Role of genetically determined fetal hemostatic disorders in the development of severe forms of placental insufficiency

Objective. To study the specific features of development of genetically determined fetal hemostatic disorders and their role in the genesis of severe forms of placental insufficiency. Subjects and methods. Seventy married couples and their newborns underwent clinical and laboratory examinations and constituted two groups: a study group (n = 50), in which their pregnancy was complicated by sub- or decompensated forms of placental insufficiency, and a control group (n = 20) without a compromised obstetric history, with current physiological pregnancy. The polymorphic variants of the genes involved in blood aggregation and folate metabolism were investigated by real-time polymerase chain reaction; the blood coagulation system was evaluated in women and babies. Results. The women in the study group were found to have statistically significant differences in the frequency of polymorphic variants of the genes: PAI-1, ITGB3, F7, F13, and MTHFR; the men in this group had PAI-1, ITGA2 807; their newborn babies had PAI-1 and MTHFR. In addition, in the study group the women and babies were detected to have the clotting disorders indicating the activation of intravascular microcoagulation. Conclusion. Clinically significant fetal thrombophilia makes a considerable contribution to the development of severe forms of placental insufficiency.

placental insufficiency, inherited thrombophilia, neonatal hemostasis, thromboelastography