Clearance of hepatitis B surface antigen and risk of hepatocellular carcinoma in a cohort chronically infected with hepatitis B virus

Authors

  • Josephine Simonetti,

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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  • Lisa Bulkow,

    1. Arctic Investigations Program, National Center for Preparedness, Detection and Control of Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK
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  • Brian J. McMahon,

    Corresponding author
    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
    2. Arctic Investigations Program, National Center for Preparedness, Detection and Control of Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK
    • Liver Disease and Hepatitis Program, Alaska Native Tribal Health Consortium, 4315 Diplomacy Drive, Anchorage, AK 99508
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    • fax: 907-729-3429.

  • Chriss Homan,

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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  • Mary Snowball,

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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  • Susan Negus,

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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  • James Williams,

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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  • Stephen E. Livingston

    1. Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium, Anchorage, AK
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Errata

This article is corrected by:

  1. Errata: Correction Volume 62, Issue 4, 1330, Article first published online: 7 August 2015

  • Potential conflict of interest: Nothing to report.

Abstract

Some individuals who are chronically infected with hepatitis B virus (HBV) eventually lose hepatitis B surface antigen (HBsAg). Hepatocellular carcinoma (HCC) has been demonstrated to occur in a few patients after loss of HBsAg. Neither factors associated with loss of HBsAg nor the incidence of HCC thereafter have been clearly elucidated. We performed a prospective population-based cohort study in 1,271 Alaska Native persons with chronic HBV infection followed for an average of 19.6 years to determine factors associated with loss of HBsAg and risk of developing HCC thereafter. HBsAg loss occurred in 158 persons for a rate of HBsAg clearance of 0.7%/year. Older age, but not sex, was associated with clearance of HBsAg, and loss of HBsAg was not associated with any particular HBV genotypes (A, B, C, D, and F) found in this population. Participants were followed for an average of 108.9 months after HBsAg loss. Six patients, two with cirrhosis and four without, developed HCC a mean of 7.3 years after HBsAg clearance (range, 2.0–15.5 years). The incidence of HCC after clearance of HBsAg was 36.8 per 100,000 per year (95% CI 13.5–80.0) which was significantly lower than the rate in those who remained HBsAg-positive (195.7 cases per 100,000 person-years of follow-up [95% CI 141.1–264.5; P < 0.001]). After loss of HBsAg, HBV DNA was detected in the sera of 28 (18%) of those who cleared a median of 3.6 years after clearance. Conclusion: HCC can occur in persons with chronic hepatitis B who have lost HBsAg, even in the absence of cirrhosis. These persons should still be followed with periodic liver ultrasound to detect HCC early. (HEPATOLOGY 2010.)

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