Recombinant leukocyte interferon treatment of chronic hepatitis B

Authors

  • Geoffrey Dusheiko M. D.,

    Corresponding author
    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
    • University of the Witwatersrand, Department of Medicine, York Road, Parktown 2193 Johannesburg, South Africa
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  • Adrian Dibisceglie,

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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  • Sheila Bowyer,

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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  • Evelyn Sachs,

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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  • Marian Ritchie,

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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  • Barry Schoub,

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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  • Michael Kew

    1. Department of Medicine, University of the Witwatersrand, Hillbrow and Baragwanath Hospitals and the National Institute of Virology, Johannesburg, South Africa
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Abstract

We have investigated the efficacy of a relatively prolonged course of recombinant leukocyte interferon treatment in 14 chronic HBsAg-, HBeAg-, hepatitis B virus DNA- and DNA polymerase-positive carriers. α-Interferon was administered for 9 weeks. Six of 14 treated carriers have a sustained loss of HBeAg, hepatitis B virus DNA and DNA polymerase. Four subsequently lost HBsAg (28.5%). Elevated pretreatment SGPT concentrations, histologic chronic active hepatitis, an exacerbation of chronic hepatitis with an increase in SGPT concentrations in the last weeks of treatment and possibly recent onset of the carrier state was associated with complete inhibition of viral replication. None of 11 matched, untreated HBsAg-, HBeAg-, hepatitis B virus DNA- and DNA polymerase-positive carriers monitored during the same period lost HBsAg. The effect of recombinant leukocyte interferon may require an appropriate host-immune response. The efficacy of recombinant leukocyte interferon therapy is restricted, but it may be of benefit in a proportion of carriers, if these carriers can be precisely identified.

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