{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T18:43:38Z","timestamp":1791053018869,"version":"4.1.0"},"reference-count":15,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[1989,9,1]],"date-time":"1989-09-01T00:00:00Z","timestamp":620611200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Human Toxicology"],"published-print":{"date-parts":[[1989,9]]},"abstract":"<jats:p>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 \u00b1 5.2 (s.d.) to 128.5 \u00b1 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.<\/jats:p>","DOI":"10.1177\/096032718900800501","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T01:08:04Z","timestamp":1230080884000},"page":"337-344","source":"Crossref","is-referenced-by-count":52,"title":["Hyponatraemia during Oxcarbazepine Therapy"],"prefix":"10.1177","volume":"8","author":[{"given":"S.C.","family":"Pendlebury","sequence":"first","affiliation":[{"name":"Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.K.","family":"Moses","sequence":"additional","affiliation":[{"name":"Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.J.","family":"Eadie","sequence":"additional","affiliation":[{"name":"Neuropharmacology and Drug Metabolism Laboratory, Department of Medicine, University of Queensland, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1989,9,1]]},"reference":[{"key":"atypb1","unstructured":"Baltzer V. & Schmutz H. 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