No abstract

Введение. Новорожденные, родившиеся у матерей с патологией во время беременности, составляют группу высокого риска тромботических и геморрагических осложнений, которые повышаются при наличии у новорожденных перинатальной патологии. Цель исследования: оценить показатели, характеризующие состояние системы фибринолиза и сосудистой стенки в крови новорожденных, родившихся у матерей с преэклампсией (ПЭ), для прогнозирования риска тромботических и геморрагических осложнений у таких детей. Материалы и методы. Обследовано 60 новорожденных, родившихся у матерей с ПЭ. Контрольную группу составили 30 новорожденных от матерей без ПЭ. Исследовали венозную кровь, взятую у новорожденных на 3–5-е сутки жизни. В крови определяли уровень тканевого активатора плазминогена (t-РА), ингибитора тканевого активатора плазминогена (PAI-1) и тромбомодулина. Результаты. Выявлено, что у новорожденных от матерей с ПЭ на 3–5-е сутки жизни отмечаются признаки повреждения эндотелия и повышение фибринолитической активности крови, на что указывает повышение содержания t-РА, PAI-1 и тромбомодулина в крови. Заключение. Полученные данные свидетельствуют о риске развития геморрагических осложнений у таких детей. Background. Neonates born to mothers with pathology during pregnancy are at high risk of thrombotic and hemorrhagic complications that are increased if neonates have perinatal pathology. Objectives: to assess blood parameters characterizing fibrinolysis and vascular wall of neonates born to mothers with preeclampsia (РЕ), to predict the risk of hemorrhagic complications in these children. Patients/Methods. 60 neonates born to mothers with РЕ were examined. The control group consisted of 30 neonates born to mothers without РЕ. We studied levels of tissue plasminogen activator (t-PA), inhibitor of tissue plasminogen activator (PAI-1) and thrombomodulin (TM) in venous blood taken from neonates on the 3–5th days of life. Results. In neonates born to mothers with PE we revealed on the 3–5th days of life increased blood levels of t-PA, PAI-1 and TM that characterized endothelial damage and increased blood fibrinolytic activity. Conclusions. The data obtained indicate the risk of hemorrhagic complications development in these children.

The aim of the study was to develop technologies for predicting the development of preeclampsia (PE) based on biomedical and molecular-genetic predictors and the calculation of individual risks for this pregnancy complication.Materials and Methods. The study involved 457 pregnant women. Of them, 147 women had chronic arterial hypertension (CAH); 109 pregnant women had CAH and secondary preeclampsia (PE); 201 patients had PE. The control group consisted of 105 pregnant women without hypertensive disorders or proteinuria. We performed a retrospective analysis of gestation course and labor outcomes, calculated risk factors using the Open Epi system and logistic regression method. Polymorphisms of genes controlling the vascular tone were identified in venous blood.Results. There were identified risk factors for developing PE, including those in women with CAH: chronic pyelonephritis; baseline mean AP above 95 mm Hg and diastolic AP above 80 mm Hg; body mass index over 30; family history of arterial hypertension. The following were identified as additional predictors of PE: perinatal loss; premature labor; spontaneous miscarriage; PE and closed craniocerebral injuries in the past medical history; threatening miscarriage in the first trimester. Additional risk factors for PE in women with CAH were found: lack of regular antihypertensive therapy before pregnancy and in the first trimester; chronic gastritis; first pregnancy; tobacco smoking.Polymorphic variants of the NOS3 (-786)C allele in the genotype in combination with the heterozygous genotype in the AGTR2 1675G/A gene are associated with a high risk of CAH. The presence of alleles NOS3 (-786)T/C and NOS3 (-786)C, as well as a combination of alleles NOS3 (-786)C and NOS3 894G/T, is associated with PE. The presence of alleles AGT 704C, CYP11B2 (-344)T, and GNB3 825T/T in the genotype, both individually and in combination, is a risk factor for the development of PE secondary to CAH. The data obtained made it possible to develop a method for predicting the onset of PE in women with CAH and a model for calculating the individual risk of PE, which formed the basis for a computer program. Conclusion.Calculating the individual risks of PE using the technologies proposed by the authors allows identifying pregnant women belonging to the high-risk group on a timely basis, which ensures high-quality implementation of preventive measures, provides a personalized approach and the possibility to prove the need for additional examination of this category of patients.

The open arterial duct has a pathological significance in premature newborns. Closure of the ductus arteriosus is a complex process that includes functional and anatomical closure.Purpose. To identify the features of arterial duct remodeling in premature newborns.Material and methods. We conducted a retrospective clinical and morphological analysis of 35 deceased premature newborns. During their lifetime, all children were examined using clinical and laboratory-instrumental methods. In all cases, autopsies of deceased children were performed with a complex of morphological studies of the arterial duct.Results. It has been established that the open arterial duct in premature newborns plays an important role in increasing respiratory failure. It also necessitates the appointment and conduct of invasive respiratory therapy. The functioning of the arterial duct is facilitated by low partial pressure and blood oxygen saturation levels. Morphofunctional features of arterial duct remodeling were revealed. A positive correlation was established between the indicators of the gas composition of the child’s blood and the thickness of the duct wall.Conclusion. Risk factors for an open arterial duct in premature newborns are the age of the mother over 35 years, threatened miscarriage, prenatal discharge of amniotic fluid, gestational diabetes mellitus, fetoplacental insufficiency, and severe asphyxia at birth. Morphological changes in the form of thickening of the endothelial layer and the formation of intimal pillows, fragmentation and focal necrosis of the internal elastic membrane with the accumulation of mucoid matter, proliferation and migration of smooth muscle cells into the subendothelial space reflect the processes of remodeling of the arterial duct.