<scp>M</scp>aternal floor infarction: <scp>M</scp>anagement of an underrecognized pathology

Alsahan, Nada; Grynspan, David; Dadelszen, Peter von; Gruslin, Andrée

doi:10.1111/jog.12159

Cited by 15 publications

(16 citation statements)

References 12 publications

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“…Our histopathologic findings were consistent with the reported placental findings in human IUGR [46-47], where placental hypovascularity and trophoblast degeneration lead to poor blood flow and nutrient transfer to the fetus [48]. However, it should be noted that despite decreased vascularity and damaged trophoblast layers within the labyrinthine area of FR-associated placentas, placental weight was not changed.…”

Section: Discussionsupporting

confidence: 90%

Gestational food restriction decreases placental interleukin-10 expression and markers of autophagy and endoplasmic reticulum stress in murine intrauterine growth restriction

Chu¹,

Thamotharan²,

Ganguly³

et al. 2016

Nutrition Research

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Intrauterine growth restriction (IUGR) affects up to 10% of pregnancies and often results in short- and long- term sequelae for offspring. The mechanisms underlying IUGR are poorly understood, but it is known that healthy placentation is essential for nutrient provision to fuel fetal growth, and is regulated by immunologic inputs. We hypothesized that in pregnancy, maternal food restriction (FR) resulting in IUGR would decrease the overall immunotolerant milieu in the placenta, leading to increased cellular stress and death. Our specific objectives were to evaluate: (1) key cytokines (e.g. IL10) that regulate maternal-fetal tolerance, (2) cellular processes (autophagy and ER stress) that are immunologically-mediated and important for cellular survival and functioning, and (3) evaluate the resulting IUGR phenotype and placental histopathology. After subjecting pregnant mice to mild and moderate FR from gestational day (GD) 10 to 19, we collected placentas and embryos at GD19. We examined RNA sequencing data to identify immunologic pathways affected in IUGR-associated placentas and validated mRNA expression changes of genes important in cellular integrity. We also evaluated histopathologic changes in vascular and trophoblastic structures as well as protein expression changes in autophagy, ER stress, and apoptosis in the mouse placentas. Several differentially expressed genes were identified in FR compared to control mice, including a considerable subset that regulates immune tolerance, inflammation and cellular integrity. In summary, maternal food restriction decreases anti-inflammatory effect of IL10 and suppresses placental autophagic and ER stress responses, despite evidence of dysregulated vascular and trophoblast structures leading to IUGR.

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Section: Discussionsupporting

confidence: 90%

Gestational food restriction decreases placental interleukin-10 expression and markers of autophagy and endoplasmic reticulum stress in murine intrauterine growth restriction

Chu¹,

Thamotharan²,

Ganguly³

et al. 2016

Nutrition Research

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“…These high levels have long been known to be associated with an excess of placental diseases, growth restriction and IUFD, probably because of early and severe thrombo‐occlusive placental lesions. Although elevated alpha‐fetoprotein is not specific, it can be used as an early marker of recurrence . Nonetheless, no data have been published about the sensitivity of this examination.…”

Section: Discussionmentioning

confidence: 99%

Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

Devisme¹,

Chauvière

Franquet-Ansart³

et al. 2017

Prenatal Diagnosis

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Regardless of their extent, MFD that covered at least 25% of the placenta was almost always accompanied by severe growth restriction and by a high risk of intrauterine fetal death. Moreover, severe MFD tend to be associated with autoimmune diseases of the mothers, and pregnancies show more often a pathologic Doppler of the umbilical arteries and more often intrauterine fetal death that the moderate form. © 2017 John Wiley & Sons, Ltd.

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“…Maternal lesions of underperfusion are thought to mediate utero-placental ischemia, which has been proposed as a mechanism of disease in preeclampsia [55,62–73], intrauterine growth restriction [55,62–64,66–68,71,74–79], fetal death [64,66,68,80,81] and abruptio placenta (ischemic placental disease) [52–57,64,66,68,82,83], preterm labor [64,66,68,84–90], preterm prelabor rupture of membranes [64,66,68,91,92], recurrent spontaneous abortion [17,93] and massive perivillous fibrin deposition [94–108]. It is important to clarify that the nosology of maternal vascular lesions consistent with underperfusion includes acute atherosis, and that we examined its association with other villous and vascular lesions consistent with maternal vascular underperfusion.…”

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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Maternal floor infarction: Management of an underrecognized pathology

Cited by 15 publications

References 12 publications

Gestational food restriction decreases placental interleukin-10 expression and markers of autophagy and endoplasmic reticulum stress in murine intrauterine growth restriction

Gestational food restriction decreases placental interleukin-10 expression and markers of autophagy and endoplasmic reticulum stress in murine intrauterine growth restriction

Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

Placental lesions associated with acute atherosis

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