

    1. Division of Gastroenterology, Department of Internal Medicine, Graduate Institute of Clinical Medicine, Hepatitis Research Center and Department of Medical Research, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan
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A/P Seng Gee LimChief, Dept of Gastroenterology & Hepatology National University Health System 5 Lower Kent Ridge Rd Singapore 119074. Email:
Tel: 65-6779555 x4369
Fax: 65-67751518


Chronic 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.