Plasma Placenta Growth Factor Levels in Midtrimester Pregnancies

Tjoa, May Lee; Vugt, J.M.G. van; Mulders, Monique A.M.; Schutgens, R. B. H.; Oudejans, Cees; Wijk, Inge J. van

doi:10.1097/00006250-200110000-00014

Cited by 26 publications

(40 citation statements)

References 23 publications

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“…Local placental dysfunction is followed by activation of compensatory pathways in the placenta (PlGF-sFLT1-endoglin axis) and mother (TGF-β-mediated NOS-dependent vasodilation) that ultimately trigger the appearance of systemic maternal symptoms (4)(5)(6). Genetically, the HELLP syndrome and preeclampsia are distinct entities (7).…”

Section: Introductionmentioning

confidence: 99%

HELLP babies link a novel lincRNA to the trophoblast cell cycle

Dijk

Thulluru²,

Mulders³

et al. 2012

J. Clin. Invest.

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The HELLP syndrome is a pregnancy-associated disease inducing hemolysis, elevated liver enzymes, and low platelets in the mother. Although the HELLP symptoms occur in the third trimester in the mother, the origin of the disease can be found in the first trimester fetal placenta. A locus for the HELLP syndrome is present on chromosome 12q23 near PAH. Here, by multipoint nonparametric linkage, pedigree structure allele sharing, and haplotype association analysis of affected sisters and cousins, we demonstrate that the HELLP locus is in an intergenic region on 12q23.2 between PMCH and IGF1. We identified a novel long intergenic noncoding RNA (lincRNA) transcript of 205,012 bases with (peri)nuclear expression in the extravillous trophoblast using strand-specific RT-PCR complemented with RACE and FISH. siRNA-mediated knockdown followed by RNAsequencing, revealed that the HELLP lincRNA activated a large set of genes that are involved in the cell cycle. Furthermore, blocking potential mutation sites identified in HELLP families decreased the invasion capacity of extravillous trophoblasts. This is the first large noncoding gene to be linked to a Mendelian disorder with autosomal-recessive inheritance.

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Section: Introductionmentioning

confidence: 99%

HELLP babies link a novel lincRNA to the trophoblast cell cycle

Dijk

Thulluru²,

Mulders³

et al. 2012

J. Clin. Invest.

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“…This state appears to result from an imbalance in the production and circulating concentrations of angiogenic factors such as placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) and anti-angiogenic factors such as soluble VEGF receptor-1 (sVEGFR-1) and soluble endoglin (sEng). Elevated serum and plasma concentrations of sVEGFR-1 and s-Eng have been observed after the diagnosis of PE [1][2][3][7][8][9]11,12,15,18,19,[21][22][23] and before the recognition of clinical disease [4][5][6]10,13,14,16,17,20,30,32].…”

mentioning

confidence: 99%

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

Erez

Romero

Espinoza

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

273

233

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The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age, The Journal of Maternal-Fetal & Neonatal Medicine, 21:5, 279-287, DOI: 10.1080 AbstractIntroduction. An imbalance between angiogenic and anti-angiogenic factors has been proposed as central to the pathophysiology of preeclampsia (PE). Indeed, patients with PE and those delivering small-for-gestational age (SGA) neonates have higher plasma concentrations of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) and the soluble form of endoglin (s-Eng), as well as lower plasma concentrations of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) than do patients with normal pregnancies. Of note, this imbalance has been observed before the clinical presentation of PE or the delivery of an SGA neonate. The objective of this study was to determine if changes in the profile of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters are associated with a high risk for the subsequent development of PE and/or delivery of an SGA neonate. Methods. This longitudinal case-control study included 402 singleton pregnancies in the following groups: (1) normal pregnancies with appropriate for gestational age (AGA) neonates (n ¼ 201); (2) patients who delivered an SGA neonate (n ¼ 145); and (3) patients who developed PE (n ¼ 56). Maternal plasma samples were obtained at the time of each prenatal visit, scheduled at 4-week intervals from the first or early second trimester until delivery. In this study, we included two samples per patient: (1) first sample obtained between 6 and 15 weeks of gestation ('first trimester' sample), and (2) second sample obtained between 20 and 25 weeks of gestation ('second trimester' sample). Plasma concentrations of s-Eng, sVEGFR-1, and PlGF were determined by specific and sensitive immunoassays. Changes in the maternal plasma concentrations of these angiogenesis-related factors were compared among normal patients and those destined to develop PE or deliver an SGA neonate while adjusting for maternal age, nulliparity, and body mass index. General linear models and polytomous logistic regression models were used to relate the analyte concentrations, ratios, and product to the subsequent development of PE and SGA. Results.(1) An increase in the maternal plasma concentration of s-Eng between the first and second trimesters conferred risk for the development of preterm PE and SGA (OR 14.9, 95% CI 4.9-45.0 and OR 2.9, 95% CI 1.5-5.6, respectively).(2) An increase in the maternal plasma concentration of sVEGFR-1 between the first and second trimester conferred risk for the development of preterm PE (OR 3.9, 95% CI 1.2-12.6). (3) A subnormal increase in maternal plasma PlGF concentration between the first and the second trimester was a risk factor for the subsequent development of preterm and term PE (OR 4....

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“…PIGF value is also low with pregnancy complications associated with a dysfunctional placenta (SGA, preeclampsia or both) [44]. Several studies have found that low PlGF concentrations in first trimester are also predictive factor for SGA, even in the absence of preeclampsia [40,42,47].…”

Section: Reference Pz (N) Gestational Week Resultsmentioning

confidence: 99%

“…By the way this situation leads to a course of antagonizing the angiogenic factors such as PlGF. Some studies have found that low PlGF is a good predictive factor in first trimester for preeclampsia [39][40][41][42][43], while other studies showed no predictive value for PlGF in first trimester [44][45][46][47]. Most studies have found that low PlGF in the second trimester predicts later occurrence of preeclampsia [47][48][49][50][51][52][53][54].…”

Section: Placental Growth Factormentioning

confidence: 99%

Prediction of the preeclampsia: a view of biochemical markers

Bostancı

Bayram

Cevrioğlu

et al. 2013

RHC

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Preeclampsia is a diverse, multiorgan group of related disease processes that occurs in up to 5%-8% of pregnancies after 20 weeks' gestation and it is one of the leading causes of maternal and fetal morbidity and mortality. Many molecular mechanisms are contributed to the pathogenesis of preeclampsia. Although it is unknown whether the mechanisms act independently or have synergistic effects. This review describes review of primary papers investigating blood based biomarker such as PAP-A, Inhibin A, sFlt1, and PP13 in general and first trimester biochemical markers and combinations of them specifically for preeclampsia.

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Plasma Placenta Growth Factor Levels in Midtrimester Pregnancies

Cited by 26 publications

References 23 publications

HELLP babies link a novel lincRNA to the trophoblast cell cycle

HELLP babies link a novel lincRNA to the trophoblast cell cycle

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

Prediction of the preeclampsia: a view of biochemical markers

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