Evidence map›Paper›PMID 32661735›Full record

ReviewSeminars in immunopathology2020

Preterm birth and sustained inflammation: consequences for the neonate.

Alexander Humberg, Ingmar Fortmann, Bastian Siller, Matthias Volkmar Kopp, Egbert Herting, Wolfgang Göpel, Christoph Härtel, German Neonatal Network, German Center for Lung Research and Priming Immunity at the beginning of life (PRIMAL) Consortium

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 5 pooled it
16.5field-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.

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

185 citing papers in PubMed, 5 syntheses or guidelines pooled it, 279 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

125 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 3 institutions in 2 countries.

Alexander HumbergDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Ingmar FortmannDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Bastian SillerDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Matthias Volkmar KoppDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Egbert HertingDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Wolfgang GöpelDepartment of Pediatrics, University of Lübeck, Lübeck, Germany.
Christoph HärtelDepartment of Pediatrics, University of Lübeck, Lübeck, Germany. haertel_c1@ukw.de.
German Neonatal Network, German Center for Lung Research and Priming Immunity at the beginning of life (PRIMAL) Consortium
University of Lübeck · DEUniversity of Bern · CHUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Almost half of all preterm births are caused or triggered by an inflammatory process at the feto-maternal interface resulting in preterm labor or rupture of membranes with or without chorioamnionitis ("first inflammatory hit"). Preterm babies have highly vulnerable body surfaces and immature organ systems. They are postnatally confronted with a drastically altered antigen exposure including hospital-specific microbes, artificial devices, drugs, nutritional antigens, and hypoxia or hyperoxia ("second inflammatory hit"). This is of particular importance to extremely preterm infants born before 28 weeks, as they have not experienced important "third-trimester" adaptation processes to tolerate maternal and self-antigens. Instead of a balanced adaptation to extrauterine life, the delicate co-regulation between immune defense mechanisms and immunosuppression (tolerance) to allow microbiome establishment is therefore often disturbed. Hence, preterm infants are predisposed to sepsis but also to several injurious conditions that can contribute to the onset or perpetuation of sustained inflammation (SI). This is a continuing challenge to clinicians involved in the care of preterm infants, as SI is regarded as a crucial mediator for mortality and the development of morbidities in preterm infants. This review will outline the (i) role of inflammation for short-term consequences of preterm birth and (ii) the effect of SI on organ development and long-term outcome.

Indexed as

ChorioamnionitisObstetric Labor, PrematurePremature BirthFemaleHumansInfantInfant, NewbornInfant, PrematureInflammationPregnancyChronic pulmonary insufficiency of prematurityMicrobiomeNeurocognitive outcomePreterm infantsSepsisSustained inflammation

Identifiers

PMID32661735
PMCPMC7508934
OpenAlexW3043801544

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.