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

Publication date

2016-09

Authors

Berghuis, B
de Haan, G-J
van den Broek, MPHISNI 0000000393141939
Sander, J W
Lindhout, DickORCID 0000-0001-9580-624X
Koeleman, Bobby P.C.ORCID 0000-0001-7749-182XISNI 0000000391422868

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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.

Keywords

Antiepileptic drugs, Drug treatment, Epilepsy, Sodium, Vasopressin receptor 2, Journal Article, Review

Citation

Berghuis, B, de Haan, G-J, van den Broek, M P H, Sander, J W, Lindhout, D & Koeleman, B P C 2016, 'Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia', European Journal of Neurology, vol. 23, no. 9, pp. 1393-1399. https://doi.org/10.1111/ene.13069