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Abstract
Summary Background: Plasminogen activator inhibitor 1 (PAI-1) is an inhibitor of fibrinolysis. The PAI-1 4G/5G polymorphism is associated with elevated plasma levels of PAI-1. Over- expression of PAI-1 and impaired fibrinolysis in homozygous carriers of the 4G/4G PAI polymorphism may lead to abnor- mal placental formation and increased risk of fetal loss (FL). The aim of our study was to determine the frequency of this polymorphism in patients with FL in a Serbian population. Methods: The study was carried out in a group of 203 women (91 controls and 112 women with FL). The presence of PAI-1 4G/5G polymorphism was detected by PCR-RFLP analysis. Results: Slightly increased frequency of the PAI-1 4G/4G genotype was observed in the study group compared to the controls (32.1% vs. 30.8%). The frequency of PAI-1 was highest in women experiencing FL in the second trimester of pregnancy (50%), but this difference was not statistically sig- nificant. Conclusions: Our findings suggest that PAI-1 4G/4G might be a risk factor for FL occurring in the second trimester of pregnancy. Further studies are required in order to determine the role of PAI-1 4G/5G polymorphism in the etiology of FL.
Highlights
Thrombophilia refers to a group of inherited or acquired coagulation disorders leading to venous and/ or arterial thrombosis as well as reproductive disorders such as fetal loss (FL) [1,2,3]
The Plasminogen activator inhibitor 1 (PAI-1) 4G/5G polymorphism is associated with elevated plasma levels of PAI-1
Overexpression of PAI-1 and impaired fibrinolysis in homozygous carriers of the 4G/4G PAI polymorphism may lead to abnormal placental formation and increased risk of fetal loss (FL)
Summary
Thrombophilia refers to a group of inherited or acquired coagulation disorders leading to venous and/ or arterial thrombosis as well as reproductive disorders such as fetal loss (FL) [1,2,3]. The most frequent genetic risk factors associated with thrombophilia include factor V Leiden (G1691A), prothrombin G20210A and PAI-1 4G/5G gene variants [1]. The 4G/5G polymorphisms located at position –675 bp in the PAI-1 gene have alleles with four or five guanosines due to a single guanosine insertion/deletion in the promoter region [4, 7]. A 5G allele binds both a transcriptional activator and a repressor protein at the overlapping binding site, which leads to normal PAI-1 expression. A 4G allele binds only a transcriptional activator, resulting in an increased expression of PAI-1 [4]. The PAI-1 overexpression and impaired fibrinolysis may cause compromised and insufficient trophoblast invasion, leading to abnormal placental formation and increased risk of FL [9,10,11]
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