eprintid: 1504767 rev_number: 25 eprint_status: archive userid: 608 dir: disk0/01/50/47/67 datestamp: 2016-07-24 05:04:42 lastmod: 2021-10-02 00:00:14 status_changed: 2016-11-09 16:40:27 type: article metadata_visibility: show creators_name: Berghuis, B creators_name: de Haan, GJ creators_name: van den Broek, MP creators_name: Sander, JW creators_name: Lindhout, D creators_name: Koeleman, BP title: Epidemiology, pathophysiology and putative genetic basis of carbamazepine- and oxcarbazepine-induced hyponatremia ispublished: pub divisions: UCL divisions: B02 divisions: C07 divisions: D07 divisions: F81 keywords: antiepileptic drugs, drug treatment, epilepsy, sodium, vasopressin receptor 2 note: 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. 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. date: 2016-09 date_type: published official_url: http://dx.doi.org/10.1111/ene.13069 oa_status: green full_text_type: other language: eng primo: open primo_central: open_green article_type_text: Review verified: verified_manual elements_id: 1139991 doi: 10.1111/ene.13069 lyricists_name: Sander, Josemir lyricists_id: JWASS04 full_text_status: public publication: European Journal of Neurology volume: 23 number: 9 pagerange: 1393-1399 issn: 1468-1331 citation: 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 <https://doi.org/10.1111/ene.13069>. Green open access document_url: https://discovery.ucl.ac.uk/id/eprint/1504767/1/Berghuis%20Epidemiology%2C%20pathophysiology%20and%20putative%20genetic%20basis%20of%20carbamazepine-%20and%20oxcarbazepine-induced%20hyponatremia.pdf