Evidence map›Paper›PMID 21156761›Full record

ArticleAnnals of the rheumatic diseases2011

A genome-wide association study suggests contrasting associations in ACPA-positive versus ACPA-negative rheumatoid arthritis.

Leonid Padyukov, Mark Seielstad, Rick T H Ong, Bo Ding, Johan Rönnelid, Maria Seddighzadeh, Lars Alfredsson, Lars Klareskog, Epidemiological Investigation of Rheumatoid Arthritis (EIRA) study group

Open access · bronzeAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of the rheumatic diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 10 pooled it
12.9field-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

143 citing papers in PubMed, 10 syntheses or guidelines pooled it, 276 citations in OpenAlex.

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83 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

9 authors at 3 institutions in 3 countries.

Leonid PadyukovRheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. seielstadm@gis.a-star.edu.sg
Mark Seielstad
Rick T H Ong
Bo Ding
Johan Rönnelid
Maria Seddighzadeh
Lars Alfredsson
Lars Klareskog
Epidemiological Investigation of Rheumatoid Arthritis (EIRA) study group
Karolinska Institutet · SEGenome Institute of Singapore · SGUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) can be divided into two major subsets based on the presence or absence of antibodies to citrullinated peptide antigens (ACPA). Until now, data from genome-wide association studies (GWAS) have only been published from ACPA-positive subsets of RA or from studies that have not separated the two subsets. The aim of the current study is to provide and compare GWAS data for both subsets. METHODS AND

resultsGWAS using the Illumina 300K chip was performed for 774 ACPA-negative patients with RA, 1147 ACPA-positive patients with RA and 1079 controls from the Swedish population-based case-control study EIRA. Imputation was performed which allowed comparisons using 1,723,056 single nucleotide polymorphisms (SNPs). No SNP achieved genome-wide significance (2.9 × 10⁻⁸) in the comparison between ACPA-negative RA and controls. A case-case association study was then performed between ACPA-negative and ACPA-positive RA groups. The major difference in this analysis was in the HLA region where 768 HLA SNPs passed the threshold for genome-wide significance whereas additional contrasting SNPs did not reach genome-wide significance. However, one SNP close to the RPS12P4 locus in chromosome 2 reached a p value of 2 × 10⁶ and this locus can thus be considered as a tentative candidate locus for ACPA-negative RA.

conclusionsACPA-positive and ACPA-negative RA display significant risk allele frequency differences which are mainly confined to the HLA region. The data provide further support for distinct genetic aetiologies of RA subsets and emphasise the need to consider them separately in genetic as well as functional studies of this disease.

Indexed as

AdolescentAdultAgedArthritis, RheumatoidAutoantibodiesCase-Control StudiesGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMiddle AgedPeptides, CyclicPolymorphism, Single NucleotideYoung AdultAutoantibodiescyclic citrullinated peptidePeptides, Cyclic

Identifiers

PMID21156761
PMCPMC3015094
OpenAlexW2132402446

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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.