Abstract

Paracetamol is partially transformed in the liver to a toxic metabolite. The small amounts of this formed from a therapeutic dose are rapidly inactivated in the liver by reduced glutathione. When more than about 10 g of paracetamol has been taken glutathione is used up faster than it can be synthesised and the excess toxic metabolite causes hepatic necrosis. Less often it also causes acute renal tubular necrosis.¹