Evidence map›Paper›PMID 29956069›Full record

ReviewInflammation2018

Mechanisms of Hemolysis During Sepsis.

Katharina Effenberger-Neidnicht, Matthias Hartmann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Secreted phospholipase PLA2G5 acts as a hemolytic factor in sepsis.The Journal of clinical investigation · 2026
    Article
  6. Article
  7. Article
  8. Review
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  10. Intravascular hemolysis as a converging mechanism in hemolytic disorders.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
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  18. Article
  19. Article
  20. Article

10 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

2 authors at 1 institution in 1 country.

Katharina Effenberger-NeidnichtInstitute of Physiological Chemistry, University Hospital Essen, Hufelandstraße 55, D-45122, Essen, Germany. katharina.effenberger-neidnicht@uni-due.de.
Matthias HartmannDepartment of Anesthesiology and Intensive Care, University Hospital Essen, Essen, Germany.
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell-free hemoglobin is increasingly playing a more central role in the pathogenesis of sepsis being proved to be a potent predictor of patient's outcome. It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. Graphical Abstract ᅟ.

Indexed as

HemolysisHemoglobinsHumansPrognosisSepsisHemoglobinsdisseminated intravascular coagulationerythrocyteshemolysislipopolysaccharidepore formationsepsissystemic inflammationtransfusion reactions

Identifiers

PMID29956069
OpenAlexW2810192557

What OpenQuestion holds

Textmetadata
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.