Coulter D L
Department of Pediatrics, Boston University School of Medicine, MA, USA.
J Child Neurol. 1995 Nov;10 Suppl 2:S32-9.
Numerous studies have shown that plasma carnitine levels are significantly lower in patients taking valproate than in controls. Free carnitine deficiency is not uncommon in these patients and also occurs in newborns with seizures and in patients taking other anticonvulsant drugs. Carnitine deficiency in epilepsy results from a variety of etiologic factors including underlying metabolic diseases, nutritional inadequacy, and specific drug effects. The relationship between carnitine deficiency and valproate-induced hepatotoxicity is unclear. Carnitine treatment does not always prevent the emergence of serious hepatotoxicity, but it does alleviate valproate-induced hyperammonemia. These studies suggest that specific risk factors for carnitine deficiency can be identified. Preliminary data suggest that carnitine treatment may benefit high-risk, symptomatic patients and those with free carnitine deficiency. Carnitine treatment is not likely to benefit low-risk, asymptomatic patients and those with normal carnitine levels.
大量研究表明,服用丙戊酸盐的患者血浆肉碱水平显著低于对照组。游离肉碱缺乏在这些患者中并不罕见,在癫痫新生儿以及服用其他抗惊厥药物的患者中也会出现。癫痫患者的肉碱缺乏由多种病因引起,包括潜在的代谢疾病、营养不足以及特定药物作用。肉碱缺乏与丙戊酸盐所致肝毒性之间的关系尚不清楚。肉碱治疗并不总能预防严重肝毒性的出现,但确实能减轻丙戊酸盐所致的高氨血症。这些研究表明,可以确定肉碱缺乏的特定风险因素。初步数据表明,肉碱治疗可能使高危、有症状的患者以及游离肉碱缺乏的患者受益。肉碱治疗不太可能使低危、无症状的患者以及肉碱水平正常的患者受益。