The relationship of angiogenic factors to maternal and neonatal manifestations of early‐onset and late‐onset preeclampsia

Pinheiro, Cilene Carlos; Rayol, Patricia; Gozzani, Luiz; Reis, Luciene M. dos; Zampieri, G.; Dias, Cristiane Bitencourt; Woronik, Viktoria

doi:10.1002/pd.4432

Cited by 45 publications

(35 citation statements)

References 57 publications

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“…Although both of these lesions are generally considered to reflect activation of the innate immune response (macrophages), there is accumulating evidence suggesting participation of the adaptive limb of the immune response as well [129–145]. Specifically, T lymphocytes have been detected in the early stages of atheroma formation and they persist as the lesions grow and eventually rupture [146].…”

Section: Discussionmentioning

confidence: 99%

Placental lesions associated with acute atherosis

Kim

Chaemsaithong

Romero

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age (SGA), spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion, amniotic fluid infection, fetal vascular thrombo-occlusive disease or chronic inflammation. Material and methods A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted examine 16,457 placentas. The frequency of placenta lesions (diagnosed using the criteria of the Perinatal Section of the Society for Pediatric Pathology) was compared between pregnancies with and without atherosis. Results Among 16,457 women who were enrolled, 10.2% (1,671/16,457) were excluded, leaving 14,786 women who contributed data for analysis. Among them, the prevalence of acute atherosis was 2.2% (326/14,786). Women with acute atherosis were more than six times as likely as those without to have placental lesions consistent with maternal underperfusion (adjusted odds ratio- aOR: 6.7; 95% CI 5.2–8.6). To a lesser degree, acute atherosis was also associated with greater risks of having either lesions consistent with fetal vascular thrombo-occlusive disease (aOR 1.7; 95% CI 1.2–2.3) or chronic chorioamnionitis (aOR 1.9; 95% CI 1.3–3), but not with other chronic inflammatory lesions, after adjusting for gestational age at delivery. In contrast, women with acute atherosis were 60% less likely to have lesions consistent with amniotic fluid infecition, adjusting for gestational age at delivery (aOR 0.4; 95% CI 0.3–0.5). Conclusions Acute atherosis is associated with increased risks of having placental lesions consistent with maternal vascular underperfusion, and to a lesser extent, chronic chorioamnionitis and those consistent with fetal vascular thrombo-occlusive disease.

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Section: Discussionmentioning

confidence: 99%

Placental lesions associated with acute atherosis

Kim

Chaemsaithong

Romero

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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“…It should also be noted that the studies cited are generally based on the ‘old’ classification of preeclampsia with the requirement for proteinuria. Preeclampsia is also distinguished as early onset vs late onset preeclampsia (Moore and Redman, 1983; Paruk and Moodley, 2000) based on evidence that the two entities have distinct pathophysiologic underpinnings (Nelson et al, 2014; Pinheiro et al, 2014) Investigators have most often classified early-onset and late-onset disease as preeclampsia that prompts delivery <34 weeks or ≥34 weeks gestation, respectively.…”

Section: Complement and Hypertensive Disorders Of Pregnancymentioning

confidence: 99%

The complement system and adverse pregnancy outcomes

Regal

Gilbert

Burwick

2015

Molecular Immunology

129

106

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Adverse pregnancy outcomes significantly contribute to morbidity and mortality for mother and child, with lifelong health consequences for both. The innate and adaptive immune system must be regulated to insure survival of the feta allograft, and the complement system is no exception. An intact complement system optimizes placental development and function and is essential to maintain host defense and fetal survival. Complement regulation is apparent at the placental interface from early pregnancy with some degree of complement activation occurring normally throughout gestation. However, a number of pregnancy complications including early pregnancy loss, fetal growth restriction, hypertensive disorders of pregnancy and preterm birth are associated with excessive or misdirected complement activation, and are more frequent in women with inherited or acquired complement system disorders or complement gene mutations. Clinical studies employing complement biomarkers in plasma and urine implicate dysregulated complement activation in components of each of the adverse pregnancy outcomes. In addition, mechanistic studies in rat and mouse models of adverse pregnancy outcomes address the complement pathways or activation products of importance and allow critical analysis of the pathophysiology. Targeted complement therapeutics are already in use to control adverse pregnancy outcomes in select situations. A clearer understanding of the role of the complement system in both normal pregnancy and complicated or failed pregnancy will allow a rational approach to future therapeutic strategies for manipulating complement with the goal of mitigating adverse pregnancy outcomes, preserving host defense, and improving long term outcomes for both mother and child.

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“…On the other hand, PE is a heterogeneous disorder, and it has been suggested that early-(EO) and late-onset (LO) PE could have differing physiopathological pathways [8,9], which is why evaluating the mechanism previously described, while considering this classification, is a matter of interest.…”

Section: Introductionmentioning

confidence: 99%

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

Valencia

Zárate

Saucedo

et al. 2018

Gynecol Obstet Invest

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Objective: To evaluate the placental and decidual gene expression and maternal and umbilical serum concentrations of tumor necrosis factor alpha, interleukin 6 (IL-6), IL-8, IL-10, IL-1 receptor antagonist (IL-1RA), intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1), along with the proinflammatory/anti-inflammatory cytokine ratios in women with preeclampsia (PE) vs. women with normal pregnancy (NP), and to analyze PE classified as early- (EO) and late-onset (LO). Methods: This cross-sectional study was performed with 50 women with PE (EO n = 30, LO n = 20) and 50 women with NP. Tissue gene expression levels were measured by real-time RT-PCR. Cytokines and adhesion molecules serum concentrations were measured by immunoassays. Results: In PE, placental expression of IL-10 and IL-1RA was lower, while placental IL-8/IL-1RA ratio and maternal concentrations of VCAM-1 were higher vs. NP. In EO, placental expression of IL-10 was lower, while placental IL-8/IL-10 and IL-8/IL-1RA ratios were higher than LO and NP. Maternal concentrations of IL-6 were higher in LO than EO and NP. Throughout PE, maternal VCAM-1 concentrations were higher vs. NP. No significant differences were observed in the decidual expression and umbilical concentrations of the markers between the groups. Conclusion: PE associates with a proinflammatory placental state; however, EO associates with a proinflammatory placental state, while LO associates with systemic maternal inflammation. Both subtypes associated with maternal endothelial dysfunction.

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The relationship of angiogenic factors to maternal and neonatal manifestations of early‐onset and late‐onset preeclampsia

Abstract: Angiogenic imbalance is more pronounced in patients with early-onset preeclampsia and correlates with worse clinical outcomes, especially for the neonates.

Cited by 45 publications

References 57 publications

Placental lesions associated with acute atherosis

Placental lesions associated with acute atherosis

The complement system and adverse pregnancy outcomes

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

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