胎盘功能不全发病机制的新进展

S. A. Gasparyan, I. A. Orfanova, S. M. Akhmedova, I. A. Vasilenko
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摘要

的相关性。胎盘功能不全是一种多原因综合征,其特征是违反了胎儿胎盘系统的分子、细胞、组织和器官适应性稳态反应。先天免疫系统的中性粒细胞成分积极参与内皮功能障碍和血栓形成障碍的发展,这是许多妊娠并发症的基础,已被证实,这是开展探索性研究评估不同妊娠阶段孕妇中性粒细胞胞外陷阱(NETs)水平的原因。本研究的目的是确定与血栓形成相关的正常妊娠和胎盘功能不全孕妇中性粒细胞胞外陷阱形成的特征。对85例妊娠中期和晚期的孕妇进行了检查:40例正常妊娠(对照组),45例血栓形成(蛋白S/蛋白C缺乏)和胎盘欠代偿性功能不全(主组)。采用自动显微系统MECOS-C - 2,根据单层类型评估血涂片中NVL的水平。结果。研究发现,21 ~ 24周正常妊娠和胎盘功能不全孕妇的DNA trap水平分别比妊娠外高1.3倍和近2倍(p <0.05),以IIa期异位为主。到36-37周,在正常妊娠中,%NVL略有增加(16%),而在胎盘功能不全的孕妇组中,%NVL比初始数据增加了35.7%,在胚胎转化的IIa期保持了较高的细胞外结构含量(7.4%比21-24周的5.8%,p >0.05)。结论。很明显,在胎儿胎盘功能不全的发病机制中,高水平NIV的存在表明免疫防御机制的失败和炎症反应的不足,这在对孕妇的状况进行中间动态监测时是有用的。
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New aspects of the pathogenesis of placental insufficiency
Relevance . Placental insufficiency is a polycausal syndrome characterized by a violation of the molecular, cellular, tissue and organ adaptivehomeostatic reactions of the fetoplacental system. The active participation of the neutrophil component of the innate immune system in the development of endothelial dysfunction and thrombotic disorders, which underlie many complications of pregnancy, has been proven, which served as the reason for conducting exploratory studies to assess the level of neutrophil extracellular traps (NETs) in pregnant women at different stages of gestation. The purpose of the study is to identify the features of the formation of neutrophil extracellular traps in pregnant women with normal pregnancy and placental insufficiency associated with thrombophilia Material and methods . 85 pregnant women in the second and third trimester were examined: 40 women with normal pregnancy (comparison group) and 45 (main group) with thrombophilia (protein S/protein C deficiency) and subcompensated placental insufficiency. The level of NVL was assessed in blood smears according to the monolayer type using an automatic microscopic system MECOS-C 2. Results . It was found that the level of DNA traps in normal pregnancy and in pregnant women with placental insufficiency at 21–24 weeks of gestation was 1.3 and almost 2 times higher than the level outside pregnancy (p <0.05), with a predominance of phase IIa etosis. By 36–37 weeks, in a normal pregnancy, there was a slight increase in%NVL (16 %), while in the group of pregnant women with placental insufficiency,%NVL increased by 35.7 % compared to the initial data, maintaining a high content of extracellular structures in IIa phase of ethotic transformation (7.4 % versus 5.8 % at 21–24 weeks, p >0.05). Conclusion . It is obvious that the presence of a high level of NIV indicates a failure of immune defense mechanisms and the development of an inadequate inflammatory response in the pathogenesis of fetoplacental insufficiency, which can be useful when carrying out intermediate dynamic monitoring of the condition of a pregnant woman.
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