Evidence map›Paper›PMID 31242491›Full record

Trial reportJournal of innate immunity2020

The Specific Organism: Not Bacterial Gram Type: Drives the Inflammatory Response in Septic Shock.

Adam Linder, Chris D Fjell, Malin Inghammar, Joseph Hsu, Keith R Walley, John H Boyd, James A Russell

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. C-Reactive Protein: More than a Biomarker.Journal of innate immunity · 2021
    Article
  5. Some Like It Hot.Journal of innate immunity · 2021
    Article
  6. Serious, Severe, Sepsis.Journal of innate immunity · 2020
    Article
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

7 authors at 3 institutions in 3 countries.

Adam LinderDivision of Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden, adam.linder@med.lu.se.
Chris D FjellCentre for Heart Lung Innovation and Division of Critical Care Medicine, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada.
Malin InghammarDivision of Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden.
Joseph HsuPulmonary and Critical Care Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Keith R WalleyCentre for Heart Lung Innovation and Division of Critical Care Medicine, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada.
John H BoydCentre for Heart Lung Innovation and Division of Critical Care Medicine, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada.
James A RussellCentre for Heart Lung Innovation and Division of Critical Care Medicine, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada.
St. Paul's Hospital · CALund University · SEStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and hypothesisThe inflammatory response was targeted by unsuccessful therapies but ignored pathogen. We hypothesized that the inflammatory response differs according to organism in human septic shock. MATERIALS AND

methodsWe measured 39 cytokines at baseline and 24 h in patients (n = 363) in the Vasopressin and Septic Shock Trial (VASST). We compared cytokine profiles (cytokine functional class) at baseline and at 24 h by organism and used hierarchical clustering to classify cytokines according to 28-day outcomes.

resultsIn 363 patients, 88 and 176 patients had at least 1 species isolated from blood and other sites, respectively. Cytokine levels differed significantly according to organism: Neisseria meningitidis and Streptococcus pneumoniae had the highest (baseline and at 24 h), while Enterococcus faecalis (blood) had the lowest mean cytokine levels. N. meningitidis and Klebsiella pneumoniae had significantly higher cytokine levels at baseline versus 24 h (p = 0.01 and 0.02, respectively); E. faecalis had significantly higher cytokine levels at 24 h versus baseline. Hierarchical clustering heat maps showed that pathogens elicited similar cytokine responses not related to the functional cytokine class.

conclusionThe organism type induces different cytokine profiles in septic shock. Specific gram-positive and gram-negative pathogens stimulated similar plasma cytokine-level patterns.

Indexed as

BacteriaBacterial InfectionsCytokinesShock, SepticAgedFemaleHumansMaleMiddle AgedCytokinesCytokinesGram typeInflammationOrganismPathogenSeptic shock

Identifiers

PMID31242491
PMCPMC7098279
OpenAlexW2960096682

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.