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