Placental factors in the development of preterm birth in pregnant women with comorbidity

S. Heryak, N. Petrenko, V. Dobrianska
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Abstract

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<0.0001) compared to healthy pregnant women.Conclusions. In patients with comorbid pathology there are disorders in the secretion of pregnancy proteins due to a decrease in the levels of trophoblastic β1-glycoprotein and α2-microglobulin of fertility and an increase in the level of placental alfa microglobulin-1 and disorders of the hormone-producing function of the trophoblast due to a decrease in the secretion of placental lactogen, progesterone, and estradiol. The disturbance of the secretion of the pregnancy zone proteins and hormones are the early markers for the initiation of premature birth caused by placental dysfunction in pregnant women with comorbid pathology.
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有合并症的孕妇发生早产的胎盘因素
早产(PB)是一个多方面的问题,它取决于许多因素,伴随着胎盘功能能力的破坏,其代谢、激素产生和保护功能的改变。目的:确定胎盘因素在合并病理的孕妇发生PB的重要性。材料和方法。测定33例妊娠26 ~ 34周伴有不稳定缓解期病理的PB威胁孕妇(主组)的胎儿及胎盘蛋白(胎盘α -微球蛋白-1、生育α - 2微球蛋白、滋养层β -1糖蛋白)及激素(雌三醇、胎盘乳原、孕酮)水平。对照组包括26名具有胎龄代表性的健康孕妇。结果。在有共病病理的孕妇中,发现胎盘的蛋白质合成功能和滋养细胞的激素产生功能下降,这使得母体机体维持妊娠的合成毒性适应程序难以启动,随后发展为胎盘功能障碍,其结果是PB。这些疾病的标志是与健康孕妇相比,滋养层β1-糖蛋白水平降低3倍(p<0.0001),生育α2-微球蛋白浓度降低1.7倍(p<0.0001),胎盘α -微球蛋白-1浓度同时升高4倍(p<0.0001),胎盘乳原水平降低1.6倍(p<0.0001),雌二醇水平降低40% (p<0.0001),孕酮水平降低2倍以上(p<0.0001)。在有共病病理的患者中,由于生育滋养层β1-糖蛋白和α2-微球蛋白水平降低,胎盘α -微球蛋白-1水平升高,导致妊娠蛋白分泌紊乱;由于胎盘乳原、黄体酮和雌二醇分泌减少,滋养层激素分泌功能紊乱。妊娠区蛋白和激素分泌紊乱是有共病病理的孕妇胎盘功能障碍引发早产的早期标志。
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