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The article presents data on the clinical and pathogenetic variants of fetal growth restriction (FGR). FGR is one of the typical clinical manifestations of large obstetric syndromes, is associated with a high perinatal morbidity and has a significant impact on the quality and duration of human life. The emphasis is made on the differences in pathogenesis, the features of prediction, diagnosis, obstetric management and the assessment of perinatal outcomes in the early and late phenotype of the FGR. The review includes materials from domestic and foreign scientific literature that found in eLibrary and PubMed on this topic and published for the last 10 years. This article discusses the role of the formation of the embryo(feto)placental system under the influence of existing periconceptional risk factors in the implementation of various phenotypes of FGR. An analysis of the literature shows that the fetal growth potential, which genetically and epigenetically determined, changes during pregnancydepending on maternal, placental and fetal factors, which ultimately determine the final weight-growth parameters of the newborn. The issues of informativeness of clinical, laboratory and instrumental predictors, diagnostic criteria, the choice of rational obstetric management in case of FGR of various periods of manifestation are discussed in this article. Convincing data on the perinatal and long-term consequences of intrauterine growth restriction are presented. The pathogenetic variant of FGR determines the features of the functioning of the immune system, has a significant impact on the programming of metabolic and endocrine processes, the formation of fetal brain structures. Identification of pregnant women at risk for the development of FGR of various periods of manifestation, timely diagnosis, selection of the timing and method of delivery should correspond to the main directions of the "4P-model" of modern medicine and represent an integral predictive, preventive and personalized system of examination and observation based on evidence-based medicine data and the requirements of practical obstetrics and perinatology.
The article presents data on the clinical and pathogenetic variants of fetal growth restriction (FGR). FGR is one of the typical clinical manifestations of large obstetric syndromes, is associated with a high perinatal morbidity and has a significant impact on the quality and duration of human life. The emphasis is made on the differences in pathogenesis, the features of prediction, diagnosis, obstetric management and the assessment of perinatal outcomes in the early and late phenotype of the FGR. The review includes materials from domestic and foreign scientific literature that found in eLibrary and PubMed on this topic and published for the last 10 years. This article discusses the role of the formation of the embryo(feto)placental system under the influence of existing periconceptional risk factors in the implementation of various phenotypes of FGR. An analysis of the literature shows that the fetal growth potential, which genetically and epigenetically determined, changes during pregnancydepending on maternal, placental and fetal factors, which ultimately determine the final weight-growth parameters of the newborn. The issues of informativeness of clinical, laboratory and instrumental predictors, diagnostic criteria, the choice of rational obstetric management in case of FGR of various periods of manifestation are discussed in this article. Convincing data on the perinatal and long-term consequences of intrauterine growth restriction are presented. The pathogenetic variant of FGR determines the features of the functioning of the immune system, has a significant impact on the programming of metabolic and endocrine processes, the formation of fetal brain structures. Identification of pregnant women at risk for the development of FGR of various periods of manifestation, timely diagnosis, selection of the timing and method of delivery should correspond to the main directions of the "4P-model" of modern medicine and represent an integral predictive, preventive and personalized system of examination and observation based on evidence-based medicine data and the requirements of practical obstetrics and perinatology.
Introduction. Pre-eclampsia (PE) continues to be the leading problem in obstetrics. The existing methods for predicting PE show insufficient efficiency, and therefore the search for new predictors of PE remains relevant.The goal of the study. To develop a method for staged stratification of pregnant women to the risk of PE according on the basis of the revealed dismetabolic features of the pathogenesis of this complication of gestation.Material and methods. A dynamic clinical and laboratory examination of 180 pregnant women with independent factors of high risk of PE was carried out. PE was revealed in 89 women who made up group I. Group II (control) consisted of 30 healthy pregnant women with the physiological gestation.Results and discussion. A statistically significant increase in diabetogenic and atherogenic changes characteristic of physiological pregnancy, changes in hormonal, endothelial-hemostasiological, pro-inflammatory and placental parameters aimed at the energy and plastic supply of the fetus was revealed in women with PE. The results of laboratory examination, statistical data processing showed that the most significant pathogenetic mechanisms of development of PE are pathological insulin resistance (IR) and hyperinsulinemia (HI), which act as the basic link and initiate atherogenic transformation of the lipid profile, pro-inflammatory and immunometabolic disorders, prothrombotic status, hyperleptinemia, hyperuricemia, antiangiogenic state and endothelial dysfunction, which indicates a pronounced pathogenetic and clinical similarity of PE and metabolic syndrome. The revealed features of the pathogenesis of PE were reflected in the method of staged risk stratification of pregnant women: the models for assessing the individual risk of PE implementation included the levels of insulin, PlGF, PAMG-1, and TNF-α at 11–14 weeks of gestation; levels of insulin, uric acid, TNF-α, and mean platelet volume at 18-21 weeks of gestation (I trimester – AUC = 0.886, Se = 86.7%, Sp = 84.3%; II trimester - AUC = 0.874, Se = 83.3%, Sp = 87.2%, р < 0.001).Conclusion. Practical application of the developed pathogenetically substantiated method of staged stratification of pregnant women by the risk of PE implementation will justify the appointment and enhancement of preventive measures, reduce the incidence of severe and complicated forms of PE, and improve gestational and perinatal outcomes.
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