Placental pathology and neonatal encephalopathy

Fox, Aine; Doyle, Evelyn; Geary, Michael; Hayes, Breda

doi:10.1002/ijgo.14301

Cited by 21 publications

(8 citation statements)

References 34 publications

(126 reference statements)

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“…[10] Also previous studies revealed, that both macroscopic and microscopic exams are associated with hypoxic brain lesions. [11][12][13] In our study, the most common placental microscopic changes in perinatal asphyxia were from the maternal and fetal vascular malperfusion categories, unlike the control group where most placentas were normal. According to the classification of placental lesions, we can conclude that those that determined the appearance of hypoxic lesions were chronic, these results being similar to Bingham et al [14].…”

Section: Discussioncontrasting

confidence: 46%

Placental Lesions in Birth Asphyxia and Hypoxic-Ischemic Syndrome

Calomfirescu-Avramescu,

Luminița,

Demetrian

et al. 2024

Preprint

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Introduction: Birth Asphyxia is a severe condition that includes many potential pathways of occurrence both in utero and during childbirth. We aimed to identify and describe specific macroscopic and microscopic placental injuries in birth asphyxia to serve as a quick tool to stratify a newborn’s potential further evolution, as hypoxic-ischemic encephalopathy can be responsible for neonatal death or severe neurologic sequelae further compromising the affected persons’ quality of life. Materials and methods: We conducted an observational prospective study over 3 years. 62 patients diagnosed with birth asphyxia which had placental histopathological examination performed were enrolled. The control group consisted of 69 term newborns that required neonatal intensive care for at least three days, in the same period, for any other reason and that also had available placental exams. In our study, placental histopathological lesions identified in birth asphyxia have been classified according to Amsterdam Criteria. Results: We analysed data gathered from both groups by applying specific statistical tests for each type of variable and hypothesis. Thus, umbilical cord abnormalities were associated with hypoxic-ischemic encephalopathy in a statistically significant manner when comparing the birth asphyxia group of newborns with the control group. Also, we identified a high statistical level of significance for maternal and fetal vascular malperfusion and the occurrence of hypoxic-ischemic syndrome when comparing the two groups (p = .00). Conclusion: The macroscopic and microscopic placental examination can provide important information on the evolution of the disease in selected newborns according to the identified lesions.

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Section: Discussioncontrasting

confidence: 46%

Placental Lesions in Birth Asphyxia and Hypoxic-Ischemic Syndrome

Calomfirescu-Avramescu,

Luminița,

Demetrian

et al. 2024

Preprint

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“…11 Umbilical cord pathology, inflammatory changes in the placenta, and placental weight were associated with HIE. 12 Intrapartum period risk factors appear to be important for the development of HIE. 13 Placenta previa, medicals during pregnancy, fetal distress, abnormal labor stage, Apgar score, amniotic fluid contamination, and cesarean section were independent risk factors for HIE.…”

Section: Introductionmentioning

confidence: 99%

Maternal and Fetal Risk Factors for Neonatal Hypoxic-Ischemic Encephalopathy: A Retrospective Study

Chen¹,

Chen²,

Jiang³

2023

IJGM

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Background: Neonatal hypoxic-ischemic encephalopathy (HIE) leads to different degree of neurological sequelae. The incidence of HIE is relatively high, and the risk factors associated with HIE are still controversial. It is necessary to identify the risk factors associated with HIE. Methods: A total of 258 neonates (110 HIE patients and 148 controls) were enrolled in this study. The characteristics of pregnant women and fetuses during pregnancy and delivery were compared between HIE patients and controls, and the risk factors of HIE were analyzed. Results:The proportions of premature infants, low-birth-weight infants and the levels of 1-minute Apgar score, 5-minute Apgar score in HIE group were significantly lower than those in control group, while the proportion of amniotic fluid contamination in the HIE group was significantly higher than those of the controls. When HIE was taken as the end point of 1-minute Apgar score, and 5-minute Apgar score, the cut-off value of 1-minute Apgar score was 3, and 5-minute Apgar score was 7 by receiver operating characteristic (ROC) curve analysis. The results of multivariate logistic regression analysis showed that low birth weight (<2.5 kg) (

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“…Conversely, the D-NCP group, despite showing similar pathway alterations, exhibited a less severe response, which might explain the absence of cleft palate formation in this group. In the D-CP group, the exacerbated response in in ammatory and hypoxic pathways might re ect a compromised placental function, leading to more severe developmental outcomes like Preeclampsia [20][21][22]. On the other hand, the D-NCP group, while still affected, may have retained a better adaptive response, preventing the full manifestation of developmental anomalies.…”

Section: Discussionmentioning

confidence: 99%

Placental and Cleft Palate: Preliminary Insights from Integrated Metabolomic and Transcriptomic Analyses

Lin,

Wei,

Luo

et al. 2024

Preprint

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The correlation between glucocorticoids and cleft palate, a prevalent congenital abnormality, remains controversial, particularly concerning the uncertain status of placenta-palate formation. Utilizing a dexamethasone-induced cleft palate model in New Zealand rabbits, an integrated analysis of untargeted metabolomics and transcriptomics was conducted to explore the correlation between placental pathology and cleft palate. After dexamethasone treatment, approximately 60% of rabbit embryos developed cleft palates. Obvious pathologic change were observed on placenta including fibrosis, calcification, and necrosis. Transcriptomic analysis identified 4,744 differentially expressed genes in the placenta, involving pathways related to hormonal responses, vascular development, and inflammatory reactions. Metabolomic data revealed significant metabolic differences in both the placenta and amniotic fluid, with notable increases in urea levels in the placenta, while urea and arginine levels were markedly reduced in the amniotic fluid. Furthermore, metabolic disruptions in urea cycle, particularly an increase in arginase activity, may related to placental pathological changes. Overall, there is a correlation between placental pathology and cleft palate. Disruption of the urea cycle may contribute to placental lesions associated with the development of cleft palate. This offers a novel direction for understanding the mechanism of cleft palate formation, suggesting a potential significant role of placental metabolic disorders.

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Placental pathology and neonatal encephalopathy

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 21 publications

References 34 publications

Placental Lesions in Birth Asphyxia and Hypoxic-Ischemic Syndrome

Placental Lesions in Birth Asphyxia and Hypoxic-Ischemic Syndrome

Maternal and Fetal Risk Factors for Neonatal Hypoxic-Ischemic Encephalopathy: A Retrospective Study

Placental and Cleft Palate: Preliminary Insights from Integrated Metabolomic and Transcriptomic Analyses

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