Abstract
To paraphrase the Swiss philosopher and physician Paracelsus: only the dose differentiates a poison from a remedy. Paracetamol is not an exception to this rule. At therapeutic doses paracetamol is relatively benign, but when it is ingested in excessive amounts endogenous hepatic glutathione is depleted and the toxic metabolite of paracetamol (N-acetyl- p-benzoquinoneimine) binds covalently with hepatocytes causing cellular death and hepatic necrosis.2 In 1991-5 paracetamol exposure was the most common incident reported to American …

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