Evidence map›Paper›PMID 32794199›Full record

ReviewScandinavian journal of immunology2020

Proteinase 3 Autoreactivity in Anti-Neutrophil Cytoplasmic Antibody-associated vasculitis-Immunological versus clinical features.

Ravi K Sharma, Björn Lövström, Iva Gunnarsson, Vivianne Malmström

Abstract readReview
In one paragraph

Review in Scandinavian journal of immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. ANCA Status or Clinical Phenotype - What Counts More?Current rheumatology reports · 2021
    Review
  6. Review
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.

Ravi K SharmaDivision of Rheumatology, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-2658-0002
Björn LövströmDivision of Rheumatology, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Iva GunnarssonDivision of Rheumatology, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Vivianne MalmströmDivision of Rheumatology, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.

Funding

ALF Funding from Stockholm County council 2019-0662Karolinska Institutet 2019-01961Vetenskapsrådet 2019-01664
6 · The paper itself

Abstract

ANCA-associated vasculitis (AAV) is a group of chronic inflammatory diseases of small- and medium-sized vessels, which are broadly subdivided based on organ manifestations and disease-specific autoantibodies. The so called anti-neutrophil cytoplasmic antibodies (ANCA) mostly target one of the enzymes, proteinase 3 (PR3) or myeloperoxidase (MPO). Accumulating genetic data demonstrates that these two autoantibodies discriminate two distinct disease entities, more so than the clinical subdivision which is mainly criteria-based. Treatment of AAV includes heavy immunosuppression and is guided by which organs that are involved. Generally, patients with PR3-ANCA display higher risk for disease relapse than patients with MPO-ANCA. In this review, we will focus on the autoimmune features of PR3+ AAV and our current understanding of its triggers and the potential translation into clinical practice.

Indexed as

AnimalsAntibodies, Antineutrophil CytoplasmicAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisHLA-DP beta-ChainsHumansInflammationModels, ImmunologicalMyeloblastinPeroxidaseT-Lymphocyte SubsetsAntibodies, Antineutrophil CytoplasmicHLA-DPB1 antigenHLA-DP beta-ChainsMyeloblastinPeroxidaseANCA vasculitisautoreactivityimmune mechanismsproteinase 3

Identifiers

PMID32794199
PMCPMC7685112

What OpenQuestion holds

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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.