Journal ArticleDOI
A critical review of early-onset and late-onset preeclampsia.
Dahlia Raymond,Erika Peterson +1 more
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TLDR
This review summarizes the relevant research on the similarities and differences between early- and late-onset preeclampsia as it relates to pathogenesis and biomarkers, including differences in vascular endothelial growth factor, placental growth factors, vascular vascular cell adhesion molecule, toll-like receptor, plasma pentraxin 3, soluble endoglin, and lipid peroxidation.Abstract:
Preeclampsia is a leading cause of pregnancy-related morbidity and mortality in the United States. In the past 30 years, a large amount of research has been performed to investigate the pathogenesis and pathophysiology of preeclampsia, ways to treat preeclampsia, markers that can be used to predictread more
Citations
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Journal ArticleDOI
Cardiovascular Implications in Preeclampsia An Overview
TL;DR: Because the pathogenesis of preeclampsia has not been fully elucidated, the search for predictive markers and a preventative strategy remains an unfulfilled goal, and clinical management is mainly symptomatic and directed to prevent maternal morbidity and mortality.
Journal ArticleDOI
Maternal Cardiovascular Function in Normal Pregnancy: Evidence of Maladaptation to Chronic Volume Overload.
TL;DR: In this article, the authors investigated cardiac functional status in pregnancy using a comprehensive approach taking into account the simultaneous changes in loading and geometry, as well as maternal age and anthropometric indices.
Journal ArticleDOI
Placental exosomes and pre-eclampsia: Maternal circulating levels in normal pregnancies and, early and late onset pre-eclamptic pregnancies.
TL;DR: The differences in the contribution of placental-derived exosomes to total exosome in maternal circulation suggests a possible pathophysiological role of placmental-derivedExosomes in pre-eclampsia.
Journal ArticleDOI
Advances in the pathophysiology of pre-eclampsia and related podocyte injury
TL;DR: Recent findings regarding placental, endothelial, and podocyte pathophysiology in pre-eclampsia provide unique and exciting possibilities for improved diagnostic accuracy, and emerging evidence suggests that testing for urinary podocytes or their markers may facilitate the prediction and diagnosis of pre- eClampsia.
Journal ArticleDOI
First trimester preeclampsia screening and prediction
TL;DR: The use of the FMF prediction model, followed by the administration of low dose aspirin, has been shown to reduce the rate of preterm preeclampsia by 62%, which is superior to that of the traditional method by maternal risk factors alone.
References
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Journal ArticleDOI
Endovascular Trophoblast Invasion: Implications for the Pathogenesis of Intrauterine Growth Retardation and Preeclampsia
TL;DR: The reviewed data suggest that endovascular trophoblast invasion involves a side route of interstitial invasion, which is associated with maintenance of high uteroplacental vascular resistance and intrauterine growth restriction (IUGR) and preeclampsia.
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Rheological and Physiological Consequences of Conversion of the Maternal Spiral Arteries for Uteroplacental Blood Flow during Human Pregnancy
TL;DR: Dilation has a surprisingly modest impact on total blood flow, and so it is suggested the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
Journal ArticleDOI
Placental Origins of Preeclampsia Challenging the Current Hypothesis
TL;DR: Although the placenta plays a crucial role in the development of preeclampsia, the onset, severity, and progression is significantly affected by the maternal response to placentally derived factors and proteins.
Journal ArticleDOI
Subclassification of Preeclampsia
TL;DR: A first step would be to subdivide preeclampsia into early‐onset disease (< 34 + 0 weeks') and late onset disease (> 34 +0 weeks').
Journal ArticleDOI
Oxidative stress in the pathogenesis of preeclampsia.
TL;DR: A recurrent theme is that free radical reactions, promoted by "cross-talk" between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.
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