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pre-eclampsia, endometrial spiral arteries, gestational remodeling, ischemia, endoplasmic reticulum stress of the syncytiotrophoblast

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Ventskovsky, B., & Zhegulovych, V. (2019). ON THE PATHOGENESIS OF PRE-ECLAMPSIA. Medical Science of Ukraine (MSU), 15(1-2), 101-106. https://doi.org/10.32345/2664-4738.1-2.2019.15


Relevance. To date, there is no pathogenetic treatment for pre-eclampsia because the etiology and pathogenesis of this pathology are still poorly understood. Therefore, the analysis of possible causes and mechanisms of pre-eclampsia is an urgent problem, as it will help to choose the right tactics for pregnant women with pre-eclampsia.

Objective: to analyze the possible causes and mechanisms of pre-eclampsia.

Materials and methods. Review of the scientific publications in the international electronic scientometric databases PubMed, Embase and Scopus by keywords for a period of 7 years (2011-2017) and comparison of the obtained data with the results of own studies dedicated to the microhemocirculatory bed of the placenta (supravital contact microscopy) and the uterine cervix (lifetime contact microscopy) in pre-eclampsia (Reichert contact colpomicroscope (Austria).

Results. The endoplasmic reticulum stress (ER stress) in pre-eclampsia results from ischemia and reperfusion accompanied by the endometrial pathology of spiral arteries, which in turn is caused by insufficient gestational conversion due to incomplete trophoblast invasion. The ER stress of the syncytiotrophoblast synthesizes a wide range of growth factors, both proangiogenic (the placental and vascular endothelial growth proteins) and antiangiogenic (soluble FMS-like tyrosine kinase and endoglin). An imbalance of these factors leads to the endothelial dysfunction. When the endothelial cells are damaged, antiangiogenic proteins are released. They bind the vascular endothelial growth factor and induce defective gestational remodeling of spiral arteries. Therefore, the changes, which occur in the uterine vascular bed, are most likely to result in the fetal growth restriction as the intensity of blood flow slows down and the fetus experiences ischemia and hypoxia. In response to the changes in the placental-fetal complex, the activation of the release of vasoactive amines into the intervillous space with further invasion into the microcirculatory blood flow in the uterus is observed. We managed to prolong pregnancy and reduce the severity of pre-eclampsia by removing soluble FMS-like tyrosine kinase-1 (antiangiogenic factor) due to extracorporeal apheresis. It is conceivable that pre-eclampsia can be linked to the increased inflammatory response: circulating tumor necrosis factor and interleukin levels are increased in pre-eclampsia.

Conclusions. The criteria for predicting pre-eclampsia include an increase in the levels of α-fetoprotein and inhibin in the maternal blood, podocyturia, the ratio of the proangiogenic growth factor of the placenta PlGF to the antiangiogenic factor of endoglin in combination with measurements of the uterine artery pulsatility index.

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