Abstract

The relationship between a polymorphism at position −670 in the Fas gene (TNFRSF6) and preterm premature rupture of membranes (PPROM) in multifetal pregnancies was examined.Buccal swabs from 119 mother-infant sets were analyzed for an adenine (A) to guanine (G) substitution at position −670 in the TNFRSF6 promoter. Pregnancy outcome data were subsequently obtained. Analysis was by Fisher exact test.Maternal allele G homozygosity (TNFRSF6∗G) was observed in 42.4% of 33 PPROM pregnancies as opposed to 19.5% of 77 with no spontaneous preterm birth (P = .01). Similarly, TNFRSF6∗G homozygosity was present in 37.5% of 32 first-born neonates from PPROM pregnancies as opposed to 18.7% of 75 uncomplicated pregnancies (P = .04). PPROM occurred in 8 of 14 (57.1%) pregnancies in which mother and all neonates were TNFRSF6∗G homozygotes as opposed to 25 of 105 (23.8%) cases in which uniform TNFRSF6∗G homozygosity was not observed (P = .02).A genetic variant in the Fas gene is associated with an increased rate of PPROM in multifetal pregnancies.

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