Oxcarbazepine
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Reactions 407 - 27 Jun 1992 S Oxcarbazepine Hyponatraemia and cerebral ischaemia: case report Hyponatraemic coma developed in a 50-year-old woman receiving oxcarbazepine for the treatment of epilepsy. Four weeks after the initiation of oxcarbazepine 1800 mg/day, seizure control in the patient was unsatisfactory and her serum sodium concentration, which had been normal 2 days before the initiation of oxcarbazepine, was lowered to 128 mmol/l. In the following 7 months, the dosage of oxcarbazepine was increased to 2400mg; however, nausea and vomiting occurred. The dosage of oxcarbazepine was changed to 2100mg (34 mg/kg), and barbexaclone and clobazam were added to the patient’s regimen leading to complete abolition of seizures. Her serum sodium concentrations were always between 125-130 mmol/l. Approximately 10 months after the initiation of oxcarbazepine, the patient’s mother retrospectively reported progressive retardation, loss of interest and fluctuating confusion in the patient The patient was admitted 5-6 weeks later fluctuating between somnolence and coma. She had a slight motor paresis on the right side which corresponded with a cerebral ischaemic lesion and a serum sodium concentration of 115 mmol/l. Oxcarbazepine was discontinued immediately and the serum sodium concentration had increased to 131 mmol/l after 2 days. On the third day after admission the clinical status of the patient had normalised, except for the slight paresis. Author comment:Only 1 other case of hyponatraemia with clinically relevant symptoms has previously been reported in a 54-year-old woman receiving oxcarbazepine 46 mg/kg. ’We therefore believe that older patients with a high daily OXC oxcarbazepine dosage have an increased risk of developing hyponatremia.’ Steinhoff BJ, et al. Hyponatremic coma under oxcarbazepine therapy. Epilepsy Research 11: 67-70, Mar 1992 - 800142233 1 Reactions 27 Jun 1992 No. 407 0114-9954/10/0407-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Oxcarbazepine
Reactions 407 - 27 Jun 1992
SOxcarbazepine
Hyponatraemia and cerebral ischaemia: case reportHyponatraemic coma developed in a 50-year-old woman
receiving oxcarbazepine for the treatment of epilepsy.Four weeks after the initiation of oxcarbazepine 1800
mg/day, seizure control in the patient was unsatisfactory andher serum sodium concentration, which had been normal 2days before the initiation of oxcarbazepine, was lowered to128 mmol/l.
In the following 7 months, the dosage of oxcarbazepine wasincreased to 2400mg; however, nausea and vomitingoccurred. The dosage of oxcarbazepine was changed to2100mg (34 mg/kg), and barbexaclone and clobazam wereadded to the patient’s regimen leading to complete abolition ofseizures. Her serum sodium concentrations were alwaysbetween 125-130 mmol/l.
Approximately 10 months after the initiation ofoxcarbazepine, the patient’s mother retrospectively reportedprogressive retardation, loss of interest and fluctuatingconfusion in the patient The patient was admitted 5-6 weekslater fluctuating between somnolence and coma. She had aslight motor paresis on the right side which corresponded witha cerebral ischaemic lesion and a serum sodium concentrationof 115 mmol/l. Oxcarbazepine was discontinued immediatelyand the serum sodium concentration had increased to 131mmol/l after 2 days. On the third day after admission theclinical status of the patient had normalised, except for theslight paresis.
Author comment:Only 1 other case of hyponatraemia withclinically relevant symptoms has previously been reported in a54-year-old woman receiving oxcarbazepine 46 mg/kg. ’Wetherefore believe that older patients with a high daily OXCoxcarbazepine dosage have an increased risk of developinghyponatremia.’Steinhoff BJ, et al. Hyponatremic coma under oxcarbazepine therapy. EpilepsyResearch 11: 67-70, Mar 1992 - 800142233
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Reactions 27 Jun 1992 No. 4070114-9954/10/0407-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
