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NAPQI begins to accumulate once glutathione stores are depleted by about 70% Biochemical Basis of Acetaminophen Toxicity Liver damage due to excess NAPQI can occur in four circumstances Excessive intake of acetaminophen Excessive CYP2E1 activity due to induction by other drugs or chronic alcohol use Competition for conjugation enzymes Depletion of glutathione stores due to malnutrition or chronic alcohol ingestion Factors influencing toxicity Chronic alcoholics are at increased risk of developing severe hepatic disease even at therapeutic doses In contrast, acute alcohol ingestion is not a risk factor for hepatotoxicity and may even be protective by competing for CYP2E1 Alcohol acts at least in part by induction of CYP2E1, which results in enhanced generation of NAPQI Acetaminophen hepatotoxicity with regular intake of alcohol: analysis of instances of therapeutic misadventure The report describes 67 patients who developed hepatic injury after ingestion of APAP with therapeutic intent

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