Evidence map›Paper›PMID 27384912›Full record

ReviewAnnals of the New York Academy of Sciences2016

Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy.

Carl W White, Raymond C Rancourt, Livia A Veress

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.9field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mesna Improves Outcomes of Sulfur Mustard Inhalation Toxicity in an Acute Rat Model.The Journal of pharmacology and experimental therapeutics · 2024
    Article
  5. Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Therapeutic options to treat mustard gas poisoning - Review.Caspian journal of internal medicine · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Carl W WhitePediatric Airway Research Center, Department of Pediatrics, University of Colorado, Aurora, Colorado. carl.w.white@ucdenver.edu.
Raymond C RancourtPediatric Airway Research Center, Department of Pediatrics, University of Colorado, Aurora, Colorado.
Livia A VeressPediatric Airway Research Center, Department of Pediatrics, University of Colorado, Aurora, Colorado.
University of Colorado Denver · USUniversity of Colorado Hospital · US

Funding

Thiols in sulfur mustard toxicityU54ES015678 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI WHITE, CARL W · 2006 to 2015
$20.5M
NIEHS NIH HHS U54 ES015678
6 · The paper itself

Abstract

Acute lung injury due to sulfur mustard (SM) inhalation causes the formation of airway fibrin casts that obstruct airways at multiple levels, leading to acute respiratory failure and death. These pathophysiological effects are seen in rodent models of acute SM vapor inhalation, as well as in human victims of acute SM inhalation. In rat models, the initial steps in activation of the coagulation system at extravascular sites depend on tissue factor (TF) expression by airway cells, especially in the microparticle fraction, and these effects can be inhibited by TF pathway inhibitor protein. Not only does the procoagulant environment of the acutely injured lung contribute to airway cast formation, but these lesions persist in airways because of the activation of multiple antifibrinolytic pathways, including plasminogen activator inhibitor-1, thrombin-activatable fibrinolysis inhibitor, and α2-antiplasmin. Airway administration of tissue plasminogen activator can overwhelm these effects and save lives by preventing fibrin-dependent airway obstruction, gas-exchange abnormalities, and respiratory failure. In human survivors of SM inhalation, fibrotic processes, including bronchiolitis obliterans and interstitial fibrosis of the lung, are among the most disabling chronic lesions. Antifibrotic therapies may prove useful in preventing either or both of these forms of chronic lung damage.

Indexed as

Acute Lung InjuryAnimalsBlood CoagulationFibrinolytic AgentsHumansInhalation ExposureMustard GasFibrinolytic AgentsMustard Gaslung injurysulfur mustardtissue factortissue plasminogen activator

Identifiers

PMID27384912
PMCPMC5418856
OpenAlexW2472094292

What OpenQuestion holds

Textmetadata
LicenceTDM
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.