Evidence map›Paper›PMID 42470889›Full record

ArticlePlacenta2026

Placental abnormalities of malperfusion, inflammation, and meconium are associated with neonatal pulmonary vascular disease.

Stephanie M Tsoi, Cynthia Gasper, Emin Maltepe, Megan A Chidboy, Nida Ozarslan, Christine A Blauvelt, Sirirak Buarpung, Shannon Cheung, Martina Steurer, Roberta L Keller and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Placenta, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Stephanie M TsoiDivision of Critical Care Medicine, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA. Electronic address: Stephanie.Tsoi@ucsf.edu.
Cynthia GasperDepartment of Pathology and Laboratory Medicine, University of California, San Francisco, CA, USA.
Emin MaltepeDivision of Neonatology, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA.
Megan A ChidboyDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Francisco, CA, USA.
Nida OzarslanDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Francisco, CA, USA.
Christine A BlauveltDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Francisco, CA, USA.
Sirirak BuarpungDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Francisco, CA, USA.
Shannon CheungDivision of Critical Care Medicine, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA.
Martina SteurerDivision of Critical Care Medicine, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA; Division of Neonatology, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA; Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
Roberta L KellerDivision of Neonatology, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA.
Jeffrey R FinemanDivision of Critical Care Medicine, Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA.
Stephanie L GawDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Francisco, CA, USA.

Funding

TGF-ß-SOX18-Collagen metabolism in pulmonary vascular disease associated with CHDP01HL146369 · NHLBI · UNIVERSITY OF ARIZONA · PI Stephen M Black · 2020 to 2026
$18.7M
Pediatric Critical Care Scientist Development ProgramK12HD047349 · NICHD · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI HEATHER T. KEENAN, Kevin M Watt · 2004 to 2026
$17.0M
Investigating the role of maternal-fetal crosstalk on neonatal immunity in COVID-19 infection or vaccination in pregnancyR01HD111582 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Stephanie Lina Gaw · 2023 to 2026
$2.8M
Multidisciplinary Research Training in Pediatric Pulmonary Vascular DiseaseT32HL160508 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Steven Herbert Abman, Eric Douglas Austin · 2022 to 2026
$1.7M
Mentoring translational researchers in perinatal infectious diseasesK24AI188458 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Stephanie Lina Gaw · 2025 to 2026
$412k
NHLBI NIH HHS P01 HL146369NHLBI NIH HHS T32 HL160508NIAID NIH HHS K24 AI188458NICHD NIH HHS K12 HD047349NICHD NIH HHS R01 HD111582
6 · The paper itself

Abstract

objectivesThe primary objective was to elucidate whether placental histopathology representative of intrauterine insults during pulmonary vascular development are associated with a diagnosis of persistent pulmonary hypertension of the newborn (PPHN). The secondary objective was to compare placental histopathologic lesions across PPHN etiologies. STUDY

designWe conducted a case-control study of mother-infant dyads ≥35 weeks gestation who delivered at a tertiary care center between 2020 and 2025. Cases were infants diagnosed with PPHN and treated with inhaled nitric oxide; unaffected controls were infants without congenital anomalies. Placentas underwent blinded histopathologic review using standardized criteria. Multivariate logistic regression modeling was used to control for confounding maternal and infant factors.

results106 placentas were analyzed (53 PPHN, 53 controls). Placental lesions were significantly more common in PPHN placentas, including fetal vascular malperfusion (30.2% vs 9.4%, p < 0.01), placental inflammation (66.0% vs 37.7%, p < 0.01), chronic presence of meconium (43.4% vs 15.2%, p < 0.01), and chorangiosis (7.6% vs 0%, p = 0.04). In adjusted analyses compared to controls, among 41 placentas with fetal development etiologies (e.g. congenital anomalies) of PPHN, fetal vascular malperfusion, placental inflammation and fetal inflammatory response were more common. Among 12 placentas with typical causes of PPHN (e.g. meconium aspiration syndrome), placental inflammation, maternal and fetal inflammatory responses, and meconium were more common.

conclusionsPPHN placentas demonstrate lesions of malperfusion, inflammation, and chronic meconium, suggesting a complex interplay between intrauterine hypoxia and inflammation as a potential mechanism for the abnormal pulmonary vascular development and function seen in PPHN.

Indexed as

InflammationMeconiumPersistent Fetal Circulation SyndromePlacentaPlacenta DiseasesAdultCase-Control StudiesFemaleHumansInfant, NewbornMalePregnancyMaternal-fetal environmentPersistent pulmonary hypertension of the newbornPlacentaPulmonary vascular development

Identifiers

PMID42470889
PMCPMC13632599

What OpenQuestion holds

Textmetadata
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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.