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Peer-reviewedCC BY 4.0PLOS One

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 Robillard1
  • Gustaaf Dekker2
  • Nandor Gabor Than3
  • Francesco Bonsante4
  • Malik Boukerrou5
  • Marco Scioscia6
  • Phuong Lien Tran7
  • Silvia Iacobelli
7 affiliations
  1. 1Service de Néonatologie, Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre Cedex, La Réunion
  2. 2Centre d’Etudes Périnatales Océan Indien (CEPOI). Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre cedex, La réunion
  3. 3Department of Obstetrics & Gynaecology, University of Adelaide, Robinson Institute, Lyell McEwin Hospital, Adelaide, Australia
  4. 4Systems Biology of Reproduction Research Group, Institute of Molecular Life Sciences, HUN-REN Research Center for Natural Sciences, Budapest, Hungary
  5. 5Department of Obstetrics and Gynaecology, School of Medicine, Semmelweis University, Budapest, Hungary
  6. 6Service ‌‌de Gynécologie et Obstétrique. Centre Hospitalier Universitaire Sud Réunion, Saint-Pierre cedex, La réunion
  7. 7Department of Obstetrics and Gynaecology, Mater Dei Hospital, Bari, Italy
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Abstract

Objectives: To 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. Design: Observational population-based cohort study over 24.5 years at a university maternity center. Results: Among 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). Conclusions: This 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.

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Cite

BibTeXRIS
BibTeX
@article{robillard2026only,
  title = {{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}},
  author = {Pierre-Yves Robillard and Gustaaf Dekker and Nandor Gabor Than and Francesco Bonsante and Malik Boukerrou and Marco Scioscia and Phuong Lien Tran and Silvia Iacobelli},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0354687},
  url = {https://doi.org/10.1371/journal.pone.0354687},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - 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
AU  - Pierre-Yves Robillard
AU  - Gustaaf Dekker
AU  - Nandor Gabor Than
AU  - Francesco Bonsante
AU  - Malik Boukerrou
AU  - Marco Scioscia
AU  - Phuong Lien Tran
AU  - Silvia Iacobelli
PY  - 2026
DA  - 2026/09/18
JO  - PLOS One
DO  - 10.1371/journal.pone.0354687
UR  - https://doi.org/10.1371/journal.pone.0354687
AB  - Objectives: To 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. Design: Observational population-based cohort study over 24.5 years at a university maternity center. Results: Among 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). Conclusions: This 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.
SN  - 1932-6203
ER  -