Glutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome

Eur J Clin Pharmacol. 2009 May;65(5):483-91. doi: 10.1007/s00228-009-0617-8. Epub 2009 Jan 29.

Abstract

Purpose: The aim of this pilot study was to assess the association between polymorphisms in genes that encode for proteins involved in the pharmacokinetics/pharmacodynamics of glucocorticoids and the occurrence of respiratory distress syndrome (RDS) in preterm infants born to mothers treated with a complete course of betamethasone.

Methods: Sixty-two preterm infants were enrolled. The C1236T, G2677T, and C3435T polymorphisms in the ABCB1 gene, BclI, N363S and ER22/23EK in the NR3C1 gene, I105V in the GST-P1 gene and GST-M1 and GST-T1 deletions were analyzed, and their association with the occurrence of RDS was assessed.

Results: In univariate analysis, the heterozygous and homozygous presence of the I105V variant in the GST-P1 gene seemed to confer protection against the occurrence of RDS (P = 0.032), while no association for all other polymorphisms was observed. In multivariate analysis, selection from the reference model of independent variables based on AIC (Akaike information criteria) maintained three variables in the model: gestation, C3435T, and GST-P1 genotype.

Conclusions: Polymorphisms of the GST-P1 gene may influence the effect of antenatal steroids on the newborn lung.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Betamethasone / therapeutic use*
  • Birth Weight
  • Female
  • Gestational Age
  • Glucocorticoids / therapeutic use*
  • Glutathione S-Transferase pi / genetics
  • Glutathione Transferase / genetics*
  • Humans
  • Infant, Newborn
  • Infant, Premature
  • Male
  • Pilot Projects
  • Polymorphism, Genetic*
  • Respiratory Distress Syndrome, Newborn / prevention & control*

Substances

  • Glucocorticoids
  • Betamethasone
  • Glutathione S-Transferase pi
  • Glutathione Transferase