1st International AIDS Society Conference on HIV Pathogenesis and Treatment Buenos Aires, Argentina - July 8-11, 2001

[ABSTRACT:] Drug induced hepatotoxicity in HIV subjects has become of increasing importance in the era of HAART, especially with the high incidence of viral hepatitis and non alcoholic steatohepatitis in these subjects. Toxins can be classified based on presumed mechanism (direct injury or idiosyncratic, hypersensitivity or allergic reaction); on type of liver injury (cholestatic or cytotoxic or mixed); or by intrinsic toxicity versus host idiosyncracy. Intrinsic hepatotoxins cause reproducible injury, which is dose dependent (e.g. acteominophen or C-17 alkylated anabolic steroids). Idiosyncratic reactions in contrast, have a low incidence and result from drug allergy (sulfonamides) or toxic metabolites (isoniazid). Understanding in which category various drug belong, is of importance in evaluating the relative risk of certain agents and possible drug interactions. Fulminant hepatic failure has resulted from multiple drugs, including NSAIDS, lipid lowering agents, antibiotics (cephalexin, clindamycin), fluconazole, anti- tuberculous drugs, psychotropic medications and niacin. In addition, ecstasy, Chinese herbs and mushrooms have caused liver failure in some patients. In patients with pre-existing necroinflammatory disease HAART may be very difficult to manage. There is a high rate of discontinuation of certain drugs (NVP, EFV and DEL) because of toxicity. In addition, it is unclear when ALT rises, if it is due to the drug or underlying liver disease. Careful reporting of all abnormal LFTs and concommitant liver disease is necessary to determine the true incidence and early diagnosis of HAART induced heaptotoxicity.

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