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JAC Advance Access originally published online on July 1, 2003
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Journal of Antimicrobial Chemotherapy (2003) 52, 149-151
© 2003 The British Society for Antimicrobial Chemotherapy

Leading Article

A prospect for pharmacogenomics in the interferon therapy of chronic viral hepatitis

Shiou-Hwei Yeh1, Ding-Shinn Chen2,3 and Pei-Jer Chen2,4,*

1 Division of Molecular and Genomic Medicine, National Health Research Institutes, Taipei; 2 Hepatitis Research Center, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 100; 3 Department of Internal Medicine College of Medicine, National Taiwan University, Taipei; 4 Graduate Institute of Clinical Medicine, National Taiwan University, Taipei, Taiwan

Keywords: antivirals, genetic polymorphism, hepatitis virus

The first 150 words of the full text of this article appear below.

Globally, hepatitis B or C virus persistently infects 350 million or 100 million people, respectively.1,2 Following recurrent chronic inflammatory hepatitis, eventually ~20%–30% of chronic viral hepatitis patients develop liver cirrhosis and hepatocellular carcinoma (HCC), which usually carries a very poor prognosis.1,2 For these patients, the best strategy to prevent progression to end-stage liver diseases is to control or eradicate hepatitis B virus (HBV or hepatitis C virus (HCV)) as early as possible. In support of this, recent studies from Japan have reported an impressive reduction in the incidence of HCC following treatment of chronic hepatitis C patients with interferon (IFN).3

Current therapies for chronic viral hepatitis include two regimens, IFN or antiviral nucleoside/nucleotide analogues such as lamivudine, adefovir dipivoxil, and ribavirin.4,5 IFN or lamivudine alone can control hepatitis B in about one-third of patients.4,6 A combination of IFN with ribavirin is standard therapy for hepatitis C and has resulted in . . . [Full Text of this Article]


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