| Literature DB >> 807299 |
N M Van Gelder, A L Sherwin, C Sacks, F Anderman.
Abstract
Amino acid analysis of plasma and urine obtained from 12 patients with epilepsy indicated that the plasma concentrations of taurine and glutamic acid were much higher than might have been expected. Glutamic acid in urine was also increased in these patients. Oral administration of taurine did not appreciably affect the levels of amino acids in plasma or urine with the exception of that of glutamic acid. In patients with an abnormal plasma concentration of glutamic acid, the administration of taurine caused glutamic acid levels to change in the direction of normal values along with a decrease in the urinary excretion of this amino acid. This action of taurine was independent of either its initial or final plasma concentration. Amino acid concentrations in the CSF were within normal range and were not influenced by taurine administration. The selective elevation of both taurine and glutamic acid in the plasma, combined with previous findings of a deficiency of these same amino acids in human and experimental epileptogenic brain, implies that some patients with epilepsy may suffer from an aberration in taurine and glutamic acid metabolism. Taurine administration appears to partially correct these biochemical abnormalities. Theoretically, such normalization of the amino acid profile in epileptogenic brain may be beneficial, but clinical signs of improvement may only become apparent after a long delay. The present study was designed to determine only the biochemical parameters implicated in taurine administration and no definite conclusions can be drawn as to the clinical efficacy of the amino acid in epilepsy. However, this study suggests that in future clinical trials investigating the potential use of taurine as an antiepileptic agent, the oral dose of taurine should not exceed 1.0 g/day and optimal doses may be as low as 0.1-0.5 g/day. In one patient who received 2.0-2.5 g of taurine/day for 2 weeks, a generalized amino aciduria occurred.Entities:
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Year: 1975 PMID: 807299 DOI: 10.1016/0006-8993(75)90063-3
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252