Polymorphism in β-fibrinogen and Integrin beta-3 Genes and Risk of Recurrent Spontaneous Miscarriage in Gaza Strip

Abstract

Background: Recurrent pregnancy loss (RPL) is an important clinical and stressful problem that has been studied tremendously. RPL affects about 1-5% of women who conceive. RPL has been defined as three or more consecutive pregnancy losses before 24 weeks of gestation. Despite extensive researches to explain the causative effects of RPL, about 50% of RPLs are still idiopathic. Common polymorhisms of β –fibrinogen (-455 G>A) and Integrin beta-3 genes have been indicated as risk factors for RPL in certain populations. Objective: This study was designed in order to investigate the relationbetween RPL and common polymorphisms in β -fibrinogen (-455 G>A) and Integrin beta-3 (L33P) genes among Palestinian women experiencing RPL in Gaza Strip. Methods: This study is an association study with a case-control design. Using molecular biological techniques, the β–fibrinogen (-455 G>A), and Integrin beta-3 (L33P) common polymorphisms were determined for 102 women who had at least three constitutive abortions and 97 controls without a previous history of abortion. Results: The β–fibrinogen 455A/A polymorphism was present in 3.9% of the patients and in 4.1% of the controls (P= 0.9422). Similarly there was no significant difference detected in the distribution of the HPA-1 (b/b) polymorphism which was detected in 2.0 % of the patients and in 2.1% of the controls (P= 0.9595). The frequency of β–fibrinogen – 455 A allele is 20.1% and the frequency of HPA-1b allele is 19% in the Palestinian population. Conclusion: Results of the present study revealed that there is no significant association between the β–fibrinogen (-455 G>A) or Integrin beta-3 (L33P) common polymorphisms and the occurrence of first trimester RPL. This non-significant relation indicates that the investigated polymorphisms do not constitute a tangible risk factor for RPL in our population. Future work should focus on association of other polymorphisms and genes contributing to thrombophilia.