A clinical significance of acquired and hereditary forms of thrombophilia in the pathogenesis of fetal growth retardation syndrome
The authors carried out a complex dynamic examination of 65 women with various forms of fetoplacental insufficiency. The study established a pathogenetic role of congenital and hereditary thrombophilias in the pathogenesis of PI. The incidence of mutations correlates with the severity of FPI. In decompensated FPI, a combination of several mutations prevails. The number of detected mutations in one patient correlates with the severity of FPI. The presence of combinations of several mutations and polymorphisms leads to development of subcompensated and decompensated forms of PI and FGRS. Prognostically, multifactor genesis and polymorphism of genetic forms of thrombophilia seem to be most important. Acquired thrombophilias have a significant prognostic value in development of PI and FGRS. Concentrations of antiphospholipid antibodies above 0.6 U/ml is indicative of a high risk for rapid progress of fetoplacental insufficiency and gestosis. The levels of antibodies to annexin V above 0.2 U/ml correlate with long-term gestosis and a subcompensated form of fetal growth retardation syndrome. The most unfavorable prognosis for development of a decompensated form of PI is a combination of increased APA concentrations and antibodies to prothrombin I.