Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers

Preeclampsia is both a vascular and inflammatory disorder. Since the placenta is a conduit for fetal development, preeclampsia should be a presumed cause of adverse infant outcomes. Yet, the relationship of placental pathology, inflammation and neurological outcomes after preeclampsia are understudi...

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Main Authors: Alexandra Sotiros, Dianne Thornhill, Miriam D. Post, Virginia D. Winn, Jennifer Armstrong
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2021-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8592443/?tool=EBI
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author Alexandra Sotiros
Dianne Thornhill
Miriam D. Post
Virginia D. Winn
Jennifer Armstrong
author_facet Alexandra Sotiros
Dianne Thornhill
Miriam D. Post
Virginia D. Winn
Jennifer Armstrong
author_sort Alexandra Sotiros
collection DOAJ
description Preeclampsia is both a vascular and inflammatory disorder. Since the placenta is a conduit for fetal development, preeclampsia should be a presumed cause of adverse infant outcomes. Yet, the relationship of placental pathology, inflammation and neurological outcomes after preeclampsia are understudied. We prospectively examined a cohort of maternal-infant dyads with preeclampsia for maternal inflammatory cytokines at time of preeclampsia diagnosis and delivery, and fetal cord blood cytokines (IL-1β, IL-6, IL-8, and TNF-α). Placentas were analyzed for inflammatory and vascular pathologies. Neurodevelopmental assessment of infants utilizing the Pediatric Stroke Outcome Measure (PSOM) was conducted at 6-month corrected gestational age. Eighty-one maternal-newborn dyads were examined. Worse neurological outcomes were not associated with elevated maternal / fetal cytokines. Early preterm birth (gestational age ≤ 32 weeks) was associated with worse neurological outcomes at 6-months regardless of maternal/ fetal cytokine levels, placental pathology, or cranial ultrasound findings (OR 1.70, [1.16–2.48], p = 0.006). When correcting for gestational age, elevated IL-6 approached significance as a predictor for worse developmental outcome (OR 1.025 [0.985–1.066], p = 0.221). Pathological evidence of maternal malperfusion and worse outcomes were noted in early preterm, although our sample size was small. Our study did not demonstrate an obvious association of inflammation and placental pathology in preeclampsia and adverse neurodevelopmental outcome at 6-month corrected age but does suggest maternal malperfusion at earlier gestational age may be a risk factor for worse outcome.
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spelling doaj.art-ee8649ec665345b59a9aea6cb1c43e032022-12-21T21:52:58ZengPublic Library of Science (PLoS)PLoS ONE1932-62032021-01-011611Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothersAlexandra SotirosDianne ThornhillMiriam D. PostVirginia D. WinnJennifer ArmstrongPreeclampsia is both a vascular and inflammatory disorder. Since the placenta is a conduit for fetal development, preeclampsia should be a presumed cause of adverse infant outcomes. Yet, the relationship of placental pathology, inflammation and neurological outcomes after preeclampsia are understudied. We prospectively examined a cohort of maternal-infant dyads with preeclampsia for maternal inflammatory cytokines at time of preeclampsia diagnosis and delivery, and fetal cord blood cytokines (IL-1β, IL-6, IL-8, and TNF-α). Placentas were analyzed for inflammatory and vascular pathologies. Neurodevelopmental assessment of infants utilizing the Pediatric Stroke Outcome Measure (PSOM) was conducted at 6-month corrected gestational age. Eighty-one maternal-newborn dyads were examined. Worse neurological outcomes were not associated with elevated maternal / fetal cytokines. Early preterm birth (gestational age ≤ 32 weeks) was associated with worse neurological outcomes at 6-months regardless of maternal/ fetal cytokine levels, placental pathology, or cranial ultrasound findings (OR 1.70, [1.16–2.48], p = 0.006). When correcting for gestational age, elevated IL-6 approached significance as a predictor for worse developmental outcome (OR 1.025 [0.985–1.066], p = 0.221). Pathological evidence of maternal malperfusion and worse outcomes were noted in early preterm, although our sample size was small. Our study did not demonstrate an obvious association of inflammation and placental pathology in preeclampsia and adverse neurodevelopmental outcome at 6-month corrected age but does suggest maternal malperfusion at earlier gestational age may be a risk factor for worse outcome.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8592443/?tool=EBI
spellingShingle Alexandra Sotiros
Dianne Thornhill
Miriam D. Post
Virginia D. Winn
Jennifer Armstrong
Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
PLoS ONE
title Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
title_full Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
title_fullStr Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
title_full_unstemmed Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
title_short Inflammatory cytokines, placental pathology, and neurological outcomes in infants born to preterm preeclamptic mothers
title_sort inflammatory cytokines placental pathology and neurological outcomes in infants born to preterm preeclamptic mothers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8592443/?tool=EBI
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