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

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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 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 ≥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.