Hyperglycaemia induced by paracetamolSir, 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 A 61 -year-old man was admitted because of uncontrollable seizures. His past medical history was irrelevant except for epilepsy diagnosed at the age of 30, and a progressive decline in mental functions in the last two years, to the point that he was unable to perform everyday tasks. On physical examination he was in apparent good health but apathetic and incoherent, he had no dysmorphic features, and his heart, lungs, abdomen, extremities, and neurologic examination were normal. Every five or ten minutes he suffered brief generalised tonicoclonic convulsive attacks, without complete loss of consciousness or urinary incontinence, that responded poorly to anticonvulsant therapy.Blood analysis revealed a moderate leucocytosis with left deviation, calcium 5.5 mg/dl (albumin 3.7 g/dl), phosphate 4.8 mg/dl, intact parathyroid hormone 1.2 pg/ml, creatine kinase 2220 U/1, alanine aminotransferase 190 U/1, aspartate aminotransferase 121 U/1 and lactic dehydrogenase 435 U/1. An electrocardiogram showed a prolonged QT interval. Radiographs of the chest were normal. A computed tomographic scan of the brain disclosed calcifications, particularly in the basal ganglia.When blood calcium levels were received, an intravenous calcium infusion was instituted and the convulsive attacks ceased. Oral calcium and vitamin D were then initiated. In the following weeks his mental functions moderately improved and he began to perform some daily activities by himself.Symptoms of IH usually begin in childhood, but sometimes appear later. Epilepsy was probably the first manifestation of IH in our patient, but his illness was not diagnosed until the age of 61, when dementia, probably related to brain calcifications,2 had developed. IH is one of the few causes of reversible dementia, but other cases3 and ours show that adequate treatment may not produce complete recovery of mental functions. This emphasises the importance of an early diagnosis.As in other cases of IH,46 serum muscle enzymes were increased in our patient, probably as a consequence of rhabdomyolysis secondary to hypocalcemia and/or recurrent seizures.6'7 B ROCA C MINGUEZ
