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After taking paracetamol regularly in therapeutic doses, a non-cirrhotic alcoholic subject developed hepatic necrosis and acute renal failure. This case is compared with 13 others found in the literature, and the clinical, biochemical and histological characteristics of such accidents are described. The severity of the acute renal failure is proven by the fact that 50% of the patients had to be put under dialysis. The potentiation of acetaminophen renal and hepatic toxicity by alcohol toxicity is discussed. The principal mechanism of enhancement is the activation of the cytochrome P 450 system associated with depletion of intracellular glutathione.
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