Hepatitis B viral loads in southern African Blacks with hepatocellular carcinoma

Authors

  • Raquel Viana,

    1. MRC/University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa
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  • Renwei Wang,

    1. Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota
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  • Mimi C. Yu,

    1. Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota
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  • Robert Welschinger,

    1. MRC/University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa
    2. Department of Medicine, Recipient of the Hillel Friedland Postdoctoral Fellowship, University of Witwatersrand Medical School, Johannesburg, South Africa
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  • Chien-Yu Chen,

    1. MRC/University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa
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  • Michael C. Kew

    Corresponding author
    1. MRC/University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa
    2. Department of Medicine, Groote Schuur Hospital, Cape Town, South Africa
    3. Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa
    • Department of Medicine, K Floor, Old Hospital Building, Groote Schuur Hospital, Main Road, Observatory 7925, Cape Town, South Africa.
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Abstract

Although viral loads are known to influence the development of hepatitis B virus-induced hepatocellular carcinoma in a number of populations, little information is available in the Black African population. Black African patients with hepatocellular carcinoma differ from those in other populations in having a lower frequency of e antigen-positivity and in other respects that might affect viral loads. Hepatitis B viral loads were measured using real-time polymerase chain reaction assay in 124 Black Africans with hepatocellular carcinoma and compared with those in 125 Black adult asymptomatic viral carriers. The geometric mean viral load in the cancer patients was 553,618 copies/ml (95% CI 301,953–1,015,033 copies/ml), with 62.1% having loads >1 × 105 copies/ml and 87.1% >1 × 104 copies/ml, whereas that in the carriers was 16,084 copies/ml (95% CI 9,184–28,168 copies/ml), with only 15.2% having values >1 × 105 copies/ml and 49.6% >1 × 104 copies/ml (P < 0.001 in each instance). Mean viral load was significantly higher in e antigen-positive than e antigen-negative cancer patients (5,905,357 copies/ml [1,362,847–25,588,520] cf 238,173 copies/ml [97,200–685,730]: P < 0.001) after adjusting for age and sex. No statistically significant difference existed between patients in different age groups, in men and women, or in patients infected with genotype A or D after adjusting for the other variables. Conclusion: Black Africans with hepatocellular carcinoma have high hepatitis B viral loads in spite of the relative infrequency of e antigen-positivity. J. Med. Virol. 81:1525–1530, 2009. © 2009 Wiley-Liss, Inc.

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