Evidence map›Paper›PMID 20833643›Full record

ArticleRheumatology (Oxford, England)2010

Anti-citrullinated peptide antibody-negative RA is a genetically distinct subset: a definitive study using only bone-erosive ACPA-negative rheumatoid arthritis.

Koichiro Ohmura, Chikashi Terao, Etsuko Maruya, Masaki Katayama, Kenichiro Matoba, Kota Shimada, Akira Murasawa, Shigeru Honjo, Kiyoshi Takasugi, Shigeto Tohma and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

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  16. Genetic landscape of interactive effects ofJournal of medical genetics · 2017
    Article
  17. Article
  18. Article
  19. Recent Advances in Defining the Genetic Basis of Rheumatoid Arthritis.Annual review of genomics and human genetics · 2016
    Review
  20. 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

20 authors at 1 institution in 1 country.

Koichiro OhmuraDepartment of Rheumatology and Clinical Immunology, Center for Genomic Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawahara-cho Sakyo-ku, Kyoto 606-8507, Japan. ohmurako@kuhp.kyoto-u.ac.jp
Chikashi Terao
Etsuko Maruya
Masaki Katayama
Kenichiro Matoba
Kota Shimada
Akira Murasawa
Shigeru Honjo
Kiyoshi Takasugi
Shigeto Tohma
Keitaro Matsuo
Kazuo Tajima
Naoichiro Yukawa
Daisuke Kawabata
Takaki Nojima
Takao Fujii
Ryo Yamada
Hiroo Saji
Fumihiko Matsuda
Tsuneyo Mimori
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesACPA is a highly specific marker for RA. It was recently reported that ACPA can be used to classify RA into two disease subsets, ACPA-positive and ACPA-negative RA. ACPA-positive RA was found to be associated with the HLA-DR shared epitope (SE), but ACPA negative was not. However, the suspicion remained that this result was caused by the ACPA-negative RA subset containing patients with non-RA diseases. We examined whether this is the case even when possible non-RA ACPA-negative RA patients were excluded by selecting only patients with bone erosion.

methodsWe genotyped HLA-DRB1 alleles for 574 ACPA-positive RA, 185 ACPA-negative RA (including 97 erosive RA) and 1508 healthy donors. We also tested whether HLA-DR SE is associated with RF-negative or ANA-negative RA.

resultsACPA-negative RA with apparent bone erosion was not associated with SE, supporting the idea that ACPA-negative RA is genetically distinct from ACPA-positive RA. We also tested whether these subsets are based on autoantibody-producing activity. In accordance with the ACPA-negative RA subset, the RF-negative RA subset showed a clearly distinct pattern of association with SE from the RF-positive RA. In contrast, ANA-negative as well as ANA-positive RA was similarly associated with SE, suggesting that the subsets distinguished by ACPA are not based simply on differences in autoantibody production.

conclusionsACPA-negative erosive RA is genetically distinct from ACPA-positive RA.

Indexed as

AgedAntibodies, Anti-IdiotypicArthritis, RheumatoidAutoantibodiesBiomarkersCase-Control StudiesFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedPeptides, CyclicStatistics as TopicAntibodies, Anti-IdiotypicAutoantibodiesBiomarkerscyclic citrullinated peptidePeptides, Cyclic

Identifiers

PMID20833643
PMCPMC2981512
OpenAlexW2150052171

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Registered trials

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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.