Hyperglycaemia induced by paracetamol.

Sir, Hypoglycaemia is a well-recognised feature of paracetamol overdose, after the development of fulminant hepatic failure, but we are aware of only one previous description of hyperglycaemia and that was in a patient with a family history of diabetes mellitus.' Over recent months we have seen five patients, all male, aged 17 to 40, who have had random blood sugars of 7.2-12.8 mmol/l (mean 9.1 mmol/l) at the time of their initial paracetamol level, taken 6-12 h after the overdose (paracetamol levels of 50-184 mg/l, mean 147 mg/l). Hepatic failure, but with full recovery, developed in two patients. None were known to have diabetes, although two had a family history of non-insulindependent diabetes mellitus. Paracetamol has previously been shown to interfere in glucose measurements,2 although YSI have modified their method and this is now less of a problem. However, none of the instruments used in the emergency laboratories in the Leicester area employ this method, and we investigated the spiking of sera with known glucose levels with paracetamol to see if the glucose results altered. Over a paracetamol concentration range of 10-400 mg/l, there was no change; thus paracetamol does not interfere with glucose measurements. It would thus appear that hyperglycaemia is a feature of a significant paracetamol overdose over the first 12 hours. Whether this is due to release of stress hormones or a direct effect of either paracetamol or its metabolites on the pancreas or liver is unclear. IG LAWRENCE