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Carcinogenesis Advance Access published online on November 13, 2007
Carcinogenesis, doi:10.1093/carcin/bgm252
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Long-term tracking of hepatitis B viral load and the relationship with risk for hepatocellular carcinoma in men

Chih-Feng Wu1, Ming-Whei Yu1,*, Chih-Lin Lin2, Chun-Jen Liu3, Wei-Liang Shih1, Keh-Sung Tsai4 and Chien-Jen Chen5

1 Research Center for Genes, Environment and Human Health and Graduate Institute of Epidemiology, College of Public Health, National Taiwan University
2 Department of Gastroenterology, Ren-Ai Branch, Taipei City Hospital
3 Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine
4 Department of Laboratory Medicine, National Taiwan University Hospital
5 Genomics Research Center, Academia Sinica–all in Taipei, Taiwan

* To whom correspondence should be addressed: Ming-Whei Yu, Ph.D., Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Room 522 No.17, Xuzhou Road Zhongzheng District, Taipei City 10055, Taiwan. Fax: 886-2-23511955. E-mail: yumw{at}ntu.edu.tw.

Little is known about the longitudinal course of hepatitis B virus (HBV) load and its relationship with the development of hepatocellular carcinoma (HCC). We conducted a case-cohort study nested within a cohort of 2874 HBV surface antigen-positive male Taiwanese government employees aged 30 years or older. HBV genotype and DNA levels (i.e., viral load) were tested using polymerase chain reaction-based assays on plasma samples from 112 cases and 1031 noncases. Prediagnostic plasma levels of HBV DNA were measured in multiple samples collected from each man (total 7706 samples), taken over periods of up to 16 years before diagnosis. Baseline viral load influenced HBV genotype-specific HCC risks and predicted the persistence of high viral load (≥4.39 log copies/mL) that can cause HCC. Moderate to high tracking of viral load was observed within 9 years. Hepatitis B e antigen (P<0.0001), genotype C HBV infection (P=0.0369), and longitudinal alanine aminotransferase (ALT) elevation (defined as ALT abnormality in ≥50% of the visits) (P=0.0005) were positively related to longer duration of persistence for high viral load. After multivariate adjustment, HBV genotype C (odds ratio [OR]= 5.97, 95% confidence interval [CI]=3.44-10.34), high viral load detected at ≥50% of the visits (compared with sustained low viral load: OR=5.04, 95% CI=2.31-11.00), and longitudinal ALT elevation (compared with sustained normal ALT levels: OR=2.84, 95% CI=1.46-5.51) accounted for 43.5%, 57.2%, and 24.9% of HCCs, respectively. The results suggest that maintenance of viral load below 4.39 log copies/mL was associated with sustained normalization of ALT levels and decreased risk of HCC.

Key Words: DNA • genotype • HBeAg • hepatitis B virus • hepatocellular carcinoma

Received August 17, 2007; revised October 23, 2007; accepted November 4, 2007.


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