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Journal ArticleDOI

Fetal growth retardation and the maternal arterial supply of the human placenta in the absence of sustained hypertension

TLDR
In five patients with fetal growth retardation in pregnancies with no or only a moderate and transient rise in blood pressure, vascular lesions in the placental bed spiral arteries were found, indicating the first clinical manifestation of underlying reno‐vascular disease.
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This article is published in British Journal of Obstetrics and Gynaecology.The article was published on 1980-08-01. It has received 159 citations till now.

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Citations
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Journal ArticleDOI

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

TL;DR: Findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre‐eclampsia and in SGA, a feature not seen beyond the second trimester in normal pregnancy.
Journal ArticleDOI

Preeclampsia: an excessive maternal inflammatory response to pregnancy.

TL;DR: It is argued that preeclampsia arises when a universal maternal intravascular inflammatory response to pregnancy decompensates in particular cases, which may occur because either the stimulus or the maternal response is too strong.
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Maternal body mass index and the risk of preeclampsia: a systematic overview.

TL;DR: Most observational studies demonstrate a consistently strong positive association between maternal prepregnancy body mass index and the risk of preeclampsia, and increasing obesity in developed countries is likely to increase the occurrence of preeClampsia.
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Current topic: pre-eclampsia and the placenta.

TL;DR: The earlier theories for the causation of pre-eclampsia assumed that deportation was the cause of eclamptic fits, but later evidence that it is a feature of normal human pregnancy has nullified this supposition.
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The myometrial junctional zone spiral arteries in normal and abnormal pregnancies: a review of the literature.

TL;DR: In this article, the authors examined the mechanisms that control decidualization and subsequent trophoblast invasion in normal and abnormal pregnancies, and explored the possibility that disruption of the decideual process in the secretory phase of the menstrual cycle triggers a cascade of events resulting in failed deep placentation.
References
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Intrauterine growth as estimated from liveborn birth-weight data at 24 to 42 weeks of gestation.

TL;DR: The median weights of Colorado babies were found to be lower at 40 weeks of gestation than the national median, and mean weights at 40 and 42 weeks were lower than those given by other authors.
Journal ArticleDOI

Fetal growth retardation and the arteries of the placental bed

TL;DR: It is believed that there exists an arteriopathy which is common to hypertensive and normotensive pregnancies complicated by fetal growth retardation, and in all patients with hypertension and a baby with low birth weight the physiological changes were restricted to the decidual segments of the spiral arteries.
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The ultrastructure of the arterial supply of the human placenta in pregnancy complicated by fetal growth retardation.

TL;DR: The ultrastructure of the arterial supply of the human placenta was studied in 15 pregnancies with severe fetal growth retardation and in both hypertensive and normotensive patients the spiral arteries and basal arteries of the decidua showed occlusive atheromatous lesions with considerable fibrin deposition and accumulation of lipid‐laden cells.
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The ultrastructure of acute atherosis in hypertensive pregnancy.

TL;DR: Acute atherosis of the myometrial segments of the uteroplacental arteries from pre-eclamptic pregnancies was studied by electron microscopy.
Journal ArticleDOI

On the pathogenesis of placental infarcts in pre‐eclampsia

TL;DR: Although placental infarction is apparently a direct result of the occlusive hypertensive lesions in the spiral arteries, it is also to be considered as the ultimate evidence of failure of adequate placentation.
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