Evidence map›Paper›PMID 11094436›Full record

ReviewArthritis research2000

What you should know about PR3-ANCA. An introduction.

A Wiik

Open access · diamondAbstract readReview
In one paragraph

Review in Arthritis research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Lupus Vasculitis: An Overview.Biomedicines · 2021
    Review
  6. Article
  7. Article
  8. ANCA-Associated Vasculitis Pathogenesis: A Commentary.Current rheumatology reports · 2017
    Review
  9. The immunopathology of ANCA-associated vasculitis.Seminars in immunopathology · 2014
    Review
  10. Article
  11. Fulminant Wegener's granulomatosis presenting as epistaxis.Emergency medicine journal : EMJ · 2007
    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

1 author at 1 institution in 1 country.

A WiikDepartment of Autoimmunology, Statens Serum Institut, Copenhagen, Denmark. ipo@ssi.dk
Statens Serum Institut · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-neutrophil cytoplasmic antibodies (ANCA) have become important diagnostic markers of small vessel vasculitides characterized by focal necrotizing lesions of vessel walls and accumulation of lymphocytes and macrophages around the affected vessels. IgG class ANCA directed to proteinase 3 (PR3) of neutrophils and monocytes seem to be directly involved in the pathophysiology of vascular damage by causing excessive neutrophil activation and vessel wall destruction. PR3 and elastase are important players in the mechanisms of vascular necrosis. Methods of detecting ANCA have now been defined but are not uniformly used, even though clinical decisions heavily depend on correct ANCA results.

Indexed as

AnimalsAntibodies, Antineutrophil CytoplasmicBiomarkersHumansMonocytesMyeloblastinNeutrophilsSerine EndopeptidasesVasculitisAntibodies, Antineutrophil CytoplasmicBiomarkersMyeloblastinSerine Endopeptidases

Identifiers

PMID11094436
PMCPMC130013
OpenAlexW1536309339

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.