The state of hemostasis changes significantly during pregnancy. These changes are necessary for the normal and safe development of pregnancy and for stopping bleeding during childbirth, but activation of the hemostasis system in pregnant women is accompanied by a 4-5-fold increase in the risk of thromboembolic complications.
AIM
To study the distribution of genetic defects in the hemostasis system in patients with a history of reproductive losses in order to choose a rational tactics for managing pregnancy.
MATERIAL AND METHODS
The survey included 324 patients of the early reproductive period with a history of reproductive losses. Determination of genetic polymorphisms associated with the risk of thrombophilia was carried out by the method of polymerase chain reaction («DNA-Technology», Moscow). The patients underwent a study of the genotypes of eight distinct genes of the plasma proteins and vascular-platelet compartment of the hemostatic system. Statistical analysis of the obtained results was carried out on the basis of standard methods of medical statistics.
RESULTS
The analysis of the obtained results showed that in 98.77% of patients the presence of mutations in the genes of plasma proteins and vascular-platelet hemostasis was revealed. The frequency of the most dangerous combination of gene mutations that increases the risk of thrombus formation was 42.50% in total. There were simultaneous combinations of defects in the genes of FV Leiden, fibrinogen, α2 and 3β integrin, serpin 1 among them. Mutations were represented by both heterozygous and homozygous forms.
CONCLUSION
An increased tendency to thrombus formation creates conditions for disruption of the processes of implantation, placentation, and fetal growth. Against this background, systemic endothelial dysfunction develops further, the pro-inflammatory response is activated and the procoagulational potential of the blood coagulation system is formed, as a result of which not only thrombotic, but also obstetric complications are realized in carriers of genetic mutations.