Change in Amniotic Fluid Levels of Multiple Anti-Angiogenic Proteins before Development of Preeclampsia and Intrauterine Growth Restriction

Wang, Chao‐Nin; Chang, Shuenn‐Dyh; Peng, Hsiu-Huei; Lee, Yun‐Shien; Chang, Yao‐Lung; Cheng, Po‐Jen; Chao, An‐Shine; Wang, Tzu‐Hao; Wang, Hsin-Shih

doi:10.1210/jc.2009-1954

Cited by 59 publications

(49 citation statements)

References 71 publications

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“…29 In fact it is possible that the local vascular concentrations of ET-1 were even higher, since its secretion is polarized, and the circulating levels are usually lower. In a recent study, Wang et al 30 showed increased levels of ET-1 and sFLt-1 in the amniotic fluid obtained at 16-19 weeks of gestation in women who later developed PE, and noted a positive correlation between the two. Some limitations of this study must be acknowledged.…”

Section: Discussionmentioning

confidence: 95%

The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia

et al. 2011

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Placental overproduction of anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) has a key role in the development of preeclampsia (PE). Circulating endothelin-1 (ET-1) levels are also elevated in PE. In this study, we investigated the correlation between ET-1 and sFlt-1, placental growth factor (PlGF), sEng levels during uncomplicated normotensive pregnancy and PE. A total of 218 pregnant primigravid women were enrolled: 110 with PE and 108 uncomplicated normotensive pregnancies. PE was defined as new onset of elevated blood pressure (BP) 4140/90 mm Hg and X2 þ proteinuria on two occasions after 20 weeks of gestation in previously normotensive pregnant women. Circulating ET-1, sFlt-1, sEng and PlGF levels were estimated using enzyme immunoassays, and correlation between variables was ascertained. Women with PE showed higher levels of sFlt-1 (41.5 ± 15.7 vs 6.15 ± 3.4 ng ml -1 , Po0.001), sEng (84.9 ± 38.8 vs 13.2 ± 6.3 ng ml -1 , Po0.001), ET-1 (1.52 ± 0.55 vs 0.88±0.35 pg ml -1 , Po0.001) and sFlt-1:PlGF ratio (591.1±468.4 vs 18.3±2.1, Po0.001); and lower levels of PlGF (96.3 ± 47.2 vs 497.6 ± 328.2pg ml -1 , Po0.001). BP levels showed an independent relationship with sFlt-1:PlGF ratio in normotensive pregnant women and with sFlt-1:PlGF ratio and ET-1 in PE. sFlt-1 and sFlt-1:PlGF ratio correlated with proteinuria. ET-1 correlated significantly with sFlt-1, sEng and sFlt-1:PlGF ratio in PE. Our results show an association between elevation of sFlt-1 and sEng and ET-1 in the maternal circulation in PE, and strengthen the possibility that ET-1 may be a mediator in genesis of PE syndrome secondary to anti-angiogenic factors released by the placenta.

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Section: Discussionmentioning

confidence: 95%

The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia

et al. 2011

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“…[9][10][11][12][13][14][15][16] Apart from being expensive, laboratories at majority of centers are not equipped with facilities of measurements of these markers. Measurement of maternal serum ferritin has also been used as a predictive marker of increase risk of IUGR.…”

Section: Introductionmentioning

confidence: 99%

Role of maternal serum ferritin as a predictive marker in intrauterine growth restriction

Bindal

Godha

Kohli

et al. 2015

Int J Reprod Contracept Obstet Gynecol

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“…[98][99][100][101] Placental overproduction of soluble VEGF receptor-1 (soluble fms-like tyrosine kinase-1 [sFlt-1]), which inhibits VEGF signaling through trapping free VEGF, 102 causes maternal endothelial dysfunction and plays a central role in the pathogenesis of preeclampsia. 99,103,104 Intraamniotic sFlt-1 administration during late gestation impairs lung VEGF signaling and increases apoptosis of endothelial cells in newborn rats, which is followed by reductions in alveolarization and vascular growth, along with biventricular hypertrophy during infancy. 98 Similarly, intrauterine growth restriction has been associated with an increased risk for PH in BPD infants 105 and has also been associated with disruption of VEGF signaling and pulmonary vascular growth in experimental intrauterine growth restriction.…”

Section: Pvd In Bpdmentioning

confidence: 99%

The Robyn Barst Memorial Lecture: Differences between the Fetal, Newborn, and Adult Pulmonary Circulations: Relevance for Age‐Specific Therapies (2013 Grover Conference Series)

et al. 2014

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Pulmonary arterial hypertension (PAH) contributes to poor outcomes in diverse diseases in newborns, infants, and children. Many aspects of pediatric PAH parallel the pathophysiology and disease courses observed in adult patients; however, critical maturational differences exist that contribute to distinct outcomes and therapeutic responses in children. In comparison with adult PAH, disruption of lung vascular growth and development, or angiogenesis, plays an especially prominent role in the pathobiology of pediatric PAH. In children, abnormalities of lung vascular development have consequences well beyond the adverse hemodynamic effects of PAH alone. The developing endothelium also plays critical roles in development of the distal airspace, establishing lung surface area for gas exchange and maintenance of lung structure throughout postnatal life through angiocrine signaling. Impaired functional and structural adaptations of the pulmonary circulation during the transition from fetal to postnatal life contribute significantly to poor outcomes in such disorders as persistent pulmonary hypertension of the newborn, congenital diaphragmatic hernia, bronchopulmonary dysplasia, Down syndrome, and forms of congenital heart disease. In addition, several studies support the hypothesis that early perinatal events that alter lung vascular growth or function may set the stage for increased susceptibility to PAH in adult patients ("fetal programming"). Thus, insights into basic mechanisms underlying unique features of the developing pulmonary circulation, especially as related to preservation of endothelial survival and function, may provide unique therapeutic windows and distinct strategies to improve short-and long-term outcomes of children with PAH.Keywords: pulmonary vascular development, angiogenesis, alveolarization, persistent pulmonary hypertension of the newborn, congenital diaphragmatic hernia, bronchopulmonary dysplasia, Down syndrome, pediatric pulmonary hypertension. Pulmonary arterial hypertension (PAH) is a devastating and progressive disease that is characterized by abnormalities of vascular tone and reactivity, vessel wall structure, growth, and thrombosis. 1 Mechanisms contributing to PAH and its progression are complex and remain incompletely understood. Insights into vascular biology over the past few decades have led to remarkable improvements in the clinical course, outcomes, and survival in adults with PAH, yet relatively few studies have been performed in children. As in adults, PAH contributes to poor outcomes in diverse cardiac, pulmonary, and systemic diseases in newborns, infants, and children (Table 1). 2 There is a clear need to define the natural history of pediatric PAH in diverse settings; to develop new strategies to identify at-risk patients early in their course; and to establish novel approaches to better diagnose, evaluate, and treat children with PAH. 3,4 Despite many similarities between pediatric and adult PAH, critical differences exist that currently limit our clinical appr...

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Change in Amniotic Fluid Levels of Multiple Anti-Angiogenic Proteins before Development of Preeclampsia and Intrauterine Growth Restriction

Cited by 59 publications

References 71 publications

The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia

The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia

Role of maternal serum ferritin as a predictive marker in intrauterine growth restriction

The Robyn Barst Memorial Lecture: Differences between the Fetal, Newborn, and Adult Pulmonary Circulations: Relevance for Age‐Specific Therapies (2013 Grover Conference Series)

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