Evidence map›Paper›PMID 38573766›Full record

Trial reportThe Journal of clinical investigation2024

Inflammatory and tissue injury marker dynamics in pediatric acute respiratory distress syndrome.

Nadir Yehya, Thomas J Booth, Gnana D Ardhanari, Jill M Thompson, L K Metthew Lam, Jacob E Till, Mark V Mai, Garrett Keim, Daniel J McKeone, E Scott Halstead and 6 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 20 citations in OpenAlex.

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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

16 authors at 8 institutions in 2 countries.

Nadir YehyaDivision of Pediatric Critical Care, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia and.
Thomas J BoothDivision of Pediatric Critical Care, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia and.
Gnana D ArdhanariDivision of Pediatric Cardiac Critical Care Medicine, Children's Heart Institute, Memorial Hermann Hospital, University of Texas Health McGovern Medical School, Houston, Texas, USA.
Jill M ThompsonDivision of Pediatric Critical Care, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia and.
L K Metthew LamDivision of Pulmonary, Allergy, and Critical Care, Department of Medicine, Department of Medicine and.
Jacob E TillDivision of Hematology-Oncology, Department of Medicine, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Mark V MaiDivision of Pediatric Critical Care Medicine, Department of Pediatrics, Children's Healthcare of Atlanta and Emory University, Atlanta, Georgia, USA.
Garrett KeimDivision of Pediatric Critical Care, Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia and.
Daniel J McKeoneDivision of Pediatric Hematology and Oncology, Department of Pediatrics and.
E Scott HalsteadDivision of Pediatric Critical Care Medicine, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.
Patrick LahniDivision of Critical Care Medicine, Department of Pediatrics, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Brian M VariscoSection of Critical Care, Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Research Institute, Little Rock, Arkansas, USA.
Wanding ZhouCenter for Computational and Genomic Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Erica L CarpenterDivision of Hematology-Oncology, Department of Medicine, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Jason D ChristieDivision of Pulmonary, Allergy, and Critical Care, Department of Medicine, Department of Medicine and.
Nilam S MangalmurtiDivision of Pulmonary, Allergy, and Critical Care, Department of Medicine, Department of Medicine and.
Children's Hospital of Philadelphia · USPulmonary and Allergy Associates · USPennsylvania State University · USUniversity of Pennsylvania · USArkansas Children's Hospital · USCincinnati Children's Hospital Medical Center · USEmory University · USMemorial Hermann · US

Funding

Linking Endotypes and Outcomes in Pediatric Acute Respiratory Distress SyndromeR01HL148054 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI YEHYA, NADIR · 2019 to 2023
$4.1M
Clinical and Proteomic Characterization of Nucleosomes in Pediatric Acute Respiratory Distress SyndromeK23HL136688 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI YEHYA, NADIR · 2017 to 2020
$694k
NHLBI NIH HHS K23 HL136688NHLBI NIH HHS R01 HL148054
6 · The paper itself

Abstract

BACKGROUNDThe molecular signature of pediatric acute respiratory distress syndrome (ARDS) is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes to outcomes is unknown. Therefore, we profiled inflammation and tissue injury dynamics over the first 7 days of ARDS, and associated specific biomarkers with mortality, persistent ARDS, and persistent multiple organ dysfunction syndrome (MODS).METHODSIn a single-center prospective cohort of intubated pediatric patients with ARDS, we collected plasma on days 0, 3, and 7. Nineteen biomarkers reflecting inflammation, tissue injury, and damage-associated molecular patterns (DAMPs) were measured. We assessed the relationship between biomarkers and trajectories with mortality, persistent ARDS, or persistent MODS using multivariable mixed effect models.RESULTSIn 279 patients (64 [23%] nonsurvivors), hyperinflammatory cytokines, tissue injury markers, and DAMPs were higher in nonsurvivors. Survivors and nonsurvivors showed different biomarker trajectories. IL-1α, soluble tumor necrosis factor receptor 1, angiopoietin 2 (ANG2), and surfactant protein D increased in nonsurvivors, while DAMPs remained persistently elevated. ANG2 and procollagen type III N-terminal peptide were associated with persistent ARDS, whereas multiple cytokines, tissue injury markers, and DAMPs were associated with persistent MODS. Corticosteroid use did not impact the association of biomarker levels or trajectory with mortality.CONCLUSIONSPediatric ARDS survivors and nonsurvivors had distinct biomarker trajectories, with cytokines, endothelial and alveolar epithelial injury, and DAMPs elevated in nonsurvivors. Mortality markers overlapped with markers associated with persistent MODS, rather than persistent ARDS.FUNDINGNIH (K23HL-136688, R01-HL148054).

Indexed as

BiomarkersInflammationRespiratory Distress SyndromeAdolescentChildChild, PreschoolCytokinesFemaleHumansInfantMaleMultiple Organ FailureProspective StudiesBiomarkersCytokinesEndothelial cellsInflammationInnate immunityProteomicsPulmonology

Identifiers

PMID38573766
PMCPMC11093602
OpenAlexW4393950764

What OpenQuestion holds

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LicenceCC BY
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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.