A functional polymorphism in the SCN1A gene does not influence antiepileptic drug responsiveness in Italian patients with focal epilepsy

Epilepsia. 2011 May;52(5):e40-4. doi: 10.1111/j.1528-1167.2011.03097.x.

Abstract

A splice site variation (c.603-91G>A or rs3812718) in the SCN1A gene has been claimed to influence efficacy and dose requirements of carbamazepine and phenytoin. We investigated the relationship between c.603-91G>A polymorphism and response to antiepileptic drugs (AEDs) in 482 patients with drug-resistant and 401 patients with drug-responsive focal epilepsy. Most commonly used AEDs were carbamazepine and oxcarbazepine. The distribution of c.603-91G>A genotypes was similar among drug-resistant and drug-responsive subjects, both in the entire population and in the groups treated with carbamazepine or oxcarbazepine. There was no association between the c.603-91G>A genotype and dosages of carbamazepine or oxcarbazepine. These findings rule out a major role of the SCN1A polymorphism as a determinant of AED response.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anticonvulsants / pharmacology
  • Anticonvulsants / therapeutic use*
  • Carbamazepine / analogs & derivatives
  • Carbamazepine / pharmacology
  • Carbamazepine / therapeutic use
  • Drug Resistance
  • Epilepsies, Partial / drug therapy*
  • Epilepsies, Partial / genetics
  • Female
  • Genotype
  • Humans
  • Italy / ethnology
  • Male
  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins / genetics*
  • Oxcarbazepine
  • Pharmacogenetics
  • Polymorphism, Genetic*
  • Sodium Channels / genetics*
  • White People / genetics

Substances

  • Anticonvulsants
  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins
  • SCN1A protein, human
  • Sodium Channels
  • Carbamazepine
  • Oxcarbazepine