Evidence map›Paper›PMID 34109491›Full record

ReviewClinical rheumatology2021

Mechanisms of thrombosis in ANCA-associated vasculitis.

Durga Prasanna Misra, Koshy Nithin Thomas, Armen Yuri Gasparyan, Olena Zimba

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

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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 3 institutions in 3 countries.

Durga Prasanna MisraDepartment of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, India. durgapmisra@gmail.com.ORCID http://orcid.org/0000-0002-5035-7396
Koshy Nithin ThomasDepartment of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, India.ORCID http://orcid.org/0000-0002-0781-6884
Armen Yuri GasparyanDepartments of Rheumatology and Research and Development, Dudley Group NHS Foundation Trust (Teaching Trust of the University of Birmingham, UK), Russells Hall Hospital, Dudley, West Midlands, UK.ORCID http://orcid.org/0000-0001-8749-6018
Olena ZimbaDepartment of Internal Medicine #2, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine.ORCID http://orcid.org/0000-0002-4188-8486
Sanjay Gandhi Post Graduate Institute of Medical Sciences · INDanylo Halytsky Lviv National Medical University · UARussells Hall Hospital · GB

Funding

SGPGIMS intramural Research Grant REF No. PGI/DIR/RC/656/2020
6 · The paper itself

Abstract

Patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) have a two- to threefold greater risk of developing venous as well as arterial thrombotic events. Although such thrombotic events are more commonly seen during phases of active AAV, they are also recognized to occur during AAV in remission. Endothelial injury is a key pathogenic event in AAV. Endothelial injury can be caused by neutrophil activation and release of thrombogenic tissue factor into the circulation. Neutrophil activation further results in the formation of neutrophil extracellular traps (NETs). NETs contribute to thrombosis by expressing tissue factor. NETs have also been detected in cutaneous thrombi from patients with AAV induced by hydralazine. Activated neutrophils in AAV patients release thrombogenic microparticles loaded with tissue factor which further enhances clotting of blood. Antiphospholipid antibodies (APLs) have been detected in up to a third of AAV and might also be induced by drugs such as cocaine adulterated with levamisole and propylthiouracil, which are known to trigger AAV. Such APLs further drive the thrombosis in AAV. Once thrombogenesis occurs, the homeostatic mechanisms resulting in clot dissolution are further impaired in AAV due to anti-plasminogen antibodies. The ongoing pandemic of coronavirus disease 2019 (COVID-19) is associated with endothelial injury and NETosis, mechanisms which are in common with AAV. Reports of new-onset AAV following COVID-19 have been described in the literature, and there could be shared mechanisms driving these processes that require further evaluation.

Indexed as

Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCOVID-19Extracellular TrapsThrombosisAntibodies, Antineutrophil CytoplasmicHumansNeutrophilsSARS-CoV-2Antibodies, Antineutrophil CytoplasmicAnti-neutrophil cytoplasmic antibody-associated vasculitisAntiphospholipid antibodiesDeep vein thrombosisEmbolism and thrombosisNeutrophil extracellular trapsVascular endothelium

Identifiers

PMID34109491
PMCPMC8189705
OpenAlexW3166112320

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.