Affiliations: Department of Pediatrics, Faculty of Medicine, Tanta
University, Tanta, Egypt | Department of Clinical Pathology, Faculty of Medicine,
Tanta University, Tanta, Egypt
Note: [] Correspondence: Sahar A. Abd El-Aziz, Assistant Professor of
Pediatric Neurology, Department of Pediatrics, Faculty of Medicine, Tanta
University, Tanta, Egypt. Tel.: +20 1002415438; E-mail:
[email protected], [email protected]
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.
Keywords: Carnitine, children, epilepsy, antiepileptic drug
