Longitudinal changes in maternal serum placental growth factor and soluble fms‐like tyrosine kinase‐1 in women at increased risk of pre‐eclampsia

Khalil, Asma; Maíz, Nerea; Garcia-Mandujano, R.; Penco, José María Pérez; Nicolaides, Kypros H.

doi:10.1002/uog.15750

Cited by 42 publications

(26 citation statements)

References 44 publications

(76 reference statements)

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“…Our study revealed signifi cantly higher serum levels of sFlt-1 and sFlt-1/PIGF ratio in pre-eclamptic women in early second trimester as compared to the normotensive pregnant women, these being associated with signifi cantly lower PlGF levels. This is in agreement with the fi ndings of a prospective longitudinal study carried out from 15 weeks' gestation onward [14]. Similarly, another prospective study measured serum sFlt-1 and PlGF levels at 10, 18, 26 and 35 weeks of gestation [15].…”

Section: Discussionsupporting

confidence: 89%

PlGF, sFlt-1 and sFlt-1/PlGF ratio: Promising markers for predicting pre-eclampsia

Marwa¹

2018

J Gynecol Res Obstet

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Pre-eclampsia is a hypertensive disorder complicating 5-8% of pregnancies [1]. It is characterized by hypertension and proteinuria and is a leading cause of maternal mortality in 15-20% of pregnant women in developed countries versus 40-80% in developing countries [2,3]. Pre-eclampsia is a state of angiogenic imbalance associated with endothelial dysfunction within specifi c vascular beds (4). The abnormalities in the development of the placental vasculature could occur early, weeks to months before the development of the clinical manifestations of pre-eclampsia [5]. Placental growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, is one of the main factors that play a key role in the remodeling process of maternal arteries in normal pregnancy. This growth factor is released into the bloodstream by the migrating trophoblasts [6]. The soluble fms-like tyrosine kinase-1 (sFlt-1), also known as soluble VEGF receptor-1, is a variant of the VEGF receptor, which is secreted from endothelial cells, monocytes, and placenta. The sFlt-1 is capable of binding with both VEGF and PlGF, consequently regulating their action [7]. Alterations in maternal serum concentrations of PlGF and sFlt-1 have been reported to precede the onset of clinically identifi able preeclampsia as early as the fi rst trimester [6]. The aim of our study is to assess the clinical utility of PlGF and sFlt-1 as early predictors of preeclampsia.

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Section: Discussionsupporting

confidence: 89%

PlGF, sFlt-1 and sFlt-1/PlGF ratio: Promising markers for predicting pre-eclampsia

Marwa¹

2018

J Gynecol Res Obstet

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“…For all these predictors, the performance was better for early than for late PE, and was better when assessed later in pregnancy than at 11–13 weeks, i.e. closer to the development of PE.…”

Section: Combined Screening Strategiesmentioning

confidence: 96%

“…Multiple studies have shown that women who go on to develop PE have, on average, higher mean arterial pressure, higher concentrations of maternal serum soluble fms‐like tyrosine kinase‐1 (sFlt‐1) and alpha‐fetoprotein (AFP), and lower concentrations of pregnancy‐associated plasma protein‐A (PAPP‐A) and PlGF, along with higher resistance in the uterine arteries, compared with women who do not. For all these predictors, the performance was better for early than for late PE, and was better when assessed later in pregnancy than at 11–13 weeks, i.e. closer to the development of PE.…”

Section: Combined Screening Strategiesmentioning

confidence: 99%

“…Second‐trimester prediction of PE appears to be at least as sensitive as prediction in the first trimester, but its value is limited by the lack of effective interventions at this gestational stage. While aspirin commenced in the first trimester appears to reduce the development of PE, the same intervention seems ineffective when started after 20 weeks.…”

Section: Management After Screeningmentioning

confidence: 99%

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ISUOG Practice Guidelines: role of ultrasound in screening for and follow‐up of pre‐eclampsia

Sotiriadis

Hernández‐Andrade

Costa

et al. 2018

Ultrasound in Obstet & Gyne

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138

115

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RESUMEN Pautas de práctica de ISUOG: la función del ultrasonido en la detección y seguimiento de la preeclampsia Introducción La hipertensión en el embarazo afecta hasta el 10% de las mujeres embarazadas y la incidencia global combinada de la preeclampsia (PE) es de aproximadamente el 3%. Las diferencias significativas entre los países desarrollados y en desarrollo pueden atribuirse a diferencias reales o a diferencias derivadas de la adquisición de datos. La PE y sus complicaciones contribuyen en gran medida a la morbilidad y mortalidad materna y perinatal en todo el mundo. Dado que la atención oportuna y efectiva puede mejorar los resultados de la PE, el desarrollo de estrategias eficaces de predicción y prevención ha sido uno de los principales objetivos de la atención prenatal y de la investigación. La PE es una enfermedad multisistémica de origen multifactorial: está relacionada con placentación defectuosa, estrés oxidativo, autoinmunidad, activación de plaquetas y trombina, inflamación intravascular, disfunción endotelial, desequilibrio en la angiogénesis y mala adaptación cardíaca materna. La invasión defectuosa de la placenta está fuertemente asociada con la mayoría de los casos de PE temprana y grave. En contraste, la placentación defectuosa parece ser menos importante para el desarrollo de la PE que se manifiesta más tarde en el embarazo, por ejemplo después de las 34 semanas. En comparación con los embarazos afectados por la enfermedad de aparición temprana, en aquellos complicados con PE a término o cerca de este, la frecuencia de anomalías histológicas de las placentas es significativamente menor, y los factores maternos (p. ej. el síndrome metabólico o la hipertensión crónica) tienen una importancia relativamente mayor. También se observan diferencias entre la PE de aparición temprana y la de aparición tardía en los factores de riesgo, la capacidad de respuesta vascular materna, el rendimiento del cribado y la eficacia de la prevención. El conocimiento cada vez mayor sobre la fisiopatología de la PE se refleja en las estrategias de cribado actuales, que se basan en el historial, la demografía, los biomarcadores (como la presión arterial) y el Doppler de la arteria uterina. Actualmente hay más de 10 000 artículos de PubMed relacionados con la detección de la PE, lo que indica el gran interés en este tema. Menos de una quinta parte de estos se refieren a la detección temprana, lo que constituye un avance de la última década. El objetivo de estas Pautas es revisar la evidencia más reciente y, en lo posible, proporcionar recomendaciones basadas en la evidencia con respecto a la función del ultrasonido en el cribado y seguimiento de la PE. Las Pautas se centran en los aspectos técnicos y clínicos del cribado, sin incluir los aspectos económicos y políticos de la salud, como la conveniencia y la rentabilidad del cribado. Además, estas Pautas se elaboraron partiendo del supuesto de que se dispone de los recursos necesarios para la realización del cribado y el seguimiento (equipo, examinadores y conocimient...

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“…A disturbance in the balance of pro‐ and anti‐angiogenic factors has been repeatedly reported in women with preeclampsia. Of the most studied anti‐angiogenic factors, sFlt‐1 and sEng are two soluble anti‐angiogenic factors released after the damaging inflammatory response occurs in the placenta and significantly increased in the circulation of women with preeclampsia . Soluble Flt‐1, a splice variant of Flt‐1, is primarily released by the placenta and binds to circulating free VEGF and PlGF .…”

Section: Targeting Anti‐angiogenic Factorsmentioning

confidence: 99%

Targeting the vascular dysfunction: Potential treatments for preeclampsia

et al. 2019

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Preeclampsia is a pregnancy-specific disorder clinically characterized by new-onset hypertension (>20 weeks' gestation) with one or more of proteinuria and maternal organ dysfunction such as renal insufficiency, liver dysfunction, neurological complications, fetal growth restriction, or uteroplacental dysfunction. 1,2 Each year, preeclampsia is the principal cause of death in over 60 000 women and in more than 500 000 babies globally. 3 The pathophysiological mechanisms underlying the disease are still not entirely clear. Briefly, In 2017, Sarah was awarded her PhD at the University of Melbourne, Australia, and is currently an NHMRC Peter Doherty Research Fellow in the Department of Obstetrics and Gynecology at Monash University, Australia. The focus of her research is to assess the potential of new and old therapeutics to target the vascular dysfunction of preeclampsia, and translate these studies into clinical application. AbstractPreeclampsia is a pregnancy-specific disorder, primarily characterized by new-onset hypertension in combination with a variety of other maternal or fetal signs. The pathophysiological mechanisms underlying the disease are still not entirely clear.Systemic maternal vascular dysfunction underlies the clinical features of preeclampsia. It is a result of oxidative stress and the actions of excessive anti-angiogenic factors, such as soluble fms-like tyrosine kinase, soluble endoglin, and activin A, released by a dysfunctional placenta. The vascular dysfunction then leads to impaired regulation and secretion of relaxation factors and an increase in sensitivity/production of constrictors. This results in a more constricted vasculature rather than the relaxed vasodilated state associated with normal pregnancy. Currently, the only effective "treatment" for preeclampsia is delivery of the placenta and therefore the baby.Often, this means a preterm delivery to save the life of the mother, with all the attendant risks and burdens associated with fetal prematurity. To lessen this burden, there is a pressing need for more effective treatments that target the maternal vascular dysfunction that underlies the hypertension. This review details the vascular effects of key drugs undergoing clinical assessment as potential treatments for women with preeclampsia.

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Longitudinal changes in maternal serum placental growth factor and soluble fms‐like tyrosine kinase‐1 in women at increased risk of pre‐eclampsia

Abstract: Objectives To investigate longitudinal changes in maternal serum levels of placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFlt-1) in pregnant women who develop pre-eclampsia (PE) or gestational hypertension (GH). Methods

Cited by 42 publications

References 44 publications

PlGF, sFlt-1 and sFlt-1/PlGF ratio: Promising markers for predicting pre-eclampsia

PlGF, sFlt-1 and sFlt-1/PlGF ratio: Promising markers for predicting pre-eclampsia

ISUOG Practice Guidelines: role of ultrasound in screening for and follow‐up of pre‐eclampsia

Targeting the vascular dysfunction: Potential treatments for preeclampsia

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