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卡马西平和奥卡西平所致低钠血症的流行病学、病理生理学及推测的遗传基础

Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia.

作者信息

Berghuis B, de Haan G-J, van den Broek M P H, Sander J W, Lindhout D, Koeleman B P C

机构信息

Stichting Epilepsie Instellingen Nederland (SEIN), Zwolle, The Netherlands.

Department of Clinical Pharmacy, University Medical Center Utrecht, Utrecht, The Netherlands.

出版信息

Eur J Neurol. 2016 Sep;23(9):1393-9. doi: 10.1111/ene.13069. Epub 2016 Jun 23.

Abstract

The use of carbamazepine (CBZ) and oxcarbazepine (OXC) as first-line antiepileptic drugs in the treatment of focal epilepsy is limited by hyponatremia, a known adverse effect. Hyponatremia occurs in up to half of people taking CBZ or OXC and, although often assumed to be asymptomatic, it can lead to symptoms ranging from unsteadiness and mild confusion to seizures and coma. Hyponatremia is probably due to the antidiuretic properties of CBZ and OXC that are, at least partly, explained by stimulation of the vasopressin 2 receptor/aquaporin 2 pathway. No known genetic risk variants for CBZ- and OXC-induced hyponatremia exist, but likely candidate genes are part of the vasopressin water reabsorption pathway.

摘要

卡马西平(CBZ)和奥卡西平(OXC)作为治疗局灶性癫痫的一线抗癫痫药物,其使用受到低钠血症这一已知不良反应的限制。服用CBZ或OXC的人群中,高达一半会出现低钠血症,尽管通常认为其无症状,但它可导致从步态不稳、轻度意识模糊到癫痫发作和昏迷等一系列症状。低钠血症可能是由于CBZ和OXC的抗利尿特性,这至少部分是由血管加压素2受体/水通道蛋白2途径的刺激所解释的。目前尚无已知的与CBZ和OXC诱导的低钠血症相关的遗传风险变异,但可能的候选基因是血管加压素水重吸收途径的一部分。

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