Evidence map›Paper›PMID 42758683›Full record

Observational studyPloS one2026

Why only one-quarter of placental fetal growth restriction triggers preeclampsia? Clinical risk factors in 2060 cases in a 24-year cohort of 90,000 births.

Pierre-Yves Robillard, Gustaaf Dekker, Nandor Gabor Than, Francesco Bonsante, Malik Boukerrou, Marco Scioscia, Phuong Lien Tran, Silvia Iacobelli

Abstract readObservational Study
In one paragraph

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

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0cells of the map it votes in
0citing papers in PubMed
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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

8 authors.

Pierre-Yves RobillardService de Néonatologie, Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre Cedex, La Réunion.ORCID https://orcid.org/0000-0001-8916-9045
Gustaaf DekkerDepartment of Obstetrics & Gynaecology, University of Adelaide, Robinson Institute, Lyell McEwin Hospital, Adelaide, Australia.
Nandor Gabor ThanSystems Biology of Reproduction Research Group, Institute of Molecular Life Sciences, HUN-REN Research Center for Natural Sciences, Budapest, Hungary.
Francesco BonsanteService de Néonatologie, Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre Cedex, La Réunion.
Malik BoukerrouCentre d'Etudes Périnatales Océan Indien (CEPOI). Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre cedex, La réunion.
Marco SciosciaDepartment of Obstetrics and Gynaecology, Mater Dei Hospital, Bari, Italy.
Phuong Lien TranService ‌‌de Gynécologie et Obstétrique. Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre cedex, La réunion.ORCID https://orcid.org/0000-0003-3283-1450
Silvia IacobelliService de Néonatologie, Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre Cedex, La Réunion.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo compare risk factors between preeclampsia-associated fetal growth restriction (PFGR) and non-preeclamptic vascular FGR (VFGR) in a cohort of 96,094 consecutive singleton non-malformed pregnancies (≥22 weeks gestation) to identify susceptibility and protective factors differentiating maternal tolerance from overt hypertensive disease.

designObservational population-based cohort study over 24.5 years at a university maternity center.

resultsAmong 94,435 non-malformed births, 9,356 (10.0%) were SGA, with 2,060 (22%) classified as FGR based on abnormal Doppler indices: 529 PFGR (25.7%) and 1,531 VFGR (74.3%). VFGR predominated in late-onset cases (≥34 weeks; 78% vs. 46% early-onset <34 weeks). Compared to VFGR, PFGR mothers were older (mean 28 vs. 27 years), had higher pre-pregnancy BMI (25.9-26.8 vs. 24.0-24.4 kg/m2), and greater gestational weight gain (by 1-3 kg). Obesity (BMI ≥ 30 kg/m2) increased PFGR risk (OR 1.4-2.1), while underweight (BMI < 18.5 kg/m2) (OR 0.36-0.50) and smoking (OR 0.36-0.51) was protective for PFGR. Chronic hypertension (OR 2.8-3.0), previous preeclampsia (OR 3.3-9.9 in multiparas), primipaternity (OR 2.1-6.8), and renal disease (OR 5.0-7.8) were key risks for PFGR, with stronger effects in early-onset. Neonatal outcomes were similarly poor in early-onset PFGR/VFGR but worse in late-onset PFGR (e.g., higher prematurity, fetal death). Multivariable models confirmed independent associations of PFGR with age, BMI, chronic hypertension, primipaternity, previous abortion, and smoking (protective).

conclusionsThis study reveals VFGR as the majority of placental-mediated FGR, with PFGR distinguished by metabolic, vascular, and immunological risks. These insights prioritize research into maternal protective mechanisms, potentially enabling targeted predictions and interventions to mitigate FGR's impacts on mothers and offspring.

Indexed as

Fetal Growth RetardationPre-EclampsiaAdultCohort StudiesFemaleGestational AgeHumansInfant, NewbornPlacentaPregnancyRisk Factors

Identifiers

PMID42758683
PMCPMC13588347

What OpenQuestion holds

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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.