Zelinka-Khobzey M. M., Tarasenko K. V.

ENDOTHELIAL DYSFUNCTION IN PREGNANT WOMEN WITH OBESITY AS PATHOGENETIC BASIS OF MATERNAL AND NEONATAL COMPLICATIONS


About the author:

Zelinka-Khobzey M. M., Tarasenko K. V.

Heading:

LITERATURE REVIEWS

Type of article:

Scentific article

Annotation:

This review article is aimed at highlighting and analyzing the manifestations of endothelial dysfunction in overweight pregnant women that has been recognized as one of the most challenging issues in current obstetrics. Obesity has already been stated as one of the most widespread diseases around the world. According to the World Health Organization, more than 25% of women are diagnosed as overweight, and there is a tendency toward an increase in the obesity incidence in pregnant women. Obesity in pregnant women can cause maternal and prenatal complications, and namely, pre-eclampsia, miscarriage, placental dysfunction, fetus intrauterine growth retardation. In Ukraine, preeclampsia occurs in 12-17% of cases and develops in 8-12% of healthy pregnant women and in 20-40% of pregnant women with intercurrent pathology. Therefore, determining the causes of preeclampsia in pregnant women with concomitant obesity is an important task. The trigger mechanism for the development of this complication of pregnancy results from the endothelial damage to the vessels in the pre-pregnancy period and is typically associated with such factors as arterial hypertension, obesity, dyslipidemia. The development of placental dysfunction and its clinical manifestations including intrauterine growth retardation syndrome and chronic fetal distress is an essential aspect in the course of pregnancy that causes high prenatal morbidity and mortality. The placental process starts with the interaction between the cytotrophoblast and the decidual tissue of the endometrium. The intensity of utero-placental blood flow is the main factor determining the oxygen supply to the placenta. In the case of uncomplicated pregnancy, placental vessels are dilated and do not respond to contractile stimuli that ensures smooth regular supply of oxygen and nutrients to the fetus. Endothelial dysfunction is a universal pathogenetic mechanism of most diseases, as the endothelium not only regulates the vascular tone, but also takes part in the processes of atherogenesis, thrombosis, and provides the protection of the vascular wall the integrity. In addition, the endothelium produces a large number of biologically active substances that affect the tone and vascular angiogenesis, regulate hemostasis, immune and anti-inflammatory response. The reduction in the synthesis of nitric oxide (NO), which is the main vasodilator, and also is involved in the functioning of various systems of the human body, and in particular, cardiovascular, immune, and endocrine, is considered as a key element of endothelial dysfunction. Nitric oxide is derived from L-arginine under the action of the NO-synthase enzyme. It is the L-arginine – NO system that according to the current views in obstetrics plays a leading vasoregulatory role during the gestation. The presence of endothelial dysfunction in pregnant women with preeclampsia can be due to the low level of substances responsible for vasodilation. Consequently, obesity in women of child-bearing age is associated with a number of systemic and reproductive problems that leads to a decrease in fertility. Pregnancy and childbirth are complicated by preeclampsia, the threat of abortion, miscarriage and intrauterine damage of the fetus. All this indicates a further need to improve measures aimed at prenatal fetal protection and reducing the frequency of maternal and fetal complications in this group of pregnant women, and states the necessity for early detection of women with an increased risk of placental syndromes (preeclampsia, fetal delay, etc.).

Tags:

obesity, pregnancy, endothelial dysfunction, preeclampsia.

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Publication of the article:

«Bulletin of problems biology and medicine» Issue 1 Part 2 (149), 2019 year, 34-40 pages, index UDK 618.2-056.5:611.018.74

DOI: