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Serum Carnitine Levels During Oxcarbazepine and Carbamazepine Monotherapies / Kurul, Dirik, and Iscan
553
bazepine monotherapy and 20 patients (12 boys, 8 girls) with
might induce carnitine deficiency. It has been suggested
that antiepilepsy drugs inhibited mitochondrial ꢀ-oxida-
tion of fatty acids, and increased intermediate metabolites,
which are excreted in the urine as carnitine esters lead to
hypocarnitinemia.12 Camina and colleagues reported that the
deficiency of serum carnitine in patients treated with other
anticonvulsants was possibly attributable to their decreased
tubular resorption of free carnitine.11 Treatment of carnitine
deficiency in patients receiving antiepilepsy drug therapy is
debatable. It has been reported that patients at greatest
risk for carnitine deficiency were particularly young children
who were taking multiple antiepilepsy drugs, and it has
been suggested that the serum carnitine levels in these
patients need to be monitored and that carnitine should be
administered if the patient has laboratory or clinical evidence
of carnitine deficiency.7
Oxcarbazepine is essentially a keto analogue of car-
bamazepine. However, this small change in chemical struc-
ture confers a major change in metabolism. Unlike
carbamazepine, it is metabolized by reduction and might
not induce hepatic monoxygenase enzymes. Oxcarbazepine
is consistently as efficacious as carbamazepine in the
treatment of generalized tonic-clonic or partial seizures.19
Carnitine deficiency during carbamazepine therapy has
been demonstrated in some studies. However, it has not
been reported previously if oxcarbazepine might cause
carnitine deficiency. Although the sample size in our study
was small, our results suggest that neither oxcarbazepine
nor carbamazepine as monotherapy causes carnitine defi-
ciency in otherwise healthy children with primary idio-
pathic epilepsy.
newly diagnosed primary idiopathic epilepsy who were receiving
carbamazepine monotherapy were included in the study. The
selection criteria were good general condition, normal nutri-
tional status, no evidence of any congenital metabolic or hepatic
disease, no previous use of any antiepilepsy drug, and good intel-
lectual capability. Written and verbal information was provided
to the families, and consent was obtained before the study. Plasma
levels of total and free carnitine and routine biochemistry deter-
minations, including ammonia, glucose, electrolytes, liver func-
tion, and lactate and pyruvate levels, were performed between 3
and 6 months after the initiation of the anticonvulsive therapy. A
spectrophotometric assay was used to measure carnitine levels
in blood.16 Reference ranges for serum total and free carnitine were
between 24 and 97 ꢁmol/L for total carnitine and between 18 and
79 ꢁmol/L for free carnitine.16 Data were analyzed statistically with
the Mann-Whitney U-test.
RESULTS
The mean age of the patients treated with oxcarbazepine
monotherapy was 10.1 3.2 years (range 6–17 years) and
of those treated with carbamazepine monotherapy 9.6
3.1 years (range 6–16 years). There was no significant dif-
ference in age between the two groups (P = .758). Liver func-
tions and fasting plasma ammonia levels were normal in all
patients in both of the groups. The average daily dose of car-
bamazepine was 20 mg/kg and of oxcarbazepine 30 mg/kg.
During the study period, children in the carbamazepine
group had blood levels within the therapeutic range.
The mean values of serum total and free carnitine lev-
els in patients receiving carbamazepine monotherapy were
63.0 20.7 ꢁmol/L (range 32–90 ꢁmol/L) and 49.1 16.7
ꢁmol/L (range 25–78 µmol/L), respectively. The mean val-
ues of serum total and free carnitine levels in patients
receiving oxcarbazepine monotherapy were 64.2 17.4
ꢁmol/L (range 32.4–96 ꢁmol/L) and 50.3 13.7 ꢁmol/L
(range 25.9–77.8 ꢁmol/L), respectively. The values were all
between normal ranges. No significant difference was
observed in the level of total and free carnitine levels
between the two groups (P = .529, P = .862).
References
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