Hyperammonemic encephalopathy induced by a combination of valproate and pivmecillinam.

We describe the clinical and neurophysiological findings in a case of hyperammonemic encephalopathy. A 72-year-old woman taking valproate (VPA), as monotherapy for her partial epilepsy developed urinary tract infection. She was treated with pivmecillinam 600 mg daily. The following days she deteriorated and became stuporous. At admission her serum ammonia level was increased (113 mmol/l) but the liver function appeared normal. EEG showed bilateral triphasic waves and continuous high-amplitude delta-theta wave. The patient recovered rapidly after discontinuation of VPA and i.v. treatment with cefuroxime for her urinary tract infection. VPA-induced hyperammonemic encephalopathy in adults is a rare phenomenon, especially when VPA is used as monotherapy. It has been suggested that the VPA-induced hyperammonemic encephalopathy is due to reduced serum carnitine concentration. Pivmecillinam, a widely used antibiotic for treatment of urinary tract infections, is also known to decrease the serum carnitine concentration. Our case shows that caution is required when treatment with VPA is combined with pivmecillinam due to the risk of developing hyperammonemic encephalopathy.

Effects of central oxytocin administration on intraoral intake of glucose in deprived and nondeprived rats.

We evaluated the effects of lateral intracerebroventricular administration of oxytocin (OT) and/or a selective oxytocin-receptor antagonist (OTX), 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-OT, on ingestion of intraorally delivered 12.5% glucose in rats that were either nondeprived or deprived of food for 20 h. In deprived rats, OT delivered 30 min before an initial intake test yielded a dose-related reduction of intraoral glucose intake. The highest dose tested, 20 nmol, reduced intraoral glucose intake by 45%. The effect was short-lived, however. Intraoral intake for a second test, initiated 60 min after the termination of the first, increased as a function of OT dose so that total session intake was unaffected by OT treatment. The suppression of intraoral intake by 20 nmol OT was reversed by pretreatment (45 min before testing) with OTX. In nondeprived rats, by contrast, OT yielded no effect on first-test, second-test, or total session intakes. Significant increases in first-test and total session intakes were obtained when OTX (20 nmol) was administered alone both in deprived (32% increase in first-test intake) and nondeprived (31% increase) rats. In general, the results obtained are consistent with the suggestion that OT contributes to the control of meal size and, in particular, to the process of satiation, which is the aspect of ingestive control highlighted by the specialized intake test used in the present study.