Paracetamol is metabolised by multiple pathways: urinary excretion of an oral dose is 55% as glucuronide conjugates, 30% as cysteine conjugates, 4% as mercapturic acid and cysteine conjugates (3). The mercapturic and cysteine conjugates are derived from a toxic intermediary metabolite, produced by oxidative metabolism by CYP2E1, and to a lesser degree CYP3A4 and CYP1A2 (4). At doses of up to 1500 mg the metabolism appears to be unchanged but there is no data for doses at or above 90 mg/kg (5). It has been proposed that paracetamol metabolism becomes saturated at higher doses and saturation of sulfation has been observed in rats (6). However saturation of either sulfation or glucuronidation has not been observed in cultured human hepatocytes (6).