Evidence map›Paper›PMID 28730407›Full record

ReviewJournal of thrombosis and thrombolysis2017

Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians.

Eduardo Vazquez-Garza, Carlos Jerjes-Sanchez, Aline Navarrete, Jorge Joya-Harrison, David Rodriguez

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of thrombosis and thrombolysis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 8 pooled it
12.0field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 8 syntheses or guidelines pooled it, 171 citations in OpenAlex.

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33 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

5 authors at 2 institutions in 1 country.

Eduardo Vazquez-GarzaCentro de Investigacion Biomedica del Hospital Zambrano Hellion, TecSalud. Escuela de Medicina y Ciencias de la Salud, Tecnologico de Monterrey, Batallón de San Patricio 112, Real San Agustin, 66278, San Pedro Garza Garcia, Nuevo Leon, Mexico.ORCID http://orcid.org/0000-0001-7149-8334
Carlos Jerjes-SanchezCentro de Investigacion Biomedica del Hospital Zambrano Hellion, TecSalud. Escuela de Medicina y Ciencias de la Salud, Tecnologico de Monterrey, Batallón de San Patricio 112, Real San Agustin, 66278, San Pedro Garza Garcia, Nuevo Leon, Mexico. jerjes@prodigy.net.mx.ORCID http://orcid.org/0000-0003-3222-7405
Aline NavarretePrograma Multicéntrico de Residencias Médicas - Tecnologico de Monterrey, San Pedro Garza Garcia, Nuevo Leon, Mexico.ORCID http://orcid.org/0000-0002-9704-0900
Jorge Joya-HarrisonPrograma Multicéntrico de Residencias Médicas - Tecnologico de Monterrey, San Pedro Garza Garcia, Nuevo Leon, Mexico.ORCID http://orcid.org/0000-0003-3253-3488
David RodriguezInstituto de Cardiología y Medicina Vascular, TecSalud and Centro de Investigacion Biomedica del Hospital Zambrano Hellion, Escuela de Medicina y Ciencias de la Salud, Tecnologico de Monterrey, San Pedro Garza Garcia, Nuevo Leon, Mexico.ORCID http://orcid.org/0000-0002-0811-4235
Hospital Zambrano Hellion · MXTecnológico de Monterrey · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Venous thromboembolism (VTE) is a worldwide disease related with mortality, cardiovascular disability, impaired quality of life and, cause major long-term complications. Clinicians related to the acute and long-term patients care must be involved in the molecular mechanisms of thrombosis. The vessel wall and its inner lining of the endothelium are critical to the maintenance of a patent vasculature. After endothelial disruption, collagen (first line of endothelial defense) and intravascular tissue factor (second line of endothelial defense) are exposed to blood flow, starting the formation of a thrombus. Anticoagulant endovascular proteins and endogenous fibrinolysis have an active role in hemostasis. Currently, the process of coagulation is a cell surface-based model that includes three overlapping phases: initiation, amplification, and propagation. From a simple view, inflammation is one of the first responses of the immune system to infection; inflammation is driven by eicosanoids and cytokines, which are released by injured or infected cells. Common cytokines, which regulate inflammatory response, include interleukins (mainly interleukin-6) that are responsible for communication among white blood cells, chemokines that promote chemotaxis, and interferons that have anti-viral effects. Acute infections have been associated with a transient increase in the risk of myocardial infarction, stroke and recently with venous thrombosis, supporting the notion that systemic and respiratory infections increase the risk of thromboembolic events. Recently, immunothrombosis, another thrombosis mechanism that includes innate immune mechanisms, the neutrophil extracellular genetic traps, and the immunothrombosis dysregulation, could explain some cases of "unprovoked" VTE especially in elderly, a high-risk population for thrombosis.

Indexed as

HemostasisHumansImmunity, InnateInflammationThrombosisVenous ThromboembolismImmunothrombosisInflammationThrombosisVenous thromboembolism

Identifiers

PMID28730407
OpenAlexW2738685539

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.