Long-term clinical and histopathological follow-up of chronic posttransfusion hepatitis

Authors

  • Adrian M. di Bisceglie M.D.,

    Corresponding author
    1. Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    • Liver Diseases Section, Building 10, Room 4D 52, National Institutes of Health, Bethesda, MD 20892
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  • Zachary D. Goodman,

    1. Department of Hepatic and Gastrointestinal Pathology, Armed Forces Institute of Pathology, Washington, D.C. 20306-6000
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  • Kamal G. Ishak,

    1. Department of Hepatic and Gastrointestinal Pathology, Armed Forces Institute of Pathology, Washington, D.C. 20306-6000
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  • Jay H. Hoofnagle,

    1. Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
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  • Jacqueline J. Melpolder,

    1. Immunology Section, Department of Transfusion Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892
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  • Harvey J. Alter

    1. Immunology Section, Department of Transfusion Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892
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Abstract

We have evaluated the clinical and histopathological outcomes of patients who contracted chronic non A, non B hepatitis as a result of transfusions administered during heart surgery at the National Institutes of Health. Posttransfusion hepatitis developed in 65 of 1,070 (6.1%) patients and became chronic in 45 (69%) of those cases. Antibody to hepatitis C virus was detectable in 53 patients (82%) with posttransfusion non A, non B hepatitis. Thirty-three patients with chronic non A, non B hepatitis agreed to liver biopsy (group 1). In addition, six other patients with chronic posttransfusion non A, non B hepatitis were evaluated (group 2). These 39 patients were followed between 1 and 24 yr (mean = 9.7 yr). Cirrhosis developed in 8 patients (20%) between 1.5 and 16 yr after blood transfusion. Of the 33 patients in group 1, 11 (33%) died during follow-up. In two cases (6%), this was related to liver failure. At this writing, two additional patients (6%) have decompensated cirrhosis and one (3%) has debilitating fatigue. Twenty of 33 patients (61%) with histological evidence of chronic active hepatitis or cirrhosis are asymptomatic and have no clinical evidence of liver disease.

Thus chronic non A, non B posttransfusion hepatitis appeared to be due to hepatitis C virus infection in most cases. It was associated with the development of cirrhosis in approximately 20% of cases and end-stage liver disease in 12% of patients followed prospectively. Most patients with histological evidence of cirrhosis or chronic active hepatitis, however, had minimal clinical evidence of liver disease within the time frame of this study. (HEPATOLOGY 1991;14:969–974.)

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