Abstract
One-third of all individuals with epilepsy are resistant to antiepileptic drug (AED) treatment. Antiepileptic treatment response has been suggested to be modulated by genetic polymorphisms of drug efflux transporters. Several polymorphic variants within the multidrug resistance 1 (MDR1) gene, which encodes the major transmembrane efflux transporter P-glycoprotein, have been proposed to be associated with AED resistance in epilepsy patients. The aim of this study was to evaluate the effect of C3435T and G2677T/A polymorphisms of MDR1 on AED resistance in Turkish children with epilepsy. MDR1 C3435T and G2677T/A were genotyped in 152 patients with epilepsy, classified as drug-resistant in 69 and drug-responsive in 83. Genotypes of the C3435T and G2677T/A polymorphisms were determined by polymerase chain reaction followed by restriction fragment length polymorphism. Genotype and allele frequencies of C3435T and G2677T/A polymorphisms of the MDR1 gene did not differ between drug-resistant and drug-responsive epilepsy patients. Our results suggest that MDR1 C3435T and G2677T/A polymorphisms are not associated with AED resistance in Turkish epileptic patients. To clarify the exact clinical implication of the MDR1 polymorphisms on the multidrug resistance in epilepsy, further investigations in various ethnic populations would be necessary.
Highlights
Epilepsy is one of the most prevalent serious chronic neurological disorders, effecting approximately 1–2 % of the population [1]
The aim of this study was to evaluate the effect of C3435T and G2677T/A polymorphisms of multidrug resistance 1 (MDR1) on antiepileptic drug (AED) resistance in Turkish children with epilepsy
Our results suggest that MDR1 C3435T and G2677T/A polymorphisms are not associated with AED resistance in Turkish epileptic patients
Summary
Epilepsy is one of the most prevalent serious chronic neurological disorders, effecting approximately 1–2 % of the population [1]. Some potential mechanisms have been suggested regarding the transporters of the AEDs. There is accumulating evidence to suggest that an increase of functional expression of multidrug transporters produces pharmacokinetic changes that modify the access of AEDs to central nervous system targets [5]. There is accumulating evidence to suggest that an increase of functional expression of multidrug transporters produces pharmacokinetic changes that modify the access of AEDs to central nervous system targets [5] Genetic polymorphisms in these transporters could account for their increased expression and/or functional activity. These genetic variations could be linked to changes on pharmacokinetic or pharmacodynamic of AEDs and effective responsiveness to AEDs [6]
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