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Journal of Clinical Microbiology, June 2009, p. 1830-1836, Vol. 47, No. 6
0095-1137/09/$08.00+0     doi:10.1128/JCM.00029-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Evaluation of Impact of Serial Hepatitis B Virus DNA Levels on Development of Hepatocellular Carcinoma {triangledown}

Henry Lik-Yuen Chan,* Vincent Wai-Sun Wong, Grace Lai-Hung Wong, Angel Mei-Ling Chim, Larry Hin Lai, and Joseph Jao-Yiu Sung

Department of Medicine and Therapeutics and Institute of Digestive Disease, The Chinese University of Hong Kong, Shatin, Hong Kong

Received 6 January 2009/ Returned for modification 30 March 2009/ Accepted 10 April 2009

We aimed to investigate the impact of hepatitis B virus (HBV) DNA on the development of hepatocellular carcinoma (HCC). We conducted a case/control study based on 506 chronic HBV patients followed up since 1997. Forty-one patients developed HCC, and each of them was age and gender matched with two simultaneously recruited controls without HCC. HBV DNA was measured at the initial visit, at yearly intervals, and at the last visit. Patient age at the time of HCC development was 55 ± 9 years. Forty-nine (40%) patients experienced antiviral treatment. The median time from diagnosis to the development of HCC was 17 months, and the control patients were followed for 92 months. At the trough level (defined as lowest level among all studied visits), more (27 patients; 66%) HCC patients had HBV DNA levels of >10,000 copies/ml than the controls (17 patients; 21%). The area under the receiver operating characteristic curve of the trough log HBV DNA level for HCC was 0.79 (95% confidence interval [CI], 0.69 to 0.89). Trough log HBV DNA (odds ratio, 11.4; 95% CI, 3.6 to 37.6; P < 0.0001) and liver cirrhosis (odds ratio, 11.4; 95% CI, 3.6 to 36.2; P < 0.0001) levels were independently associated with HCC after an adjustment for age, gender, antiviral treatment, and HBV genotype. The difference in the trough HBV DNA level was more obvious among untreated patients (5.7 ± 1.4 log copies/ml in HCC patients versus 3.2 ± 1.3 log copies/ml in control patients; P < 0.0001) than among those who had received antiviral treatment (3.0 ± 1.4 log copies/ml in HCC patients versus 2.5 ± 0.9 log copies/ml in control patients; P = 0.38). A high trough HBV DNA level was associated with a higher risk of HCC. Whether antiviral treatment could prevent HCC was uncertain.

* Corresponding author. Mailing address: Department of Medicine and Therapeutics, 9/F Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, Hong Kong. Phone: 852-26323593. Fax: 852-26373852. E-mail: hlychan{at}cuhk.edu.hk

{triangledown} Published ahead of print on 22 April 2009.

Journal of Clinical Microbiology, June 2009, p. 1830-1836, Vol. 47, No. 6
0095-1137/09/$08.00+0     doi:10.1128/JCM.00029-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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