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Carcinogenesis Advance Access originally published online on November 13, 2007
Carcinogenesis 2008 29(1):106-112; 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 Wu, Ming-Whei Yu*, Chih-Lin Lin1, Chun-Jen Liu2, Wei-Liang Shih, Keh-Sung Tsai3 and Chien-Jen Chen4

Research Center for Genes, Environment and Human Health and Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Xuzhou Road Zhongzheng District, Taipei 10055, Taiwan
1 Department of Gastroenterology, Ren-Ai Branch, Taipei City Hospital, Taipei 10629, Taiwan
2 Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei 10002, Taiwan
3 Department of Laboratory Medicine, National Taiwan University Hospital, Taipei 10002, Taiwan
4 Genomics Research Center, Academia Sinica, Taipei 11529, Taiwan

* To whom correspondence should be addressed. Tel: +886 2 33228031; Fax: +886 2 23511955; Email: 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 non-cases. 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 <4.39 log copies/ml was associated with sustained normalization of ALT levels and decreased risk of HCC.

Abbreviations: ALT, alanine aminotransferase; CI, confidence interval; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; OR, odds ratio; PAR, population attributable risk; PCR, polymerase chain reaction

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


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