Evidence map›Paper›PMID 40851246›Full record

ArticleRomanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie

Dynamic TyG-inflammation-endothelial trajectories and placental histopathology synergistically define a maternal-fetal vascular risk phenotype.

Biliana Alexandra Belovan, Adrian Claudiu Raţiu, Ioan Sas, Loredana Gabriela Stana

Abstract read
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Article in Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Biliana Alexandra BelovanDepartment of Obstetrics and Gynecology, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania; ratiu.adrian@umft.ro.
Adrian Claudiu Raţiu
Ioan Sas
Loredana Gabriela Stana

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaternal dysmetabolism and low-grade inflammation accelerate fetal aortic wall thickening. Whether concomitant placental vascular or inflammatory lesions amplify this risk is unknown. Participants, Materials and Methods: 88 women with singleton, anatomically normal pregnancies were phenotyped at 24-26 weeks (visit 1, V1) and 32-34 weeks (visit 2, V2). Dynamic maternal markers [(Δ triglyceride-glucose (TyG) index, Δ interleukin-6 (IL-6), Δ high-sensitivity C-reactive protein (hsCRP), Δ flow-mediated dilation (FMD)] again generated three metabolic inflammatory response phenotypes (MIRP-1∕-2∕-3). Placentas were examined by pathologists. A placental malperfusion-inflammation composite (PMIC) score (0-10) summed semiquantitative grades of maternal vascular malperfusion (MVM), distal villous immaturity, chronic villitis of unknown etiology (CVUE) and acute chorioamnionitis.

resultsAdequate placental tissue was obtained from 84 (95%) dyads. Median PMIC rose step wise from MIRP-1 = 2 [interquartile range (IQR) 1-3] to MIRP-2 = 5 [IQR 3-6] and MIRP-3 = 7 [IQR 6-9] (p<0.001). In mixed effects modelling, PMIC independently predicted fetal abdominal aorta intima-media thickness (IMT) progression [β=+0.012 mm per PMIC point; 95% confidence interval (CI): 0.007-0.017; p<0.001] alongside Δ TyG and Δ IL-6 (R² conditional = 0.61). Mothers in the high risk combined phenotype (MIRP-3 + PMIC ≥7; n=25) exhibited a mean IMT increment of +0.21±0.05 mm vs. +0.06±0.03 mm in the double low reference group (MIRP-1 + PMIC ≤3; n=22; p<0.001). A five variable XGBoost model [Δ TyG, Δ IL-6, Δ FMD, PMIC, baseline body mass index (BMI)] identified fetuses with late gestation high IMT (≥90th percentile) with area under the receiver operating characteristic (AUROC) 0.91, outperforming the parent model lacking PMIC (AUROC 0.88).

conclusionsPlacental vascular and inflammatory lesions potentiate the impact of adverse maternal metabolic inflammatory trajectories on fetal arterial remodeling. Integrating rapid placental histology with dynamic TyG inflammation endothelial indices could refine perinatal risk stratification and guide both ante and postpartum surveillance.

Indexed as

FetusInflammationPlacentaAdultFemaleHumansPhenotypePregnancyRisk Factorsfetal vascular remodelingplacental histopathologytriglyceride-glucose index

Identifiers

PMID40851246
PMCPMC12509501

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LicenceCC BY-NC-SA
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.