Van Gelder N M, Sherwin A L, Sacks C, Anderman F
Brain Res. 1975 Aug 29;94(2):297-306. doi: 10.1016/0006-8993(75)90063-3.
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.
对12例癫痫患者的血浆和尿液进行氨基酸分析表明，血浆中牛磺酸和谷氨酸的浓度比预期的要高得多。这些患者尿液中的谷氨酸也有所增加。口服牛磺酸除了对谷氨酸水平有影响外，对血浆或尿液中的氨基酸水平没有明显影响。在血浆谷氨酸浓度异常的患者中，给予牛磺酸会使谷氨酸水平朝着正常值方向变化，同时该氨基酸的尿排泄量减少。牛磺酸的这种作用与其初始或最终血浆浓度无关。脑脊液中的氨基酸浓度在正常范围内，不受牛磺酸给药的影响。血浆中牛磺酸和谷氨酸的选择性升高，再加上之前在人类和实验性致痫脑内发现这些相同氨基酸缺乏，这意味着一些癫痫患者可能存在牛磺酸和谷氨酸代谢异常。给予牛磺酸似乎可以部分纠正这些生化异常。从理论上讲，致痫脑内氨基酸谱的这种正常化可能是有益的，但临床改善迹象可能要经过很长时间才会显现。本研究仅旨在确定与给予牛磺酸相关的生化参数，关于该氨基酸对癫痫的临床疗效无法得出明确结论。然而，本研究表明，在未来研究牛磺酸作为抗癫痫药物潜在用途的临床试验中，牛磺酸的口服剂量不应超过1.0克/天，最佳剂量可能低至0.1 - 0.5克/天。在一名每天接受2.0 - 2.5克牛磺酸，持续2周的患者中，出现了全身性氨基酸尿。
