The sFlt-1/PlGF ratio as a predictor for poor pregnancy and neonatal outcomes

Chang, Yu Shan; Chen, Chi Nien; Jeng, Suh‐Fang; Su, Yi Ning; Chen, Chien-Yi; Chou, Hung-Chieh; Tsao, Po‐Nien; Hsieh, Wu‐Shiun

doi:10.1016/j.pedneo.2016.10.005

Cited by 39 publications

(28 citation statements)

References 30 publications

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“…However, there are studies that prove not such a strong connection between the said parameter and birth weight. The correlation does exist, however it is considerably lower from those between the PAPP -A and the birth weight [21]. Our research did not prove this connection (p=>0.05) and the results gained comply with Nilgun et al [22].…”

Section: Mom In Prediction Of Birth Weightcontrasting

confidence: 50%

Diagnostic validity of a marker model of first trimester in pregnancy in prediction of birth weight

et al. 2022

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Background/Aim. Nowadays, low birth weight is considered to be one of the main causes of cardiovascular diseases or metabolic syndrome occurring later in life. Many studies have shown a strong impact of abnormal birth weight onto the future development, however, due to its stronger influence onto the development, a special emphasis is placed on low birth weight as compared to higher one. There is still no high-percentage accuracy test that will clearly classify expectant women under the risk of giving birth to a child too low or too big for gestational age. The aim of this paper was to set up a model that may indicate future low or high birth weight. Methods. This study included 191 expectant women who were divided into three groups, based on the birth weight (group 1: ? 3,000 g; group 2: 3,000?4,000 g; group 3: ? 4,000 g). The values of biochemical (pregnancy associated plasma protein A ? PAPP-A, free ? human chorionic gonadotropin) and ultra-sonographic markers (nuchal translucency) as well as their multiple of the median (MoM) were determined and com-pared among groups. Results. It was shown that the values of PAPP-A MoM were considerably lower in groups of expectant women that had a fetus with low body weight (p = 0.003, p = 0.001). Statistically significant correlation between PAPP-A MoM and the newborn?s weight (rs = 0.221, p = 0.001) was proven among the groups examined within this study. Conclusion. The usage of a combination of biochemical parameters, sonographic and demographic data in screening program increases the chances for early identification of fetuses that are under higher risk for growth restriction or increased growth. Al-so, the increase in the value of PAPP- A MoM causes the increase of fetus? body weight.

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Section: Mom In Prediction Of Birth Weightcontrasting

confidence: 50%

Diagnostic validity of a marker model of first trimester in pregnancy in prediction of birth weight

et al. 2022

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“…Overexpression of the soluble isoform of the human VEGF receptor, sFLT1, in mouse embryos induces pre-eclampsia like symptoms in pregnant dams, including IUGR, hypertension, and proteinuria, which can be ameliorated by PGF induction suggesting that PGF works antagonistically with sFLT1 to regulate placental angiogenesis ( 94 ). Dysregulated expression of sFLT1, PGF, and other angiogenic factors has been observed in human pregnancies complicated by IUGR and early onset pre-eclampsia complicated by IUGR ( 95 – 97 ). Indeed, determination of the sFLT1:PGF ratio, in combination with ultrasound findings, shows promise as a test of pre-eclampsia risk in the clinic, with an elevated ratio as an indicator of disease risk in pregnant women before the clinical onset of symptoms ( 98 , 99 ).…”

Section: Placental Structures Linked To Embryonic Growthmentioning

confidence: 99%

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

2018

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The placenta is the chief regulator of nutrient supply to the growing embryo during gestation. As such, adequate placental function is instrumental for developmental progression throughout intrauterine development. One of the most common complications during pregnancy is insufficient growth of the fetus, a problem termed intrauterine growth restriction (IUGR) that is most frequently rooted in a malfunctional placenta. Together with conventional gene targeting approaches, recent advances in screening mouse mutants for placental defects, combined with the ability to rapidly induce mutations in vitro and in vivo by CRISPR-Cas9 technology, has provided new insights into the contribution of the genome to normal placental development. Most importantly, these data have demonstrated that far more genes are required for normal placentation than previously appreciated. Here, we provide a summary of common types of placental defects in established mouse mutants, which will help us gain a better understanding of the genes impacting on human placentation. Based on a recent mouse mutant screen, we then provide examples on how these data can be mined to identify novel molecular hubs that may be critical for placental development. Given the close association between placental defects and abnormal cardiovascular and brain development, these functional nodes may also shed light onto the etiology of birth defects that co-occur with placental malformations. Taken together, recent insights into the regulation of mouse placental development have opened up new avenues for research that will promote the study of human pregnancy conditions, notably those based on defects in placentation that underlie the most common pregnancy pathologies such as IUGR and pre-eclampsia.

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“…The sFlt‐1/PIGF ratio at 26–30 gestational weeks has been shown to be negatively associated with neonatal birth weight . In a study of 25 pregnant women who had either pre‐eclampsia or IUGR, a sFlt‐1/PIGF ratio above 85 at 16–36 gestational weeks was associated with a higher incidence of fetal demise, early pregnancy termination, preterm delivery, low birth weight, and respiratory distress syndrome . The use of these biomarkers to monitor pregnancies complicated by pre‐eclampsia can reduce fetal and maternal deaths.…”

Section: Role Of Angiogenic Factors In the Management Of Pre‐eclampsiamentioning

confidence: 99%

Role of angiogenic factors in the pathogenesis and management of pre‐eclampsia

Ngene

Moodley

2018

Intl J Gynecology & Obste

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The cause of pre-eclampsia is unknown. Different postulates have been developed to explain its pathogenesis. The two-stage theory and angiogenic imbalance are two notable postulates of the disease. Together, they propose that there is a lack of cytotrophoblastic invasion of the uterine spiral arteries in pre-eclampsia. The lumen of these arteries remains narrow instead of converting to the wide channels seen in normal pregnancy, and result in poor placental perfusion. Coupled with maternal susceptibility, this process leads to the release of mediators, including an excess of anti-angiogenic factors that result in the clinical manifestations of the disease. Circulating levels of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 increase, whereas pro-angiogenic factors such as placental growth factor decrease. Assessment of the circulating concentrations of these angiogenic factors, such as the soluble fms-like tyrosine kinase-1/placental growth factor ratio, has diverse clinical relevance in pre-eclampsia. The present review describes the role of angiogenic factors in the pathogenesis and management of pre-eclampsia.

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The sFlt-1/PlGF ratio as a predictor for poor pregnancy and neonatal outcomes

Abstract: High sFlt-1/PlGF ratio in pregnant women is associated with poor pregnancy and neonatal outcomes. Therefore, the monitoring of sFlt-1/PlGF ratio in pregnant women with fetal IUGR and timely management for placenta-associated diseases are recommended.

Cited by 39 publications

References 30 publications

Diagnostic validity of a marker model of first trimester in pregnancy in prediction of birth weight

Diagnostic validity of a marker model of first trimester in pregnancy in prediction of birth weight

Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models

Role of angiogenic factors in the pathogenesis and management of pre‐eclampsia

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