Evidence map›Paper›PMID 27906045›Full record

ArticleArthritis research & therapy2016

Smoking is associated with the concurrent presence of multiple autoantibodies in rheumatoid arthritis rather than with anti-citrullinated protein antibodies per se: a multicenter cohort study.

Tineke J van Wesemael, Sofia Ajeganova, Jennifer Humphreys, Chikashi Terao, Ammar Muhammad, Deborah P M Symmons, Alex J MacGregor, Ingiäld Hafström, Leendert A Trouw, Annette H M van der Helm-van Mil and 7 more

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

Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 3 pooled it
6.3field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 65 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

17 authors at 9 institutions in 5 countries.

Tineke J van WesemaelDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands. tinekevanwesemael@gmail.com.
Sofia AjeganovaDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Jennifer HumphreysArthritis Research UK Centre for Epidemiology, University of Manchester, Manchester, UK.
Chikashi TeraoCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Ammar MuhammadDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Deborah P M SymmonsArthritis Research UK Centre for Epidemiology, University of Manchester, Manchester, UK.
Alex J MacGregorNorwich Medical School, University of East Anglia, Norwich, UK.
Ingiäld HafströmRheumatology Unit, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
Leendert A TrouwDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Annette H M van der Helm-van MilDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Tom W J HuizingaDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Tsuneyo MimoriDepartment of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
René E M ToesDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Fumihiko MatsudaCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Björn SvenssonDepartment of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden.
Suzanne M M VerstappenArthritis Research UK Centre for Epidemiology, University of Manchester, Manchester, UK.
Diane van der WoudeDepartment of Rheumatology C1-R, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Leiden University Medical Center · NLKyoto University · JPVersus Arthritis · GBBrigham and Women's Hospital · USKarolinska Institutet · SEKarolinska University Hospital · SELund University · SEUniversity of East Anglia · GBUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe contribution of smoking to rheumatoid arthritis (RA) is hypothesized to be mediated through formation of anti-citrullinated protein antibodies (ACPA). In RA, however, autoantibodies such as ACPA, rheumatoid factor (RF), and anti-carbamylated protein antibodies (anti-CarP) often occur together, and it is thus unclear whether smoking is specifically associated with some autoantibodies rather than others. We therefore investigated whether smoking is only associated with ACPA or with the presence of multiple RA-related autoantibodies.

methodsA population-based Japanese cohort (n = 9575) was used to investigate the association of smoking with RF and anti-cyclic citrullinated peptide antibodies (anti-CCP2) in individuals without RA. Furthermore, RA patients fulfilling the 1987 criteria from three early arthritis cohorts from the Netherlands (n = 678), the United Kingdom (n = 761), and Sweden (n = 795) were used. Data on smoking, RF, anti-CCP2, and anti-CarP were available. A total score of autoantibodies was calculated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated by logistic regression.

resultsIn the population-based non-RA cohort, no association was found between smoking and one autoantibody (RF or anti-CCP2), but smoking was associated with double-autoantibody positivity (OR 2.95, 95% CI 1.32-6.58). In RA patients, there was no association between smoking and the presence of one autoantibody (OR 0.99, 95% CI 0.78-1.26), but smoking was associated with double-autoantibody positivity (OR 1.32, 95% CI 1.04-1.68) and triple-autoantibody positivity (OR 2.05, 95% CI 1.53-2.73).

conclusionsSmoking is associated with the concurrent presence of multiple RA-associated autoantibodies rather than just ACPA. This indicates that smoking is a risk factor for breaking tolerance to multiple autoantigens in RA.

Indexed as

AdultAgedArthritis, RheumatoidAutoantibodiesAutoantigensCitrullineCohort StudiesEnzyme-Linked Immunosorbent AssayFemaleFluorescent Antibody TechniqueHumansJapanMaleMiddle AgedPeptides, CyclicRheumatoid FactorAutoantibodiesAutoantigensCitrullinePeptides, CyclicRheumatoid FactorAnti-carbamylated protein antibodiesAnti-citrullinated protein antibodiesRheumatoid arthritisRheumatoid factorRisk factorSmoking

Identifiers

PMID27906045
PMCPMC5134292
OpenAlexW2557882437

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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.