Serum inhibin A and angiogenic factor levels in pregnancies with previous preeclampsia and/or chronic hypertension: are they useful markers for prediction of subsequent preeclampsia?

Sibai, Bahaeddine M; Koch, Matthew; Freire, Sálvio; Silva, João Luiz Pinto e; Rudge, Marilza Vieira Cunha; Costa, Sérgio Hofmeister de Almeida Martins; Bartz, Janet; Santos, Cleide de Barros; Cecatti, José Guilherme; Costa, Roberto Antônio de Araújo; Ramos, José Geraldo Lopes; Spinnato, Joseph A.

doi:10.1016/j.ajog.2008.06.071

Cited by 69 publications

(68 citation statements)

References 21 publications

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“…We did not collect data on angiogenic factors in normotensive pregnant controls, thus we cannot determine whether the levels in chronic hypertensives who did not develop PE were similar to normotensive pregnant women, although results from other published studies suggest that they are. 17,18 The levels that we report in women who developed SPE are also similar to previous reports in women who developed SPE and who were sampled only twice during pregnancy. 17 Our study, in which angiogenic factors were measured every 8 weeks and postpartum in the same patients, both confirms and adds to these previous reports.…”

Section: Discussionsupporting

confidence: 79%

“…17,18 The levels that we report in women who developed SPE are also similar to previous reports in women who developed SPE and who were sampled only twice during pregnancy. 17 Our study, in which angiogenic factors were measured every 8 weeks and postpartum in the same patients, both confirms and adds to these previous reports. The 9 women with early onset SPE had different baseline characteristics compared with the other groups.…”

Section: Discussionsupporting

confidence: 79%

“…14 -16 Alterations in the levels of circulating factors in women with chronic hypertension are beginning to be appreciated primarily after crosssectional analyses of subgroups. [17][18][19] The current investigation was designed to characterize the levels of circulating sFlt1, sEng, and PlGF in women with preexisting hypertension and to investigate whether longitudinal profiling can help distinguish chronically hypertensive pregnant women who develop SPE from those who do not develop SPE. In this study, we have leveraged and performed a secondary analysis of the peripheral blood specimens originally collected longitudinally in the context of a placebocontrolled, double-blinded randomized trial of calcium supplementation in chronically hypertensive pregnant women and demonstrate significant alterations in sFlt1, sEng, and PlGF before the clinical diagnosis of early onset (Ͻ34 weeks) SPE and at the time of diagnosis in women with both early and late-onset SPE.…”

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confidence: 99%

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Angiogenic Factors in Superimposed Preeclampsia

et al. 2012

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Abstract-Imbalances in circulating angiogenic factors contribute to the pathogenesis of preeclampsia. To characterize levels of angiogenic factors in pregnant women with chronic hypertension, we prospectively followed 109 women and measured soluble fms-like tyrosine kinase 1 (sFlt1), soluble endoglin, and placental growth factor at 12, 20, 28, and 36 weeks' gestation and postpartum. Superimposed preeclampsia developed in 37 (34%) and was early onset (Ͻ34 weeks) in 9 and later onset (Ն34 weeks) in 28. Circulating levels of sFlt1 and the ratio of sFlt1 to placental growth factor were higher before clinical diagnosis at 20 weeks' gestation in women who subsequently developed early onset preeclampsia between 28 and 34 weeks compared with levels in women who never developed preeclampsia (Pϭ0.001) or who developed late-onset preeclampsia (Pϭ0.001). Circulating levels of sFlt1, soluble endoglin, and the ratio of sFlt1:placental growth factor were also significantly higher, and placental growth factor levels were significantly lower at the time of clinical diagnosis of superimposed preeclampsia in women with either early or late-onset superimposed preeclampsia compared with levels at similar gestational ages in those with uncomplicated chronic hypertension. We conclude that alterations in angiogenic factors are detectable before and at the time of clinical diagnosis of early onset superimposed preeclampsia, whereas alterations were observed only at the time of diagnosis in women with late-onset superimposed preeclampsia. Key Words: superimposed preeclampsia Ⅲ angiogenic factors Ⅲ chronic hypertension in pregnancy P reeclampsia (PE), a syndrome that manifests in the latter half of pregnancy and is characterized by maternal hypertension and proteinuria, develops in Ϸ3% to 5% of pregnant women. 1 PE may also develop in women with chronic (preexisting) hypertension and occurs 3 to 5 times more frequently compared with women who are normotensive at conception. [2][3][4] The diagnosis of superimposed PE (SPE) is often difficult, because women already have hypertension and some even have proteinuria. SPE is associated with even greater maternal and fetal morbidity and mortality than PE in women without preexisting hypertension. 2,5 The pathogenesis of PE, as well as SPE, is likely to involve placental vascular remodeling, leading to defective placentation, 6,7 placental ischemia, 8,9 and maternal endothelial cell dysfunction. 10 Emerging data suggest that placental ischemia is associated with increased production of placental proteins, which, on release into the maternal circulation, cause maternal systemic inflammation and endothelial cell dysfunction. 11,12 In particular, an imbalance in circulating proangiogenic and antiangiogenic factors released by the hypoxic placenta has gained currency as a critical link between placental dysfunction and several maternal manifestations of PE, particularly endothelial dysfunction and proteinuria. 13 Results from clinical trials suggest that the soluble forms of the vascular endothelial ...

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

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Angiogenic Factors in Superimposed Preeclampsia

et al. 2012

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“…Muttukrishna et al found that maternal serum concentrations of inhibin A and activin A are more elevated in women with preeclampsia as compared to normotensive control women [23]. Some authors have confirmed that elevated inhibin A/activin A levels in first trimester [24,25] or in second trimester [26][27][28][29][30] could predict preeclampsia (Table II). Spence et al found that elevated inhibin A and activin A levels combined with uterine artery doppler measurement become a more accurate predictive values in second trimester [30].…”

Section: Inhibin a And Activin Amentioning

confidence: 60%

“…Most studies about the role sFlt1 in PE evaluation have shown that elevated second trimester sFlt1 predicts preeclampsia (Table V) [29,38,41,[57][58][59]. sFlt1 is a better predictor for the early-onset type of preeclampsia, which has worse pregnancy outcomes when compare with the late onset type of preeclampsia.…”

Section: Soluble Fms-like Tyrosine Kinase-1mentioning

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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Preeclampsia: Linking Placental Ischemia with Maternal Endothelial and Vascular Dysfunction

Bakrania

Spradley

Drummond

et al. 2020

Comprehensive Physiology

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Preeclampsia (PE), a hypertensive disorder, occurs in 3% to 8% of pregnancies in the United States and affects over 200,000 women and newborns per year. The United States has seen a 25% increase in the incidence of PE, largely owing to increases in risk factors, including obesity and cardiovascular disease. Although the etiology of PE is not clear, it is believed that impaired spiral artery remodeling of the placenta reduces perfusion, leading to placental ischemia. Subsequently, the ischemic placenta releases antiangiogenic and pro-inflammatory factors, such as cytokines, reactive oxygen species, and the angiotensin II type 1 receptor autoantibody (AT1-AA), among others, into the maternal circulation. These factors cause widespread endothelial activation, upregulation of the endothelin system, and vasoconstriction. In turn, these changes affect the function of multiple organ systems including the kidneys, brain, liver, and heart. Despite extensive research into the pathophysiology of PE, the only treatment option remains early delivery of the baby and importantly, the placenta. While premature delivery is effective in ameliorating immediate risk to the mother, mounting evidence suggests that PE increases risk of cardiovascular disease later in life for both mother and baby. Notably, these women are at increased risk of hypertension, heart disease, and stroke, while offspring are at risk of obesity, hypertension, and neurological disease, among other complications, later in life. This article aims to discuss the current understanding of the diagnosis and pathophysiology of PE, as well as associated organ damage, maternal and fetal outcomes, and potential therapeutic avenues.

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Serum inhibin A and angiogenic factor levels in pregnancies with previous preeclampsia and/or chronic hypertension: are they useful markers for prediction of subsequent preeclampsia?

Cited by 69 publications

References 21 publications

Angiogenic Factors in Superimposed Preeclampsia

Angiogenic Factors in Superimposed Preeclampsia

Prediction of the preeclampsia: a view of biochemical markers

Preeclampsia: Linking Placental Ischemia with Maternal Endothelial and Vascular Dysfunction

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