Plasma carnitine levels in children with idiopathic epilepsy treated with old and new antiepileptic drugs

• Published in: Journal of pediatric neurology Vol. 10; no. 4; pp. 275 - 281
• Main Authors: Abd El-Aziz, Sahar A., El-Serogy, Hesham
• Format: Journal Article
• Language: English
• Published: New York Georg Thieme Verlag KG 01.12.2012; Stuttgart Thieme Medical Publishers Inc
• Subjects: Age; Antiepileptic agents; Carbamazepine; Carnitine; Children; Epilepsy; Family medical history; Fatty acids; lamotrigine; Metabolic disorders; Metabolism; Mitochondria; Neurology; oxcarbazepine; Pediatrics; Plasma; Studies; Valproic acid; epilepsy; antiepileptic drug; children; Carnitine
• ISSN: 1304-2580; 1305-0613; 1875-9041
• DOI: 10.3233/JPN-120582

Abstract Prolonged antiepileptic drugs (AEDs) treatment can result in secondary carnitine deficiency. Clinical studies indicate a decrease in free and total carnitine levels in children treated with old-generation AEDs (especially valproate). A number of studies on the effect of valproic acid and/or other AEDs on carnitine concentrations yielded contradictory results. The effect of new AEDs as oxcarbazepine and lamotrigine on carnitine metabolism has not been reported previously. The aim of this study was to evaluate the plasma carnitine level in children with idiopathic epilepsy treated with old AEDs (valproic acid and carbamazepine) and new AEDs (lamotrigine and oxcarbazepine). Fifty children with newly diagnosed idiopathic epilepsy were selected from those attending the pediatric neurology out-patient clinic at Tanta University Hosptial. Thirty-four males and 16 females were enrolled in the study with the mean age was (6.8 ± 3.1 yr). Patients were grouped according to their antiepileptic treatment into: group 1, 20 patients received valproic acid as monotherapy with no prior AEDs use. Group 2, 10 patients received valproic acid as polytherapy after 3 mo treatment with carbamazepine. Group 3, 10 patients received lamotrigine as monotherapy, and group 4, 10 patients received oxcarbazepine as monotherapy. Twenty healthy children served as control group with mean age was (8.5 ± 2.3 yr). Estimation of the plasma carnitine levels were done for all the studied groups. Group 1 and group 2 epileptic children, treated with valproic acid monotherapy and polytherapy respectively had significantly lower plasma carnitine levels than that of the control group ( P < 0.05). There was significant correlation between the age and the plasma carnitine in group 1 and group 2 epileptic children, the younger the age the greater the reduction in the plasma carnitine levels. Patients treated with valproic acid polytherapy had significantly lower plasma carnitine levels than those of the patients treated with valproic acid monotherapy ( P < 0.05). There was no significant difference in the plasma carnitine levels between the controls and children with epilepsy treated with oxcarbazepine and lamotrigine ( P > 0.05). In conclusion, carnitine deficiency is not uncommon among children with epilepsy and is mainly linked to valproate therapy. In contrast, new-generation AEDs probably do not cause carnitine deficiency. These findings suggest a need to monitor serum carnitine levels in children treated with valproic acid therapy.