Evidence map›Paper›PMID 31379873›Full record

ReviewFrontiers in immunology2019

Platelets in Sepsis: An Update on Experimental Models and Clinical Data.

Alice Assinger, Waltraud C Schrottmaier, Manuel Salzmann, Julie Rayes

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 4 pooled it
12.5field-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

152 citing papers in PubMed, 4 syntheses or guidelines pooled it, 269 citations in OpenAlex.

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92 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

4 authors at 2 institutions in 2 countries.

Alice AssingerCenter for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Waltraud C SchrottmaierCenter for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Manuel SalzmannCenter for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Julie RayesInstitute of Cardiovascular Science, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Medical University of Vienna · ATUniversity of Birmingham · GB

Funding

Austrian Science FundAustrian Science Fund FWF P 24978Austrian Science Fund FWF P 32064British Heart Foundation
6 · The paper itself

Abstract

Beyond their important role in hemostasis, platelets play a crucial role in inflammatory diseases. This becomes apparent during sepsis, where platelet count and activation correlate with disease outcome and survival. Sepsis is caused by a dysregulated host response to infection, leading to organ dysfunction, permanent disabilities, or death. During sepsis, tissue injury results from the concomitant uncontrolled activation of the complement, coagulation, and inflammatory systems as well as platelet dysfunction. The balance between the systemic inflammatory response syndrome (SIRS) and the compensatory anti-inflammatory response (CARS) regulates sepsis outcome. Persistent thrombocytopenia is considered as an independent risk factor of mortality in sepsis, although it is still unclear whether the drop in platelet count is the cause or the consequence of sepsis severity. The role of platelets in sepsis development and progression was addressed in different experimental

Indexed as

AnimalsBlood CoagulationBlood PlateletsHemostasisHumansInflammationModels, TheoreticalSepsisinfectioninflammationplateletssepsisthrombocytopenia

Identifiers

PMID31379873
PMCPMC6650595
OpenAlexW2956081866

What Socratic 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 Socratic graph.