Expert review: preeclampsia Type I and Type II

Yagel, Simcha; Cohen, Sarah M.; Admati, Inbal; Skarbianskis, Niv; Solt, Ido; Zeisel, Amit; Beharier, Ofer; Goldman-Wohl, Debra

doi:10.1016/j.ajogmf.2023.101203

Cited by 14 publications

(2 citation statements)

References 91 publications

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“…PE is underlined by a number of genetic, behavioral, and environmental factors, which are modified by the normal physiological changes of pregnancy with the particular relevance of an increased inflammatory response. Conditions known to increase the risk of preeclampsia include obesity, hypertension, diabetes, hyperhomocysteinemia, increased androgens, and Black race [19].…”

Section: Sars-cov-2 Infection and Chronic Placental Pathologymentioning

confidence: 99%

SARS-CoV-2 Infection in Late Pregnancy and Childbirth from the Perspective of Perinatal Pathology

Debelenko

2023

JDB

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This review focuses on SARS-CoV-2 infection in placental and fetal tissues. Viremia is rare in infected pregnant women, and the virus is seldom amplified from placental tissues. Definite and probable placental infection requires the demonstration of viral RNA or proteins using in situ hybridization (ISH) and immunohistochemistry (IHC). Small subsets (1.0–7.9%, median 2.8%) of placentas of SARS-CoV-2-positive women showed definite infection accompanied by a characteristic histopathology named SARS-CoV-2 placentitis (SP). The conventionally accepted histopathological criteria for SP include the triad of intervillositis, perivillous fibrin deposition, and trophoblast necrosis. SP was shown to be independent of the clinical severity of the infection, but associated with stillbirth in cases where destructive lesions affecting more than 75% of the placental tissue resulted in placental insufficiency and severe fetal hypoxic–ischemic injury. An association between maternal thrombophilia and SP was shown in a subset of cases, suggesting a synergy of the infection and deficient coagulation cascade as one of the mechanisms of the pathologic accumulation of fibrin in affected placentas. The virus was amplified from fetal tissues in approximately 40% of SP cases, but definite fetal involvement demonstrated using ISH or IHC is exceptionally rare. The placental pathology in SARS-CoV-2-positive women also includes chronic lesions associated with placental malperfusion in the absence of definite or probable placental infection. The direct viral causation of the vascular malperfusion of the placenta in COVID-19 is debatable, and common predispositions (hypertension, diabetes, and obesity) may play a role.

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Section: Sars-cov-2 Infection and Chronic Placental Pathologymentioning

confidence: 99%

SARS-CoV-2 Infection in Late Pregnancy and Childbirth from the Perspective of Perinatal Pathology

Debelenko

2023

JDB

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“…This study also confirmed that PLGF was mainly derived from the syncytiotrophoblast and was significantly downregulated in early-onset PE, whereas FLT1 expression was upregulated across all trophoblast cell types in the human PE placenta. As reviewed by Yagel et al (2023) [13], type I early-onset preeclampsia is characterized by placental dysfunction or malperfusion, shallow trophoblast invasion, inadequate SpA remodeling, profound syncytiotrophoblast stress, elevated sFLT1 levels, reduced PLGF levels, and high peripheral vascular resistance, often leading to FGR. Type II preeclampsia typically occurs in the later stages of pregnancy with a moderately dysfunctional placenta and a normal or slightly disturbed sFLT1/PlGF ratio.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice

Vogtmann,

Riedel,

Sassmannshausen

et al. 2024

IJMS

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Preeclampsia (PE) is characterized by maternal hypertension and placental dysfunction, often leading to fetal growth restriction (FGR). It is associated with an overexpression of the anti-angiogenic sFLT1 protein, which originates from the placenta and serves as a clinical biomarker to predict PE. To analyze the impact of sFLT1 on placental function and fetal growth, we generated transgenic mice with placenta-specific human sFLT1 (hsFLT1) overexpression. Immunohistochemical, morphometrical, and molecular analyses of the placentas on 14.5 dpc and 18.5 dpc were performed with a focus on angiogenesis, nutrient transport, and inflammation. Additionally, fetal development upon placental hsFLT1 overexpression was investigated. Dams exhibited a mild increase in serum hsFLT1 levels upon placental hsFLT1 expression and revealed growth restriction of the fetuses in a sex-specific manner. Male FGR fetuses expressed higher amounts of placental hsFLT1 mRNA compared to females. FGR placentas displayed an altered morphology, hallmarked by an increase in the spongiotrophoblast layer and changes in labyrinthine vascularization. Further, FGR placentas showed a significant reduction in placental glycogen storage and nutrient transporter expression. Moreover, signs of hypoxia and inflammation were observed in FGR placentas. The transgenic spongiotrophoblast-specific hsFLT1 mouse line demonstrates that low hsFLT1 serum levels are sufficient to induce significant alterations in fetal and placental development in a sex-specific manner.

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Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy

Schwartz,

Stanhewicz

2024

Comprehensive Physiology

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Preeclampsia, a pregnancy disorder characterized by de novo hypertension and maternal multisystem organ dysfunction, is the leading cause of maternal mortality worldwide and is associated with a fourfold greater risk of cardiovascular disease throughout the lifespan. Current understanding of the etiology of preeclampsia remains unclear, due in part to the varying phenotypical presentations of the disease, which has hindered the development of effective and mechanism‐specific treatment or prevention strategies both during and after the affected pregnancy. These maternal sequelae of preeclampsia are symptoms of systemic vascular dysfunction in the maternal nonreproductive microvascular beds that drives the development and progression of adverse cardiovascular outcomes during preeclampsia. Despite normalization of vascular disturbances after delivery, subclinical dysfunction persists in the nonreproductive microvascular beds, contributing to an increased lifetime risk of cardiovascular and metabolic diseases and all‐cause mortality. Given that women with a history of preeclampsia demonstrate vascular dysfunction despite an absence of traditional CVD risk factors, an understanding of the underlying mechanisms of microvascular dysfunction during and after preeclampsia is essential to identify potential therapeutic avenues to mitigate or reverse the development of overt disease. This article aims to provide a summary of the existing literature on the pathophysiology of maternal microvascular dysfunction during preeclampsia, the mechanisms underlying the residual dysfunction that remains after delivery, and current and potential treatments both during and after the affected pregnancy that may reduce microvascular dysfunction in these high‐risk women. © 2024 American Physiological Society. Compr Physiol 14:5703‐5727, 2024.

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Expert review: preeclampsia Type I and Type II

Cited by 14 publications

References 91 publications

SARS-CoV-2 Infection in Late Pregnancy and Childbirth from the Perspective of Perinatal Pathology

SARS-CoV-2 Infection in Late Pregnancy and Childbirth from the Perspective of Perinatal Pathology

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice

Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy

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