Evidence map›Paper›PMID 37240292›Full record

ReviewInternational journal of molecular sciences2023

Interrelationship between COVID-19 and Coagulopathy: Pathophysiological and Clinical Evidence.

Beatrice Ragnoli, Beatrice Da Re, Alessandra Galantino, Stefano Kette, Andrea Salotti, Mario Malerba

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Rethinking angiotensin receptor blocker (ARB) use in COVID-19: a class-wide call for careful dosing.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Observational
  10. Review
  11. Article
  12. Article
  13. Evaluation of d-dimer as outcome biomarker in COVID-19 acute respiratory distress patients.Revista do Instituto de Medicina Tropical de Sao Paulo · 2024
    Observational
  14. COVID-19: a multi-organ perspective.Frontiers in cellular and infection microbiology · 2024
    Review
  15. Long COVID: Molecular Mechanisms and Detection Techniques.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Frequency and Association of Polymorphisms in F2, F7, and PROS1 Coagulation Genes with Disease Severity in Coronavirus Disease 2019.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

6 authors at 2 institutions in 1 country.

Beatrice RagnoliRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.ORCID 0000-0001-5969-8501
Beatrice Da ReRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.
Alessandra GalantinoRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.
Stefano KetteRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.
Andrea SalottiRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.
Mario MalerbaRespiratory Unit, Sant'Andrea Hospital, 13100 Vercelli, Italy.ORCID 0000-0003-1246-4892
CTO Andrea Alesini · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.

Indexed as

Blood Coagulation DisordersCOVID-19ThrombophiliaThrombosisAnticoagulantsHumansInflammationSARS-CoV-2Anticoagulantsanticoagulant therapycitokine stormcoagulopathyCOVID-19 infectionendothelial dysfunctionplatelet activation

Identifiers

PMID37240292
PMCPMC10219009
OpenAlexW4377103943

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.