China
Africa
Explore chapters and articles related to this topic
Hypertensive Disorders
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
A 2017 multicenter, double-blind, placebo-controlled trial was conducted including 1776 women with singleton pregnancies who were considered high risk for preterm pre-eclampsia based on a combination of maternal factors, mean arterial pressure (MAP), uterine-artery pulsatility index, maternal serum pregnancy-associated plasma protein A (PAPP-A) and placental growth factor (PlGF) during their visit between 11 0/7 weeks through 13 6/7 weeks of gestation. Patients received either aspirin (150 mg/day) or placebo from 11–14 weeks of gestation until 36 weeks of gestation. Preterm pre-eclampsia was decreased by 62% in the aspirin group (OR, 0.38; 95% CI, 0.20 to 0.74; P = 0.004) [60].
Placenta previa and placental abruption
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The etiology of abruption is unknown. Some cases are associated with rapid changes in uterine size or shape. This is the case with maternal trauma or abruption that can occur after delivery of one fetus in a multifetal pregnancy or after reduction amniocentesis. Other cases may be related to acute vascular changes in the mother, such as that which may occur after maternal cocaine use. Abruption may also occur in association with chronic placental disease. It is known that abruption is increased, for example, in gravidas with elevated maternal serum alpha fetoprotein levels. Low Papp-A levels are similarly associated with abruption. Serum levels of placental growth factor are decreased in gravida who subsequently develop placental abruption (43). Thrombophilia disorders are common, and some studies have noted an association between thrombophilia and placental abruption (44–47). This association, however, does not establish thrombophilia as a cause of abruption. Newer prospective studies are finding little association between inherited thrombophilias and pregnancy complication such as placental abruption. Currently, there is no evidence that patients with a history of abruption and known thrombophilia should be treated with heparin during pregnancy for the prevention of abruption recurrence (48). It is reasonable to use folate to treat hyperhomocysteinemia in patients with prior abruption. Risk factors for abruption are shown in Table 2 (49–53).
Hypertension and pre-eclampsia (PET)
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
In pregnancies complicated by pre-eclampsia, invasion of trophoblast cells is confined to the decidual level of the blood vessels causing a problem with normal uterine placental blood flow. This results in a relatively under-perfused (ischaemic) placenta. This placental hypoperfusion is accompanied by an imbalance of key angiogenic factors that are important in the development of blood vessels. Soluble fms-like tyrosine kinase-1(S Flt-1) is secreted by the placenta in excess amounts in pregnancies complicated by pre-eclampsia. It has an anti-angiogenic effect and this results in systemic endothelial dysfunction and antagonises placental growth factor. Placental Growth Factor (PlGF) is produced by the syncytiotrophoblast cells of the placenta and can be identified in maternal blood from around 12 weeks’ gestation15. Concentrations of PlGF increase until around 30 weeks, after which it declines. It is important in promoting blood vessel formation and low levels of PlGF are associated with pre-eclampsia15,16. Measurement of PlGF, or the ratio of PlGF to sFlt, are the basis of a maternal blood test, which aims to identify women at greater risk of pre-eclampsia3,17.
Analysis of serum placental growth factor levels in preeclamptic and normotensive pregnant women in Lagos, Nigeria: a worthwhile screening tool?
Published in Journal of Obstetrics and Gynaecology, 2022
Ayodeji A. Oluwole, Adeolu A. Onakoya, Kehinde S. Okunade, Ochuwa A. Babah, Opeyemi Akinajo
Central to the pathophysiologic abnormalities of preeclampsia is placental ischaemia leading to the release of circulating factors such as placental growth factor (PlGF) that cause extensive endothelial cell damage (Powe et al. 2011). PlGF, an angiogenic factor, is a secondary marker of placental dysfunction commonly seen in preeclampsia (Griffin et al. 2015; Agrawal et al. 2019). In normal pregnancy, the maternal circulatory levels of PlGF increase with gestation, with concentration reaching a peak at between 26 and 30 weeks and subsequently declining towards term (Griffin et al. 2015). Numerous studies have, however, shown a drop in the levels of PlGF before the development of preeclampsia, and also a further drop in women who had severe disease (Shokry et al. 2010; Wortelboer et al. 2010; Powe et al. 2011; Dover et al. 2013; Ghosh et al. 2013; Moore Simas et al. 2014; Li et al. 2016). This reduction in PlGF level has been shown to occur throughout gestation and even as early as the first trimester, a time when angiogenesis is critical for placental invasion, thus providing evidence of its potential usefulness as a screening tool for predicting preeclampsia (Agrawal et al. 2019).
Cardiovascular and hemodynamic consequences of recombinant placental growth factor administration in Guinea pigs
Published in Hypertension in Pregnancy, 2022
Adelene Y. Tan, Ken Kearney, Courtney Jenkins, S. Ananth Karumanchi, Walter Bee, Paul Kussie
Placental growth factor (PlGF), a secreted glycoprotein that belongs to the vascular endothelial growth factor (VEGF) family of growth factors, has emerged as a key factor in the pathogenesis of preeclampsia (1). PlGF is expressed at high levels by the human placenta and has pro-angiogenic activities in a variety of in vitro and in vivo models of angiogenesis (2,3). PlGF also plays an important role in the maintenance of vascular tone through its vasodilatory properties (4). PlGF has been shown to vasodilate ex vivo isolated blood vessels in several species using several methods (5–11). PlGF therapy has been shown to reduce blood pressure in pregnant primates and rodents (12–14); however, the acute time course of these BP changes has not been characterized. The purpose of this study was to record acute cardiovascular changes induced by PlGF administered intravenously using Guinea pigs with implanted telemeters (15,16).
The Placental Growth Factor Pathway and Its Potential Role in Macular Degenerative Disease
Published in Current Eye Research, 2019
Fiona Cunningham, Tine Van Bergen, Paul Canning, Imre Lengyel, Jean H. M. Feyen, Alan W. Stitt
Placental growth factor (PlGF) is a member of the VEGF family, first discovered in the placenta43, where its elevation corresponds with placental angiogenesis.44 The human PlGF gene encodes four isoforms with distinct properties.45–47 PlGF-1 and -3 are diffusible isoforms, while PlGF-2 and -4 possess heparin-binding domains, conferring them additional ligand–receptor interactions. All four isoforms bind VEGFR1, while PlGF-2 and -4 additionally bind to neuropilins (NP-1 and NP-2), which are the VEGFR1 co-receptors highly expressed by neurons.48,49 PlGF-activated VEGFR1 signalling is distinct from VEGF-A-mediated signalling, due to the phosphorylation of different tyrosine residues on the receptors, leading to specific regulation of downstream targets.50,51