Acetaminophen hepatotoxicity.
Acetaminophen hepatotoxicity.
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DOI:
10.1016/0016-5085(80)90593-4
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发表时间:
1980
期刊:
影响因子:
29.4
通讯作者:
M. Black
中科院分区:
文献类型:
--
作者:
M. Black
Over the past five or more years, laboratory and clinical investigations aimed at elucidating the pathogenesis of acetaminophen-induced liver-cell necrosis have achieved a striking degree of success in considerably resolving the biochemical mechanisms involved, and they have identified novel therapeutic approaches to the management of the disorder. Fortuitously, these investigations have also served a number of purposes beyond their primary objectives. They have been singularly responsible for opening lines of communication between biomedical scientists whose paths had infrequently crossed previously. General internists, gastroenterologists, clinical hepatologists, pharmacologists, toxicologists, experimental pathologists, chemists, biochemists, pharmacists, and others from allied fields have increasingly sought each other’s counsel as the available information on acetaminophen hepatotoxicity extended beyond their respective areas of expertise. The lessons learned from acetaminophen hepatotoxicity also may affect the future way gastroenterologists and other internists view interactions between drugs and the liver. In the wake of the acetaminophen experience, it appears less likely that drug-induced liver injury will be as readily written off as an entirely unpredictable immunologic event whose experimental pathology resides in circulating or tissue-bound immune complexes containing the offending drug in some form or other, and whose therapy inexorably includes corticosteroids. Modern day drugs are now being recognized as often-potent compounds whose toxicities (as well as their actions) in many cases result from a chemical reaction between the drug (or metabolite) and structures(receptors) within a cell. The time may have come when Hyman Zimmerman’s message on