ETIOPATHOGENESIS OF RECURRENT PREGNANCY LOSS DUE TO GENETIC FORMS OF THROMBOPHILIA
Abstract
The aim of the study was to develop a concept of the etiopathogenesis of miscarriages due to the genetic form of thrombophilia.
Materials and methods. In a prospective cohort study, 143 pregnant women were examined, including 109 with pregnancy loss and genetic defects of hemostasis [main (M) group]; the control (K) group consisted of 34 relatively healthy pregnant women with a light history and pregnancy without risk factors for pregnancy loss. Genetic polymorphisms of coagulation factors and fibrinolysis (1691 G→A FVL, 20210 G→A prothrombin, 675 5G/4G PAI-1, 455 G→A fibrinogen β), endothelial dysfunction (677 C→T MTHFR) were studied with the help of allele-specific polymerase chain reaction.
Results. A comprehensive clinical, laboratory, instrumental and statistical analysis has determined the main risk factors for pregnancy loss. Pathological polymorphisms of hemostasis and endothelial dysfunction genes play an important role in the development of miscarriage, namely the following pathological genotypes: 1691 GA factor V Leiden - increases the risk by 5.3 times (95% CI 1.5-18.5), 20210 GA prothrombin - 26.47 times (1.6-445.7), 675 4G / 4G PAI-1 - 7.5 times (1.7-33.79), -455AA fibrinogen β - 9.7 times (1.3-74.16), 677 CT MTHFR - 2.6 times (1.0-6.2), 677TT MTHFR - 21.7 times (1.3-368.6). It has been found that multigenic forms of thrombophilia predominate in most patients with pregnancy loss - 76.1% (p <0.001, OR = 12.31, 95% CI 4.8-31.55).
Conclusions. The obtained data allowed us to form a concept of the etiopathogenesis of recurrent pregnancy loss due to genetic thrombophilia and justify the need for a personalized approach in each case of pregnancy loss.
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