SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Human & Experimental Toxicology
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Pendlebury, S.C.
Right arrow Articles by Eadie, M.J.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Pendlebury, S.C.
Right arrow Articles by Eadie, M.J.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Hyponatraemia during Oxcarbazepine Therapy

S.C. Pendlebury

Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia

D.K. Moses

Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia

M.J. Eadie

Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia

A clinical and pharmacokinetic study was carried out progressively substituting a new anticonvulsant oxcarbazepine for its congener carbamazepine in a group of patients with refractory epilepsy. Although oxcarbazepine showed possible though not statistically significant advantages of better seizure control and was probably less sedating, its use was associated with a dose-dependent reduction in plasma sodium levels in 12 of 15 patients. The mean plasma sodium level fell from 137.5 ± 5.2 (s.d.) to 128.5 ± 6.1 mE/1. Imposed restriction of fluid intake may have minimized the degree of hyponatraemia. This adverse effect may limit the role of the drug as an anticonvulsant or necessitate special precautions when it is used. However, the possibility of employing the drug in diabetes insipidus may be worth exploring.

Human & Experimental Toxicology, Vol. 8, No. 5, 337-344 (1989)
DOI: 10.1177/096032718900800501


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




Advertisement