Cocaine-induced liver cell injury: Comparison of morphological features in man and in experimental models

Authors

  • Gary C. Kanel M.D,

    Corresponding author
    1. Departments of Pathology and Hepatology, University of Southern California Liver Unit, Downey, California 90242
    • Liver Research and Education Foundation, Inc., Rancho Los Amigos Medical Center, Department of Pathology, 7705 Golondrinas-1200 Bldg., Downey, CA 90242
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  • William Cassidy,

    1. Departments of Pathology and Hepatology, University of Southern California Liver Unit, Downey, California 90242
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  • Louis Shuster,

    1. Department of Pharmacology, Tufts University School of Medicine, Boston, Massachusetts 02111
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  • Telfer B. Reynolds

    1. Departments of Pathology and Hepatology, University of Southern California Liver Unit, Downey, California 90242
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Abstract

Although investigative research of animal models in cocaine metabolism and associated liver cell injury has been fairly extensive during the past 10 yr, little evidence of hepatotoxicity has been documented in man. We report a case of fulminant hepatic failure and acute rhabdomyolysis resulting from cocaine use. Coagulative-type perivenular and midzonal necrosis and periportal microvesicular fatty change were the predominant morphological features throughout all lobules of the liver, in contrast to periportal necrosis described in the only previous case report with biopsy. Differences in zonal necrosis caused by the same drug are not typically seen in man experiencing direct or indirect intrinsic hepatotoxicity. However, experimental models have shown cocaine to have this ability, dependent on enzyme induction or inhibition, sex and dose. Therapeutic approaches for prevention of possible liver cell injury by cocaine toxicity are discussed.(HEPATOLOGY 1990; 11:646-651.)

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