PLACENTAL FACTORS IN THE DEVELOPMENT OF PRETERM BIRTH IN PREGNANT WOMEN WITH COMORBIDITY

Premature birth (PB) is a polyetiological problem that depends on many factors, accompanied by violations of the placenta functional competence, changes in its metabolic, hormone-producing and protective functions. The objective: to establish the importance of placental factors in the development of PB in pregnant women with comorbid pathology. Materials and methods. The levels of fetal and placental proteins (placental alfa microglobulin-1, α2-microglobulin of fertility, trophoblastic β1-glycoprotein) and hormones (estriol, placental lactogen, progesterone) were determined in 33 pregnant women with threat of PB at 26–34 weeks of gestation (main group), who had concomitant comorbid pathology in the stage of unstable remission. The control group included 26 healthy pregnant women who were representative for gestational age. Results. In pregnant women with comorbid pathology a decrease of the placenta protein-synthesizing function and the hormone-producing function of the trophoblast was found, which makes it difficult to launch the syntoxic adaptation programs of the mother’s organism, which are responsible for maintaining the pregnancy with the subsequent development of placental dysfunction, the result of which is PB. The markers of these disorders are a 3-fold decrease in the level of trophoblastic β1-glycoprotein (p<0.0001) and a 1.7-fold decrease in the concentration of α2-microglobulin of fertility (p<0.0001) with a simultaneous 4-fold increase of placental alfa microglobulin-1 concentration (p<0.0001) and a decrease in the levels of placental lactogen by 1.6 times (p<0.0001), estradiol by 40 % (p<0.0001) and progesterone by more than 2 times (p