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

• Published in: European journal of neurology Vol. 23; no. 9; pp. 1393 - 1399
• Main Authors: Berghuis, B., de Haan, G.-J., van den Broek, M. P. H., Sander, J. W., Lindhout, D., Koeleman, B. P. C.
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01-09-2016; John Wiley & Sons, Inc
• Subjects: Animals; Anticonvulsants - adverse effects; antiepileptic drugs; Carbamazepine - adverse effects; Carbamazepine - analogs & derivatives; drug treatment; epilepsy; Humans; Hyponatremia - chemically induced; Hyponatremia - epidemiology; Hyponatremia - genetics; Hyponatremia - physiopathology; Pharmacogenetics; sodium; vasopressin receptor 2; epilepsy; antiepileptic drugs; sodium; vasopressin receptor 2; drug treatment
• ISSN: 1351-5101; 1468-1331
• DOI: 10.1111/ene.13069

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.