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

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

Research output: Contribution to journalArticleAcademicpeer-review

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.

Original languageEnglish
Pages (from-to)1393-1399
Number of pages7
JournalEuropean Journal of Neurology
Volume23
Issue number9
DOIs
Publication statusPublished - Sept 2016

Keywords

  • Antiepileptic drugs
  • Drug treatment
  • Epilepsy
  • Sodium
  • Vasopressin receptor 2

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