Evidence map›Paper›PMID 34948438›Full record

ReviewInternational journal of molecular sciences2021

Prothrombotic Phenotype in COVID-19: Focus on Platelets.

Cristina Barale, Elena Melchionda, Alessandro Morotti, Isabella Russo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
6.0field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Platelets and Cardioprotection: The Role of Nitric Oxide and Carbon Oxide.International journal of molecular sciences · 2023
    Review
  9. Shedding Light on the Pathogenesis of Splanchnic Vein Thrombosis.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Platelets in COVID-19 disease: friend, foe, or both?Pharmacological reports : PR · 2022
    Review
  13. Article
  14. Article
  15. Review
  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

4 authors at 1 institution in 1 country.

Cristina BaraleDepartment of Clinical and Biological Sciences, Turin University, 10043 Orbassano, Turin, Italy.ORCID 0000-0003-3201-5883
Elena MelchiondaDepartment of Clinical and Biological Sciences, Turin University, 10043 Orbassano, Turin, Italy.
Alessandro MorottiDepartment of Clinical and Biological Sciences, Turin University, 10043 Orbassano, Turin, Italy.ORCID 0000-0002-8407-2903
Isabella RussoDepartment of Clinical and Biological Sciences, Turin University, 10043 Orbassano, Turin, Italy.ORCID 0000-0002-2921-1763
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 infection is associated with a broad spectrum of presentations, but alveolar capillary microthrombi have been described as a common finding in COVID-19 patients, appearing as a consequence of a severe endothelial injury with endothelial cell membrane disruption. These observations clearly point to the identification of a COVID-19-associated coagulopathy, which may contribute to thrombosis, multi-organ damage, and cause of severity and fatality. One significant finding that emerges in prothrombotic abnormalities observed in COVID-19 patients is that the coagulation alterations are mainly mediated by the activation of platelets and intrinsically related to viral-mediated endothelial inflammation. Beyond the well-known role in hemostasis, the ability of platelets to also release various potent cytokines and chemokines has elevated these small cells from simple cell fragments to crucial modulators in the blood, including their inflammatory functions, that have a large influence on the immune response during infectious disease. Indeed, platelets are involved in the pathogenesis of acute lung injury also by promoting NET formation and affecting vascular permeability. Specifically, the deposition by activated platelets of the chemokine platelet factor 4 at sites of inflammation promotes adhesion of neutrophils on endothelial cells and thrombogenesis, and it seems deeply involved in the phenomenon of vaccine-induced thrombocytopenia and thrombosis. Importantly, the hyperactivated platelet phenotype along with evidence of cytokine storm, high levels of P-selectin, D-dimer, and, on the other hand, decreased levels of fibrinogen, von Willebrand factor, and thrombocytopenia may be considered suitable biomarkers that distinguish the late stage of COVID-19 progression in critically ill patients.

Indexed as

Blood CoagulationBlood Coagulation DisordersBlood PlateletsCOVID-19Cytokine Release SyndromeEndothelial CellsFibrin Fibrinogen Degradation ProductsHemostasisHumansInflammationPhenotypePlatelet ActivationSARS-CoV-2ThrombocytopeniaThrombosisFibrin Fibrinogen Degradation Productsfibrin fragment DCOVID-19immunothrombosisinflammationplatelet activationSARS-CoV-2thrombosis

Identifiers

PMID34948438
PMCPMC8705811
OpenAlexW4200254476

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.