Diagnostic Biomarkers in Women With Suspected Preeclampsia in a Prospective Multicenter Study

Duckworth, Susan; Griffin, Melanie; Seed, Paul; North, Robyn A.; Myers, Jenny; Mackillop, Lucy; Simpson, Nigel; Waugh, Jason; Anumba, Dilly; Kenny, Louise C.; Redman, Christopher W.G.; Shennan, Andrew; Chappell, Lucy C

doi:10.1097/aog.0000000000001508

Cited by 30 publications

(18 citation statements)

References 22 publications

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“…One isoform that seems to be gaining more widespread acceptance at least as a predictive marker in PE is circulating PlGF (which preferentially binds VEGFR1). In PE, PlGF levels are decreased, whether free or sFlt-1 bound (Levine et al 2004; Robinson et al 2006) Certainly recent prospective trials suggest the sFlt:PlGF ratio may have particular value as a predictive marker (Zeisler et al 2016) while another study suggests a single marker (PlGF, sFlt-1 or endoglin) may be effective (Duckworth et al 2016). Others have reported the predictive value even at 20–34 weeks were limited (Andersen et al 2016).…”

Section: Hormones Of Preeclampsia-related Endothelial Dysfunctionmentioning

confidence: 99%

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Boeldt

Bird

2017

Journal of Endocrinology

244

152

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Maternal vascular adaptation to pregnancy is critically important in order to expand the capacity for blood flow through the uteroplacental unit to meet the needs of the developing fetus. Failure of the maternal vasculature to properly adapt can result in hypertensive disorders of pregnancy such as preeclampsia (PE). Herein, we review the endocrinology of maternal adaptation to pregnancy and contrast this with that of PE. Our focus is specifically on those hormones with directly impact endothelial cell function and dysfunction, as endothelial cell dysfunction is a hallmark of PE. A variety of growth factors and cytokines are present in normal vascular adaptation to pregnancy but have also been shown to be circulating at abnormal levels in PE pregnancies. Many of these factors promote endothelial dysfunction when present at abnormal levels by acutely inhibiting key Ca2+ signaling events and chronically promoting the breakdown of endothelial cell-cell contacts. Increasingly, our understanding of how the contributions of the placenta, immune cells, and the endothelium itself promote the endocrine milieu of PE is becoming more clear. We then describe in detail how the complex endocrine environment of PE effects endothelial cell function, why this has contributed to the difficulty in fully understanding and treating this disorder, and how a focus on signaling convergence points of many hormones may be a more successful treatment strategy.

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Section: Hormones Of Preeclampsia-related Endothelial Dysfunctionmentioning

confidence: 99%

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Boeldt

Bird

2017

Journal of Endocrinology

244

152

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“…71 In the second trimester, low levels of PlGF have superior screening performance in comparison with many potential biomarkers to predict placenta-related complications. 84 In a prospective cohort of 274 women with suspected preeclampsia presenting at 20-34 weeks' gestation, low circulating PlGF (<100 pg/mL) had high sensitivity to detect SGA births (n ¼ 96) below third customized birthweight centile (sensitivity 93%, negative predictive value [NPV] 90%), which was superior to fetal weight estimation by ultrasound (sensitivity 71%, NPV 79%). 85 An earlier multicenter study by the same group, of 592 women with reduced symphysisfundal height measurements, found that combining PlGF with ultrasound biometry increased the sensitivity from 58-69% for the detection of customized growth at the third centile (with the same 93% NPV).…”

Section: Circulating Proangiogenic and Antiangiogenic Placenta-derivementioning

confidence: 99%

A placenta clinic approach to the diagnosis and management of fetal growth restriction

Kingdom

Audette

Hobson

et al. 2018

American Journal of Obstetrics and Gynecology

127

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Effective detection and management of fetal growth restriction is relevant to all obstetric care providers. Models of best practice to care for these patients and their families continue to evolve. Since much of the disease burden in fetal growth restriction originates in the placenta, the concept of a multidisciplinary placenta clinic program, managed primarily within a maternal-fetal medicine division, has gained popularity. In this context, fetal growth restriction is merely one of many placenta-related disorders that can benefit from an interdisciplinary approach, incorporating expertise from specialist perinatal ultrasound and magnetic resonance imaging, reproductive genetics, neonatal pediatrics, internal medicine subspecialties, perinatal pathology, and nursing. The accurate diagnosis and prognosis for women with fetal growth restriction is established by comprehensive clinical review and detailed sonographic evaluation of the fetus, combined with uterine artery Doppler and morphologic assessment of the placenta. Diagnostic accuracy for placenta-mediated fetal growth restriction may be enhanced by quantification of maternal serum biomarkers including placenta growth factor alone or combined with soluble fms-like tyrosine kinase-1. Uterine artery Doppler is typically abnormal in most instances of early-onset fetal growth restriction and is associated with coexistent preeclampsia and underlying maternal vascular malperfusion pathology of the placenta. By contrast, rare but potentially more serious underlying placental diagnoses, such as massive perivillous fibrinoid deposition, chronic histiocytic intervillositis, or fetal thrombotic vasculopathy, may be associated with normal uterine artery Doppler waveforms. Despite minor variations in placental size, shape, and cord insertion, placental function remains, largely normal in the general population. Consequently, morphologic assessment of the placenta is not currently incorporated into current screening programs for placental complications. However, placental ultrasound can be diagnostic in the context of fetal growth restriction, for example in Breus' mole and triploidy, which in turn may enhance diagnosis and management. Several examples are illustrated in our figures and supplementary videos. Recent advances in the ability of multiparameter screening and intervention programs to reduce the risk of severe preeclampsia will likely increase efforts to deliver similar improvements for women at risk of fetal growth restriction. Placental pathology is important because the underlying pathologies associated with fetal growth restriction have a wide range of recurrence risks. Rare conditions such as massive perivillous fibrinoid deposition or chronic histolytic intervillositis may recur in >50% of subsequent pregnancies. Postpartum care in a placenta-focused program can provide effective counseling for modifiable maternal risk factors, and can assist in planning future pregnancy care based on the pathologic basis of fetal growth restriction.

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“…In Table 1 we report a summary of the studies that aimed to understand if PCT is a PE marker [49,[52][53][54][55][59][60][61][62][63]. At present, however, there are no plasmatic factors that can be considered PE markers with a predictive value.…”

Section: Review Series: Immunology Of Pregnancymentioning

confidence: 99%

“…Perhaps for this reason, numerous studies have been carried out during the last 5 years to verify if the PCT could be an ideal candidate for this role. In Table 1 we report a summary of the studies that aimed to understand if PCT is a PE marker [49,[52][53][54][55][59][60][61][62][63]. In general, we can deduce that PCT plasmatic levels are increased in PE and its levels correlate with the severity of the disease, but PCT has no predictive value.…”

Section: Review Series: Immunology Of Pregnancymentioning

confidence: 99%

Overview of procalcitonin in pregnancy and in pre-eclampsia

Mangogna

Agostinis

Ricci

et al. 2019

Clinical and Experimental Immunology

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Procalcitonin (PCT), a precursor for calcitonin, is a prohormone involved in the inflammatory processes, which has been poorly studied in the context of pregnancy. During severe inflammation, PCT derives from almost all cell types, including monocytes and parenchymal tissues, making it a good predictive and diagnostic marker of an inflammatory state with rapidly increased serum levels in inflammation or sepsis. In normal pregnancy, PCT is basally expressed at very low level by decidual cells, even if decidual macrophages, which in normal pregnancy are skewed to M2 macrophages, are resistant to lipopolysaccharide (LPS)-induced production of PCT. As PCT increase is associated with an inflammatory state, several research groups investigated whether PCT can be considered a marker of pre-eclampsia, a pregnancy disease characterized by systemic inflammation. The first aim of this review is to summarize what is already known about the tissues synthesizing PCT, about the stimuli that cause the increase of circulating PCT levels and how PCT acts as a proinflammatory stimulus by itself. Secondly, we will describe the role of this prohormone in normal pregnancy and in pregnancies complicated by pre-eclampsia, highlighting the involvement of the decidual macrophages and the proinflammatory cytokine tumor necrosis factor-α in the modulation of PCT expression in the decidual microenvironment.

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Diagnostic Biomarkers in Women With Suspected Preeclampsia in a Prospective Multicenter Study

Cited by 30 publications

References 22 publications

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

A placenta clinic approach to the diagnosis and management of fetal growth restriction

Overview of procalcitonin in pregnancy and in pre-eclampsia

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