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

Berghuis, B; de Haan, GJ; van den Broek, MP; Sander, JW; Lindhout, D; Koeleman, BP; (2016) Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia. European Journal of Neurology , 23 (9) pp. 1393-1399. 10.1111/ene.13069. Green open access

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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.

Type: Article
Title: Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia
Open access status: An open access version is available from UCL Discovery
DOI: 10.1111/ene.13069
Publisher version: http://dx.doi.org/10.1111/ene.13069
Language: English
Additional information: Copyright © 2016 EAN. This is the peer reviewed version of the following article: [Berghuis, B., de Haan, G.-J., van den Broek, M. P. H., Sander, J. W., Lindhout, D. and Koeleman, B. P. C. (2016), Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia. European Journal of Neurology, 23: 1393–1399. doi: 10.1111/ene.13069], which has been published in final form at http://dx.doi.org/10.1111/ene.13069. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
Keywords: antiepileptic drugs, drug treatment, epilepsy, sodium, vasopressin receptor 2
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Experimental Epilepsy
URI: https://discovery.ucl.ac.uk/id/eprint/1504767
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