Abnormal Trophoblast Invasion: The Culprit of The Major Obstetrics Problems

Q4 Medicine
S. Sulistyawati
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引用次数: 0

Abstract

Pathogenesis of preeclampsia as the consequences of the interaction failure between trophoblast and womb, mainly in the 1 st trimester leads to a stress response in the placenta. This may cause poor growth and development of the villous tree, deteriorating transfer of oxygen and nutrients to the fetus. 1 In the simultaneous way huge number of placental debris as the result of necrotic-apoptotic process is released into maternal circulation. 1,2 That of phenomenon related to syncytiotrophoblastic stress is triggering endothelial dysregulation and extreme in fl ammation process, and so do the clinical respond related, such as: hypertension, proteinuria, edema, convulsion, cerebral edema, acute renal failure, acute liver dysfunction, thrombocytopenia (which are as the maternal complications) and fetal growth restriction, preterm delivery, still birth (which are as the fetal complications). 3 Fetal growth restriction (FGR) which could be develop solely or as one entity of early-onset preeclampsia is mostly caused by the poor attitude of extravillous trophoblast cells (EVT) in doing its work on maternal spiral artery remodeling process. 4 As we can see clear from the large data of scienti fi c evidence, the only signi fi cant modality to prevent FGR until recent is by giving low-dose aspirin before 16 weeks of gestational age in selected pregnancies with high resistance index of uterine artery shown by doppler velocimetry ultrasound. 5 Beyond that, only timely delivery after series of close monitoring that will give better perinatal outcome. 6 This will often end with preterm delivery, which increases the percentage of preterm birth in general. 6 In the placenta accreta spectrum (PAS) is a condition where the trophoblast invasion is too aggressive. The development of PAS is a complex multifactorial process related to the combination of decidual-myometrial (as the results of previous c-section or other gynecological surgery), absence the basal plate
滋养细胞异常侵袭:主要产科问题的罪魁祸首
子痫前期的发病机制是滋养细胞和子宫之间相互作用失败的结果,主要发生在妊娠早期,导致胎盘产生应激反应。这可能会导致绒毛树生长发育不良,恶化氧气和营养物质向胎儿的转移。同时,大量的胎盘碎片作为坏死-凋亡过程的结果被释放到母体循环中。1,2与合胞滋养层应激相关的现象在炎症过程中引发内皮异常和极端,临床反应也与之相关,如:高血压、蛋白尿、水肿、惊厥、脑水肿、急性肾功能衰竭、急性肝功能障碍、血小板减少(作为母体并发症)和胎儿生长受限、早产、死产(作为胎儿并发症)。胎儿生长受限(FGR)可单独发展或作为早发性子痫前期的一个实体,主要是由于上皮外滋养细胞(EVT)在母体螺旋动脉重构过程中的作用不积极所致。4从大量的科学证据中我们可以清楚地看到,直到最近,唯一有效的预防FGR的方法是在孕龄16周之前,对经多普勒超声显示子宫动脉阻力指数高的孕妇给予低剂量阿司匹林。除此之外,只有经过一系列密切监测后及时分娩才能获得更好的围产期结局。这通常会导致早产,从而增加了早产的比例。在胎盘增生谱(PAS)中,滋养细胞侵袭太强。PAS的发展是一个复杂的多因素过程,与蜕膜-子宫肌瘤(作为既往剖腹产或其他妇科手术的结果)、基底板缺失的结合有关
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来源期刊
Indonesian Journal of Obstetrics and Gynecology
Indonesian Journal of Obstetrics and Gynecology Medicine-Pathology and Forensic Medicine
CiteScore
0.10
自引率
0.00%
发文量
0
审稿时长
24 weeks
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