A pharmacogenetic exploration of vigabatrin-induced visual field constriction

Epilepsy Res. 2006 Aug;70(2-3):144-52. doi: 10.1016/j.eplepsyres.2006.03.012. Epub 2006 May 3.

Abstract

Introduction: Use of the antiepileptic drug (AED) vigabatrin is severely limited by irreversible visual field constriction, an adverse reaction to the drug reported in approximately 40% of patients. Given the evidence suggesting an idiosyncratic drug response, we set out to detect genetic variation of strong, clinically relevant effect that might guide clinicians in the safe, controlled prescribing of this otherwise usefuldrug.

Methods: Patients with a history of at least 1-year exposure to vigabatrin were enrolled at two independent referral centers. Using Goldmann perimetry, visual fields and the extent of constriction were calculated for each patient. We examined the correlation between the extent of vigabatrin induced visual field constriction and genetic variation across six candidate genes (SLC6A1, SLC6A13, SCL6A11, ABAT, GABRR1 and GABRR2). We availed of HapMap data and used a tagging SNP technique in an effort to efficiently capture all common variation within these genes. We attempted to replicate any positive associations before drawing conclusions from our results.

Results: The degree of visual field constriction correlated with three SNPs and one haplotype in a cohort of 73 patients. However we were unable to replicate these findings in a second independent cohort consisting of 58 patients, suggesting the initial results were possibly false positives, or variants of weak effect.

Conclusion: Common variants of strong, clinically relevant effect do not appear to reside in the candidate genes studied here. This does not rule out the presence of genetic variants of weak effect in these genes, nor of variants of strong effect in other genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 4-Aminobutyrate Transaminase / genetics*
  • Adult
  • Anticonvulsants / adverse effects*
  • Cohort Studies
  • Epilepsy / drug therapy
  • False Positive Reactions
  • Female
  • GABA Plasma Membrane Transport Proteins / genetics*
  • Genetic Variation
  • Haplotypes
  • Humans
  • Male
  • Middle Aged
  • Pharmacogenetics
  • Polymorphism, Single Nucleotide
  • Receptors, GABA / genetics*
  • Vigabatrin / adverse effects*
  • Visual Fields / drug effects
  • Visual Fields / genetics*

Substances

  • Anticonvulsants
  • GABA Plasma Membrane Transport Proteins
  • GABA-C receptor
  • Receptors, GABA
  • SLC6A1 protein, human
  • SLC6A11 protein, human
  • SLC6A13 protein, human
  • 4-Aminobutyrate Transaminase
  • Vigabatrin