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Clinical Specialist Department of Neurology Annunziata Hospital Cosenza, Italy
Clinical Specialist Department of Neurology Annunziata Hospital
Clinical Specialist Department of Neurology Annunziata Hospital
Assistant Chair of Pharmacology Department of Experimental and Clinical Medicine Faculty of Medicine and Surgery University Magna Graecia of Catanzaro Regional Pharmacovigilance Center Mater Domini University Hospital Catanzaro, Italy
Full Professor Chair of Pharmacology Department of Experimental and Clinical Medicine Faculty of Medicine and Surgery University Magna Graecia of Catanzaro Regional Pharmacovigilance Center Mater Domini University Hospital Via T. Campanella 115 88100 Catanzaro, Italy fax 390961774424 desarro{at}unicz.it
Published Online, January 23, 2004. www.theannals.com, DOI 10.1345/aph.1D437
Case Report. A 64-year-old woman (weight 60 kg) with a 20-year history of complex partial seizures of unknown etiology being treated with oxcarbazepine 30 mg/kg/day (1800 mg/day) was admitted to our hospital for routine control. Baseline electroencephalography (EEG) disclosed mild, generalized, background alpha activity. Two months later, she was prescribed furosemide 25 mg/day for mild hypertension (165/95 mm Hg); there were no other disease states interfering with electrolytes.
About one month after the start of furosemide treatment, the woman presented with confusion, a hallucinatory phenomenon (auditory, visual), and delirium. She was not receiving medications other than oxcarbazepine and furosemide. Blood tests showed a significant decrease in sodium and chloride values, 115 mEq/L and 81 mEq/L, respectively (before oxcarbazepine treatment, the sodium level was 140 mEq/L, chloride was 100 mEq/L; before furosemide treatment, sodium was 138 mEq/L, chloride was 99 mEq/L).
Computed tomography of the brain was normal. Magnetic resonance imaging was not performed because of the cardiac pacemaker worn by the patient. An EEG disclosed theta activity mixed with activity at 14-15 Hz and isolated sharp waves bilaterally (Figure 1A). The seizure activity did not worsen during concomitant treatment using oxcarbazepine and furosemide. Therefore, those agents were immediately discontinued and substituted with valproic acid 1 g/day and amlodipine 10 mg/day.
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After 20 days, the patient was oriented, without hallucinatory phenomenon and delirium, and the serum sodium and chlorium returned to normal values. An EEG disclosed mild, generalized, background alpha activity mixed with theta activity of medium amplitude bilaterally on the temporal-occipital derivation (Figure 1B). During follow-up, performed 6 months later, we recorded complete remission of neurologic manifestations and a normalization of her baseline EEG, as well as sodium and chloride values. Use of the Naranjo probability scale indicated a probable relationship between neurologic manifestations and concomitant use of oxcarbazepine plus furosemide.3
Discussion. The mechanism responsible for hyponatremia in treatment with oxcarbazepine is complex and unclear. It is known, however, to include direct and/or indirect action on kidney osmoceptors.1,4 One study indicated that hyponatremia induced by oxcarbazepine is more likely attributable to a direct effect on kidney-collecting tubules or enhancement of their responsiveness to circulating antidiuretic hormone rather than inappropriate secretion of antidiuretic hormone syndrome.4 Indeed, older patients and patients in concomitant treatment with natriuretic drugs showed a higher risk of hyponatremia induced by oxcarbazepine.1,2 Different clinical studies showed that most cases of hyponatremia had no clinical relevance.1 On the contrary, Nielsen et al.5 demonstrated that high doses of oxcarbazepine induced hyponatremia with clinical symptoms.
Based on our experience, we believe that careful monitoring of electrolytes is required when furosemide is administered to older patients with epilepsy treated with oxcarbazepine.
References
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