Placental Morphology in Fetal Alcohol Spectrum Disorders

Tai, Marlene; Piskorski, Anna; Kao, Jennifer Chien Wen; Hess, Lynn A.; Gündoğan, Füsun

doi:10.1093/alcalc/agw088

Cited by 25 publications

(19 citation statements)

References 44 publications

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“…The risk of spontaneous abortion and stillbirth increases with the quantity of alcohol consumed during pregnancy ( 36–38 ). In utero PNAE deaths have been linked to placental insufficiency, which can result in hypoxia, and intrauterine growth restriction ( 39 ). In humans, alcohol consumption was positively correlated with placental hemorrhage and accelerated villous maturation ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

Human Brain Abnormalities Associated With Prenatal Alcohol Exposure and Fetal Alcohol Spectrum Disorder

Jarmasz

Basalah

Chudley

et al. 2017

Journal of Neuropathology &Amp; Experimental Neurology

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Fetal alcohol spectrum disorder (FASD) is a common neurodevelopmental problem, but neuropathologic descriptions are rare and focused on the extreme abnormalities. We conducted a retrospective survey (1980–2016) of autopsies on 174 individuals with prenatal alcohol exposure or an FASD diagnosis. Epidemiologic details and neuropathologic findings were categorized into 5 age groups. Alcohol exposure was difficult to quantify. When documented, almost all mothers smoked tobacco, many abused other substances, and prenatal care was poor or nonexistent. Placental abnormalities were common (68%) in fetal cases. We identified micrencephaly (brain weight <5th percentile) in 31, neural tube defects in 5, isolated hydrocephalus in 6, corpus callosum defects in 6 (including some with complex anomalies), probable prenatal ischemic lesions in 5 (excluding complications of prematurity), minor subarachnoid heterotopias in 4, holoprosencephaly in 1, lissencephaly in 1, and cardiac anomalies in 26 cases. The brain abnormalities associated with prenatal alcohol exposure are varied; cause–effect relationships cannot be determined. FASD is likely not a monotoxic disorder. The animal experimental literature, which emphasizes controlled exposure to ethanol alone, is therefore inadequate. Prevention must be the main societal goal, however, a clear understanding of the neuropathology is necessary for provision of care to individuals already affected.

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Section: Discussionmentioning

confidence: 99%

Human Brain Abnormalities Associated With Prenatal Alcohol Exposure and Fetal Alcohol Spectrum Disorder

Jarmasz

Basalah

Chudley

et al. 2017

Journal of Neuropathology &Amp; Experimental Neurology

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“…The placenta is a portal and reservoir for a number of congenital viruses which do not result in evident gross placental inflammation, such as we and others demonstrated with Zika virus. [36][37][38] Maternal obesity, 39,40 gestational diabetes, 41 and alcohol consumption 42,43 are associated with highly predictive changes in the placenta. Levels of polycyclic aromatic hydrocarbons, a carcinogenic and toxic component of tobacco smoke, have been measured from the placenta in a study of preterm birth.…”

Section: Why Study the Effect Of Tobacco And Nicotine Exposures On mentioning

confidence: 99%

The impact of tobacco chemicals and nicotine on placental development

Suter

Aagaard

2020

Prenatal Diagnosis

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Despite decades of messages warning about the dangers of tobacco use in pregnancy, 10% to 15% of pregnant women continue to smoke. Furthermore, an increased popularity of electronic nicotine delivery systems (ENDS) over the past decade in women of childbearing age raises parallel concerns regarding the effects of vaporized nicotine use in pregnancy. While research using animal models which mimic tobacco smoke and nicotine exposure in pregnancy have largely replicated findings in humans, few studies focus directly on the effects of these exposures on the placenta. Because the placenta is a fetal derived tissue, and nicotine and other components of tobacco smoke are either processed by or transported directly through the placenta, such studies help us understand the risks of these exposures on the developing fetus. In this review, we summarize research on the placenta and placental‐derived cells examining either tobacco smoke or nicotine exposure, including both histologic and subcellular (ie, epigenetic and molecular) modifications. Collectively, these studies reveal that tobacco and nicotine exposure are accompanied by some common and several unique molecular and epigenomic placental modifications. Consideration of the nature and sequelae of these molecular mediators of risk may help to better inform the public and more effectively curtail modifiable behavior.

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“…Central to this study, is maternal alcohol consumption. Chronic alcohol exposure during human gestation is associated with low birth weight (Jones and Smith, 1973;Manning and Eugene Hoyme, 2007;O'Leary et al, 2009;Tai et al, 2016), as well as placental complications, including miscarriage, preeclampsia, pre-term birth and stillbirth (Kaminski et al, 1978;Tai et al, 2016;Maconochie et al, 2007;Avalos et al, 2014;Salihu et al, 2011;Meyer-Leu et al, 2011;Marbury et al, 1983). However, one period that is potentially susceptible to alcohol exposure and has received little attention, is consumption prior to pregnancy recognition.…”

Section: Introductionmentioning

confidence: 99%

Periconceptional alcohol exposure causes female-specific perturbations to trophoblast differentiation and placental formation in the rat

et al. 2019

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The development of pathologies during pregnancy, including preeclampsia, hypertension and fetal growth restriction (FGR), often originates from poor functioning of the placenta. In vivo models of maternal stressors, such as nutrient deficiency, and placental insufficiency often focus on inadequate growth of the fetus and placenta in late gestation. These studies rarely investigate the origins of poor placental formation in early gestation, including those affecting the pre-implantation embryo and/or the uterine environment. The current study characterises the impact on blastocyst, uterine and placental outcomes in a rat model of periconceptional alcohol exposure, in which 12.5% ethanol is administered in a liquid diet from 4 days before until 4 days after conception. We show female-specific effects on trophoblast differentiation, embryo-uterine communication, and formation of the placental vasculature, resulting in markedly reduced placental volume at embryonic day 15. Both sexes exhibited reduced trophectoderm pluripotency and global hypermethylation, suggestive of inappropriate epigenetic reprogramming. Furthermore, evidence of reduced placental nutrient exchange and reduced pre-implantation maternal plasma choline levels offers significant mechanistic insight into the origins of FGR in this model.

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Placental Morphology in Fetal Alcohol Spectrum Disorders

Cited by 25 publications

References 44 publications

Human Brain Abnormalities Associated With Prenatal Alcohol Exposure and Fetal Alcohol Spectrum Disorder

Human Brain Abnormalities Associated With Prenatal Alcohol Exposure and Fetal Alcohol Spectrum Disorder

The impact of tobacco chemicals and nicotine on placental development

Periconceptional alcohol exposure causes female-specific perturbations to trophoblast differentiation and placental formation in the rat

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