An A > G polymorphism at position - 670 in the Fas (TNFRSF6) gene in pregnant women with pre-eclampsia and intrauterine growth restriction Academic Article uri icon

Overview

MeSH Major

  • Fetal Growth Retardation
  • Polymorphism, Genetic
  • Pre-Eclampsia
  • Receptors, Tumor Necrosis Factor

abstract

  • Fas-mediated apoptosis of maternal lymphocytes during pregnancy has been postulated to prevent the development of pre-eclampsia. A single adenine (A) to guanine (G) polymorphism at position -670 in the Fas gene (TNFRSF6) results in decreased Fas synthesis. The association between this polymorphism and pre-eclampsia in Hungarian women was investigated. In a case-control study, buccal swabs from 38 pregnant women with pre-eclampsia and 89 normotensive controls were analysed for the TNFRSF6-670 polymorphism. Investigators were blinded to clinical outcomes. Maternal homozygosity for the TNFRSF6-670*A occurred in 33 (37.1%) normotensive pregnant women as compared to only 5 (16.1%) of 31 pre-eclamptic pregnant women who delivered at < 37 weeks gestation (P = 0.04). The carriage rate of the TNFRSF6-670*G variant was also higher among these patients (59.7%) than among normotensive controls (42.1%; P = 0.01). There was no relation between the polymorphism and the pre-eclampsia diagnosed at > or = 37 weeks. Among pre-eclamptic patients with an intrauterine growth restriction (IUGR) neonate, eight (57.2%) were TNFRSF6-670*G homozygous as opposed to 3 (17.6%) of 17 pre-eclamptics who did not have IUGR (P = 0.03) and 19 (21.3%) normotensive controls (P = 0.008). Carriage of the TNFRSF6-670 polymorphism in the neonate was not associated with pre-eclampsia or IUGR. Maternal possession of the TNFRSF6-670*G increases the risk for pre-eclampsia and pre-eclampsia-associated IUGR in women who deliver at < 37 weeks.

publication date

  • March 2005

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1093/molehr/gah151

PubMed ID

  • 15695771

Additional Document Info

start page

  • 207

end page

  • 10

volume

  • 11

number

  • 3