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The study of acetaminophen toxicity by Kuffner et al¹ may underestimate the actual risk in alcoholic patients. Depletion of hepatic glutathione and induction of P450-CYP2E1 are the most important factors that predispose to acetaminophen toxicity. Fasting and malnutrition further decrease hepatic glutathione and contribute to acetaminophen toxicity.² In contrast, acute ethanol exposure does not appear to be a predisposing factor to acetaminophen toxicity.

The impact of alcohol on acetaminophen toxicity reflects the duration and degree of the alcohol abuse. However, the study by Kuffner et al excludes the alcoholic subjects who are likely to be at highest risk. Patients with aspartate aminotransferase or alanine aminotransferase values greater than 120 U/L were excluded. In addition, only 24% of the study population had been actively drinking for more than 6 months; more than 50% had been actively drinking for 4 weeks or less, and half of these had been actively drinking less . . . [Full Text of this Article]

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Arch Intern Med. 2001;161(18):2247-2252.
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