Evidence map›Paper›PMID 35177220›Full record

ReviewAmerican journal of obstetrics and gynecology2022

Preeclampsia and eclampsia: the conceptual evolution of a syndrome.

Offer Erez, Roberto Romero, Eunjung Jung, Piya Chaemsaithong, Mariachiara Bosco, Manaphat Suksai, Dahiana M Gallo, Francesca Gotsch

Registry-linked trialOpen access · bronzeAbstract readHistorical ArticleReview
In one paragraph

Review in American journal of obstetrics and gynecology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06352970 (Effects of Tuberculosis Infection on Placental Development and Function), which is not on this map. Cited by 120 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 4 pooled it
46.2field-weighted citation impact, top 1% of its field
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.

NCT06352970 recruitingnot on this mapstarted 2024, after this paper: background citation

Effects of Tuberculosis Infection on Placental Development and Function

TypeobservationalSponsorLund UniversityRan2024 to 2027Enrolled500ConditionsPregnancy Related, Tuberculosis Infection, Placenta DiseasesArmsTB infection
3 · Its place in the literature

Who cites it

120 citing papers in PubMed, 4 syntheses or guidelines pooled it, 258 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Phenotyping Preeclampsia Using Unsupervised Machine Learning: A Prospective Cohort Study.BJOG : an international journal of obstetrics and gynaecology · 2026
    Article
  7. Article
  8. The pathophysiology of pre-eclampsia.Nature reviews. Nephrology · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Renewed focus on reducing the burden of pre-eclampsia.Bulletin of the World Health Organization · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Review

60 more citing papers are in PubMed but not listed here.

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 at 1 institution in 3 countries.

Offer ErezPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI; Department of Obstetrics and Gynecology, HaEmek Medical Center, Afula, Israel.
Roberto RomeroPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI; Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI; Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI; Detroit Medical Center, Detroit, MI. Electronic address: prbchiefstaff@med.wayne.edu.
Eunjung JungPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.
Piya ChaemsaithongPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI; Faculty of Medicine, Department of Obstetrics and Gynecology, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Mariachiara BoscoPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.
Manaphat SuksaiPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.
Dahiana M GalloPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.
Francesca GotschPerinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, United States Department of Health and Human Services, Bethesda, MD, and Detroit, MI; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.
United States Department of Health and Human Services · US

Funding

The Role Of Subclinical Infection And Cytokines In Preterm ParturitionZIAHD002400 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI ROMERO, ROBERTO · 2009 to 2025
$254.4M
THE ROLE OF SUBCLINICAL INFECTION AND CYTOKINES IN PRETERM PARTURITIONZ01HD002400 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI ROMERO, ROBERTO · 1992 to 2008
$8.2M
Intramural NIH HHS Z01 HD002400NICHD NIH HHS HHSN275201300006C
6 · The paper itself

Abstract

Preeclampsia, one of the most enigmatic complications of pregnancy, is considered a pregnancy-specific disorder caused by the placenta and cured only by delivery. This article traces the condition from its origins-once thought to be a disease of the central nervous system, recognized by the occurrence of seizures (ie, eclampsia)-to the present time when preeclampsia is conceptualized primarily as a vascular disorder. We review the epidemiologic data that led to the recommendation to use diastolic hypertension and proteinuria as diagnostic criteria, as their combined presence was associated with an increased risk of fetal death and the birth of small-for-gestational-age neonates. However, preeclampsia is a multisystemic disorder with protean manifestations, and the condition can be present even in the absence of hypertension and proteinuria. Toxins gaining access to the maternal circulation have been proposed to mediate the clinical manifestations-hence, the term "toxemia of pregnancy," which was used for several decades. The search for putative toxins has challenged investigators for more than a century, and a growing body of evidence suggests that products of an ischemic or a stressed placenta are responsible for the vascular changes that characterize this syndrome. The discovery that the placenta can produce antiangiogenic factors, which regulate endothelial cell function and induce intravascular inflammation, has been a major step forward in the understanding of preeclampsia. We view the release of antiangiogenic factors by the placenta as an adaptive response to improve uterine perfusion by modulating endothelial function and maternal cardiovascular performance. However, this homeostatic response can become maladaptive and lead to damage of target organs during pregnancy or the postpartum period. Early-onset preeclampsia has many features in common with atherosclerosis, whereas late-onset preeclampsia seems to result from a mismatch of fetal demands and maternal supply, that is, a metabolic crisis. Preeclampsia, as it is understood today, is essentially vascular dysfunction unmasked or caused by pregnancy. A subset of patients diagnosed with preeclampsia are at greater risk of the subsequent development of hypertension, ischemic heart disease, heart failure, vascular dementia, and end-stage renal disease. However, these adverse events may be the result of a preexisting vascular pathologic process; it is not known if the occurrence of preeclampsia increases the baseline risk. Therefore, the understanding, prediction, prevention, and treatment of preeclampsia are healthcare priorities.

Indexed as

EclampsiaPre-EclampsiaAlbuminuriaEdemaFemaleFetal MortalityGene-Environment InteractionHELLP SyndromeHistory, 19th CenturyHistory, AncientHumansPlacentaPlacenta Growth FactorPregnancyProteinuriaPuerperal DisordersFLT1 protein, humanPlacenta Growth FactorVascular Endothelial Growth Factor Receptor-1acute fatty liveralbuminuriaangiogenic factorbiomarkerblood pressurecardiovascular diseasechronic hypertensionconvulsioneclampsiaedemaElevated Liver enzymes and Low Platelets (HELLP) syndromefetal deathgenetic predispositiongestational hypertensiongreat obstetrical syndromesHemolysishistoryhypertensionhysterotoninimitatorischemiaplacental growth factor (PlGF)postpartum preeclampsiapregnancy-induced hypertensionproteinuriasevere preeclampsiasmall for gestational age (SGA)soluble fms-like tyrosine kinase-1 (sFlt-1)stillbirthtoxemiatoxinuteroplacental ischemiavascular endothelial growth factor (VEGF)

Identifiers

PMID35177220
PMCPMC8941666
OpenAlexW4213172203

What OpenQuestion holds

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Registered trials

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.