Elevated circulating thrombomodulin in severe preeclampsia

Hsu, Chaur Dong; Iriye, Brian; Johnson, Timothy R.B.; Witter, Frank R.; Hong, Shih-Fen; Chan, Daniel W.

doi:10.1016/0002-9378(93)90151-8

Cited by 73 publications

(38 citation statements)

References 2 publications

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“…It is noteworthy, however, that in pre-eclampsia -a disorder characterized by endothelial injury -serum uric acid correlates with markers of endothelial damage, such as plasma levels of thrombomodulin [52] and endothelin-1 [53] . Increased production of uric acid by endothelial cells might then represent a more sensitive marker of endothelial injury, since activation of uric acid production must occur before cellular damage.…”

Section: Discussionmentioning

confidence: 99%

Uric acid in chronic heart failure: a marker of chronic inflammation

Leyva¹

1998

European Heart Journal

256

166

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Section: Discussionmentioning

confidence: 99%

Uric acid in chronic heart failure: a marker of chronic inflammation

Leyva¹

1998

European Heart Journal

256

166

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“…Although markers of systemic inflammation [79,80] and endothelial dysfunction [81][82][83][84][85][86][87][88] in maternal blood have been associated with preeclampsia, their prognostic performance for the identification of patients with preeclampsia prior to diagnosis has been disappointing [79][80][81]83,[89][90][91]. This indicates that either inflammation occurs late (even during the subclinical phase of the disease), or that the current methods available to detect intravascular inflammation are not sensitive enough.…”

Section: Introductionmentioning

confidence: 92%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Objectives: Angiogenic/anti-angiogenic factors have emerged as one of the promising biomarkers for the prediction of preeclampsia. Since not all patients with preeclampsia can be identified by these analytes, the search for additional biomarkers continues. The soluble form of ST2 (sST2), a protein capable of binding to interleukin (IL)-33 and thus contributing to a Th1-biased immune response, has been reported to be elevated in maternal plasma of women with preeclampsia. The aims of this study were to examine: (1) differences in maternal plasma concentrations of sST2 and IL-33 between women diagnosed with preeclampsia and those having uncomplicated pregnancies; (2) the relationship between sST2, umbilical and uterine artery Doppler velocimetry, and the severity of preeclampsia; and (3) the performance of sST2 and angiogenic/anti-angiogenic factors in identifying patients with preeclampsia at the time of diagnosis. Methods: This cross-sectional study included women with preeclampsia (n ¼ 106) and women with an uncomplicated pregnancy (n ¼ 131). Plasma concentrations of sST2, IL-33, soluble vascular endothelial growth factor receptor (sVEGFR)-1, soluble endoglin (sEng) and placental growth factor (PlGF) were determined by enzyme linked immune sorbent assay. Area under the receiver operating characteristic curve (AUC) for the identification of preeclampsia was examined for each analyte. Results: (1) Patients with preeclampsia had a higher mean plasma concentrations of sST2 than those with an uncomplicated pregnancy (p50.0001), while no significant difference in the mean plasma concentration of IL-33 between the two groups was observed; (2) the magnitude of this difference was greater in early-onset, compared to late-onset disease, and in severe compared to mild preeclampsia; (3) sST2 plasma concentrations did not correlate with the results of uterine or umbilical artery Doppler velocimetry (p ¼ 0.7 and p ¼ 1, respectively) among women with preeclampsia; (4) sST2 correlated positively with plasma concentrations of sVEGFR1-1 and sEng (Spearman's Rho ¼ 0.72 and 0.63; each p50.0001), and negatively with PlGF (Spearman's Rho ¼ À0.56, p50.0001); and (5) while the AUC achieved by sST2 and angiogenic/anti-angiogenic factors in identifying women with preeclampsia at the time of diagnosis were non-significantly different prior to term (537 weeks of gestation), thereafter the AUC achieved by sST2 was significantly less than that achieved by angiogenic/anti-angiogenic factors. Conclusions: Preeclampsia is associated with increased maternal plasma concentrations of sST2. The findings that sST2 concentrations do not correlate with uterine or umbilical artery Doppler velocimetry in women with preeclampsia suggest that elevated maternal plasma sST2 concentrations in preeclampsia are not related to the increased impedance to flow in the uteroplacental circulation. The performance of sST2 in identifying preeclampsia at the time of diagnosis prior to 37 weeks of gestation was comparable to that of angiogenic/anti-angiogenic f...

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“…This finding not only emphasises that PE is not merely a variant of essential hypertension but supports the concept that endothelial cells are a target in the disorder. Several markers of endothelial Increased endothelin 222 Increased prevalence of antiendothelial antibodies 80 Increased thrombomodulin 223 Increased thromboxane 224 Increased cellular fibronection (cFN) concentration a 225 Increased plasminogen activation activity (PAI-1) 226 Increased soluble VCAM 227 Increased tissue plasminogen activator 228 Increased ICAM a 229…”

Section: Journal Of Human Hypertensionmentioning

confidence: 99%

“…Blood concentrations of thrombomodulin, an endothelial protein only released with actual injury, are only increased with clinically evident PE. 72 By contrast, reduced prostacyclin production, 73 increased circulating von Willebrand factor 74 and growth factor activity, 75 features of endothelial activation are altered weeks to months before clinically evident PE. The relevance of in vitro effects of PE serum/plasma to the in vivo setting is open to question.…”

Section: Effects On Ex Vivo Vesselsmentioning

confidence: 99%

Hypertension in pregnancy

Pipkin

Roberts

2000

J Hum Hypertens

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Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as geneticallydetermined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similiar features are found in association with non-hypertensive

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Elevated circulating thrombomodulin in severe preeclampsia

Cited by 73 publications

References 2 publications

Uric acid in chronic heart failure: a marker of chronic inflammation

Uric acid in chronic heart failure: a marker of chronic inflammation

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Hypertension in pregnancy

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