TREATMENT OF PLACENTAL INSUFFICIENCY IN PREGNANT WOMEN WITH ANTIPHOSPHOLIPID SYNDROME AND VARICOSE VEINS

Abstract

In recent years, there has been an increase in the frequency of placental insufficiency (PI) in pregnant women with obstetric and somatic pathology, including in patients with varicose veins, especially in the presence of autoimmune antibodies of various etiologies. The antiphospholipid syndrome (APS) attracts more and more attention of scientists, which significantly increases both maternal and perinatal mortality [8, 9]. Most of the adverse outcomes in APS are associated with PI. One of the reasons for the development of PI are disorders of the hemostasis system in pregnant women with the presence of circulating antiphospholipid antibodies (APA). AFAs circulating in the blood plasma contribute to the activation of the platelet link of hemostasis, disruption of the hemostatic potential, and potentiation of endothelial damage. Such changes lead to local ischemia of the villous chorion, impaired placental blood flow. The consequences of pathological changes in PI in the fetoplacental system lead to hypoxia, fetal malnutrition, increase perinatal mortality, and also have adverse consequences for the development of the child [2,8,9]. Risk factors for the development of fetal malnutrition are numerous. These include various somatic diseases, disorders in the reproductive system, pregnancy complications, social factors and much more. According to the literature, in women with an autoimmune cause of miscarriage without treatment, up to 90% of pregnancies are interrupted, and the effectiveness of treatment with the most modern approaches reaches 80% or more [5, 10]. Pregnancy is a favorable condition for the implementation of the pathogenic action of AFA. The manifestation of pathological processes can occur at different times, starting from the moment of conception: the process of implantation and early embryogenesis are disrupted. According to the literature, AFAs are capable of disrupting several aspects in the process of trophoblast differentiation, which is expressed in a change in the adhesiveness of the embryo, impaired fusion of syncytium, and a decrease in the depth of trophoblast invasion; a decrease in the production of hCG, an increase in thrombotic tendencies. As a result, these changes lead to a decrease in the protein-synthesizing and hormonal functions of the placenta. In the absence of adequate therapy, thrombosis occurs in the microcirculatory bed, which causes PI, chronic hypoxia, and often fetal death due to acute circulatory disorders in the vessels of the placenta [5, 6, 10]. Among patients with PN, 16-25% of women have manifestations of varicose veins, chronic venous insufficiency and varicose veins of the pelvis. Some authors attach significant importance in the occurrence of varicose veins in pregnant women to immunological mechanisms that lead not only to functional, but also to structural changes in the vessels. As a result, a cascade of pathological changes occurs, initiated by venous stasis and hemocoagulation abnormalities, which lead to PI. Treatment of this category of patients presents significant difficulties, as it can lead to the most severe complications in obstetrics, thrombosis and pulmonary embolism [1, 3].