Evidence map›Paper›PMID 32918567›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

The coagulopathy, endotheliopathy, and vasculitis of COVID-19.

Toshiaki Iba, Jean Marie Connors, Jerrold H Levy

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 4 pooled it
9.3field-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

240 citing papers in PubMed, 4 syntheses or guidelines pooled it, 433 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

180 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

3 authors at 3 institutions in 2 countries.

Toshiaki IbaDepartment of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo Bunkyo-ku, Tokyo, 113-8421, Japan. toshiiba@juntendo.ac.jp.ORCID http://orcid.org/0000-0002-0255-4088
Jean Marie ConnorsHematology Division Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Jerrold H LevyDepartment of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Brigham and Women's Hospital · USDuke University · USJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCOVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy.

methodsThe authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19.

resultsThe primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed.

conclusionThe endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.

Indexed as

BetacoronavirusBlood Coagulation DisordersCoronavirus InfectionsCOVID-19Endothelial CellsEndothelium, VascularFibrin Fibrinogen Degradation ProductsHumansLungMicrovesselsPandemicsPneumonia, ViralPubMedPulmonary EmbolismSARS-CoV-2ThrombosisFibrin Fibrinogen Degradation Productsfibrin fragment DCoagulopathyCOVID-19EndotheliopathyThromboembolismVasculitis

Identifiers

PMID32918567
PMCPMC7486586
OpenAlexW3086407960

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.