A single nucleotide A>G polymorphism at position −670 in the Fas gene promoter: Relationship to preterm premature rupture of fetal membranes in multifetal pregnancies

医学 精确检验 等位基因 怀孕 产科 妇科 正式舞会 胎儿 胎膜早破 基因 单核苷酸多态性 基因型 遗传学 生物 内科学
作者
Robin B. Kalish,Daniel P. Nguyen,Santosha A. Vardhana,Meruka Gupta,Sriram C. Perni,Steven S. Witkin
出处
期刊:American Journal of Obstetrics and Gynecology [Elsevier]
卷期号:192 (1): 208-212 被引量:28
标识
DOI:10.1016/j.ajog.2004.06.106
摘要

Objective 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. Methods 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. Results 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). Conclusions A genetic variant in the Fas gene is associated with an increased rate of PPROM in multifetal pregnancies. 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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