A theoretical approach to the management of paracetamol overdosage.
Possible ways of treating paracetamol hepatotoxicity are briefly reviewed. This toxicity appears to be due to an oxidation metabolite which is normally detoxified by conjugation with glutathione, but when in excess, as in paracetamol overdosage, binds covalently to hepatic proteins to cause liver necrosis. Depletion of hepatic glutathione may also lead to other contributory disorders of cellular metabolism. Physical methods of preventing this would appear to be of little value, and treatments are being developed which aim to lessen the production of the toxic metabolite, antagonize its attachment to hepatic tissue or to combat this toxicity via basic cellular mechanisms. At this moment the most effective substances appear to be glutathione precursors and other compounds which interfere with oxidation of paracetamol.
D000082:Acetaminophen / Q000378:metabolism / Q000506:poisoning*; D002606:Charcoal / Q000627:therapeutic use; D003543:Cysteamine / Q000627:therapeutic use; D004358:Drug Therapy; D005978:Glutathione / Q000627:therapeutic use; D006801:Humans; D010477:Perfusion; D011433:Propranolol / Q000627:therapeutic use; D006435:Renal Dialysis; D013438:Sulfhydryl Compounds / Q000627:therapeutic use
D013438:Sulfhydryl Compounds; D002606:Charcoal; D000082:Acetaminophen; D003543:Cysteamine; D011433:Propranolol; D005978:Glutathione