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Abstract 


Acetaminophen can produce potentially fatal liver necrosis, via an intermediate toxic metabolite. Hepatic injury usually requires acute ingestion of at least 10-15 g of the drug. The patient typically feels well for one to three days before evidence of liver damage appears. Striking elevation of aminotransferases is characteristic, reflecting acute hepatocellular necrosis. In non-fatal cases, recovery is usually rapid. Liver damage can be completely prevented by oral or IV N-acetylcysteine (Mucomyst), which blocks the effect of the toxic metabolite. However, treatment is effective only if given within eight to 12 hours of acetaminophen ingestion. Hence, prompt action by the physician can prevent acetaminophen liver necrosis.

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Can Fam Physician. 1985 Nov; 31: 2155-2156, 2158.
PMCID: PMC2327744
PMID: 21274134

Acetaminophen Liver Injury

Abstract

Acetaminophen can produce potentially fatal liver necrosis, via an intermediate toxic metabolite. Hepatic injury usually requires acute ingestion of at least 10-15 g of the drug. The patient typically feels well for one to three days before evidence of liver damage appears. Striking elevation of aminotransferases is characteristic, reflecting acute hepatocellular necrosis. In non-fatal cases, recovery is usually rapid. Liver damage can be completely prevented by oral or IV N-acetylcysteine (Mucomyst), which blocks the effect of the toxic metabolite. However, treatment is effective only if given within eight to 12 hours of acetaminophen ingestion. Hence, prompt action by the physician can prevent acetaminophen liver necrosis.

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Selected References

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