Evidence map›Paper›PMID 33478589›Full record

ReviewJournal of intensive care2021

The discovery of biological subphenotypes in ARDS: a novel approach to targeted medicine?

Karin Wildi, Samantha Livingstone, Chiara Palmieri, Gianluigi LiBassi, Jacky Suen, John Fraser

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Journal of intensive care, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Clinical Subphenotypes of Staphylococcus aureus Bacteremia.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2024
    Observational
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 2 countries.

Karin WildiThe Critical Care Research Group, The Prince Charles Hospital, Clinical Sciences Building, Level 3, Chermside, Brisbane, QLD, 4032, Australia. k.wildi@uq.edu.au.ORCID http://orcid.org/0000-0002-6520-2696
Samantha LivingstoneThe Critical Care Research Group, The Prince Charles Hospital, Clinical Sciences Building, Level 3, Chermside, Brisbane, QLD, 4032, Australia.
Chiara PalmieriSchool of Veterinary Science, the University of Queensland, Brisbane, Australia.
Gianluigi LiBassiThe Critical Care Research Group, The Prince Charles Hospital, Clinical Sciences Building, Level 3, Chermside, Brisbane, QLD, 4032, Australia.
Jacky SuenThe Critical Care Research Group, The Prince Charles Hospital, Clinical Sciences Building, Level 3, Chermside, Brisbane, QLD, 4032, Australia.
John FraserThe Critical Care Research Group, The Prince Charles Hospital, Clinical Sciences Building, Level 3, Chermside, Brisbane, QLD, 4032, Australia.
The University of Queensland · AU

Funding

The Prince Charles Hospital Foundation PhD scholarshipUniversity of Queensland PhD scholarship
6 · The paper itself

Abstract

The acute respiratory distress syndrome (ARDS) is a severe lung disorder with a high morbidity and mortality which affects all age groups. Despite active research with intense, ongoing attempts in developing pharmacological agents to treat ARDS, its mortality rate remains unaltered high and treatment is still only supportive. Over the years, there have been many attempts to identify meaningful subgroups likely to react differently to treatment among the heterogenous ARDS population, most of them unsuccessful. Only recently, analysis of large ARDS cohorts from randomized controlled trials have identified the presence of distinct biological subphenotypes among ARDS patients: a hypoinflammatory (or uninflamed; named P1) and a hyperinflammatory (or reactive; named P2) subphenotype have been proposed and corroborated with existing retrospective data. The hyperinflammatory subphenotyope was clearly associated with shock state, metabolic acidosis, and worse clinical outcomes. Core features of the respective subphenotypes were identified consistently in all assessed cohorts, independently of the studied population, the geographical location, the study design, or the analysis method. Additionally and clinically even more relevant treatment efficacies, as assessed retrospectively, appeared to be highly dependent on the respective subphenotype. This discovery launches a promising new approach to targeted medicine in ARDS. Even though it is now widely accepted that each ARDS subphenotype has distinct functional, biological, and mechanistic differences, there are crucial gaps in our knowledge, hindering the translation to bedside application. First of all, the underlying driving biological factors are still largely unknown, and secondly, there is currently no option for fast and easy identification of ARDS subphenotypes. This narrative review aims to summarize the evidence in biological subphenotyping in ARDS and tries to point out the current issues that will need addressing before translation of biological subohenotypes into clinical practice will be possible.

Indexed as

Acute respiratory distress syndrome (ARDS)BiomarkerCluster analysisPrecision medicinePredictive and prognostic enrichmentSubphenotypesTargeted treatment

Identifiers

PMID33478589
PMCPMC7817965
OpenAlexW3123886734

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.