Acetaminophen is one of the most commonly purchased medications in the United States and is sold on its own or in combination with other medications. Acetaminophen at therapeutic doses can be used as an antipyretic and analgesic. However, at toxic levels it can lead to hepatic injury and failure. Every year, approximately 30 000 patients are admitted to the hospital for treatment of acetaminophen toxicity. Almost 20% of liver transplant cases are directly related to acetaminophen hepatotoxicity.1 

Acetaminophen undergoes 2 types of metabolism after ingestion: (1) primarily (approximately 90%) through phase II conjugation via glucuronidation and sulfation to nontoxic metabolites, (2) in a minor pathway (approximately 10%), through phase I oxidation to form the toxic intermediate N-acetyl-p-benzoquinone imine (NAPQI), which then is detoxified by conjugation with glutathione to a nontoxic metabolite. The nontoxic metabolites are renally excreted. If acetaminophen is ingested at toxic doses, the glucuronidation and sulfation...

You do not currently have access to this content.