Evidence map›Paper›PMID 38049984›Full record

ArticleAnnals of the rheumatic diseases2024

In early rheumatoid arthritis, anticitrullinated peptide antibodies associate with low number of affected joints and rheumatoid factor associates with systemic inflammation.

Eleftheria Pertsinidou, Saedis Saevarsdottir, Vivek Anand Manivel, Lars Klareskog, Lars Alfredsson, Linda Mathsson-Alm, Monika Hansson, Martin Cornillet, Guy Serre, Rikard Holmdahl and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
11.2field-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

17 citing papers in PubMed, 45 citations in OpenAlex.

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  9. Autoantibodies as prognostic markers in rheumatoid arthritis.Journal of translational autoimmunity · 2025
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  14. Bone-protective effects of neutralizing angiopoietin-like protein 4 monoclonal antibody in rheumatoid arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

15 authors at 5 institutions in 7 countries.

Eleftheria PertsinidouDepartment of Immunology Genetics and Pathology, Uppsala University, Uppsala, Sweden eleftheria.pertsinidou@igp.uu.se.ORCID http://orcid.org/0000-0002-8492-4045
Saedis SaevarsdottirClinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Stockholm, Sweden.
Vivek Anand ManivelDepartment of Immunology Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Lars KlareskogRheumatology Unit, Department of Medicine, Karolinska Institute, Solna, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9601-6186
Lars AlfredssonInstitute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
Linda Mathsson-AlmDepartment of Immunology Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Monika HanssonRheumatology Unit, Department of Medicine, Karolinska Institute, Solna, Stockholm, Sweden.
Martin CornilletInstitut Toulousain des Maladies Infectieuses et Inflammatoires, UMR1291 Inserm, 5051 CNRS, Université de Toulouse 3, Toulouse, France.ORCID http://orcid.org/0000-0001-7981-0927
Guy SerreInstitut Toulousain des Maladies Infectieuses et Inflammatoires, UMR1291 Inserm, 5051 CNRS, Université de Toulouse 3, Toulouse, France.
Rikard HolmdahlDepartment of Medical Inflammation Research, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4969-2576
Karl SkrinerDepartment of Medicine, Charité University Hospital, Berlin, Germany.ORCID http://orcid.org/0000-0002-5415-270X
Per-Johan JakobssonRheumatology Unit, Department of Medicine, Karolinska Institute, Solna, Stockholm, Sweden.
Helga WesterlindClinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-3380-5342
Johan AsklingClinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-0433-0616
Johan RönnelidDepartment of Immunology Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0003-1186-3226
Karolinska Institutet · SEUppsala University · SECentre National de la Recherche Scientifique · FRCharité - Universitätsmedizin Berlin · DEUniversity of Iceland · IS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate how individual rheumatoid arthritis (RA) autoantibodies associate with individual signs and symptoms at the time of RA diagnosis.

methodsIgA, IgG, IgM rheumatoid factor (RF), antibodies against cyclic citrullinated peptide version 2 (anti-CCP2) and 16 individual antibodies against citrullinated protein (ACPA) reactivities were analysed centrally in baseline sera from 1600 patients with RA classified according to the 1987 American College of Rheumatology (ACR) criteria. These results were related to C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), number of swollen and tender joints (SJC and TJC), 28-joint disease activity scores (DAS28 and DAS28CRP), global disease activity evaluated by the patients and Health Assessment Questionnaire, all obtained at baseline.

resultsIndividually, all autoantibodies except immunoglobulin G (IgG) RF associated with low SJC and TJC and with high ESR. In IgM RF-negative patients, ACPA associated strictly with low number of swollen and tender joints. This association persisted in multiple regression and stratified analyses where IgM and IgA RF instead associated with inflammation expressed as ESR. Among subjects without any ACPA peptide reactivity, there was no association between RF isotypes and ESR. The effect of RF on ESR increased with the number of ACPA reactivities, especially for IgM RF. In patients fulfilling the 1987 ACR criteria without taking RF into account, associations between IgM RF and high ESR, as well as between ACPA and low joint counts, remained.

conclusionWhereas ACPA associate with low counts of affected joints in early RA, RF associates with elevated measures of systemic inflammation in an ACPA-dependent manner. This latter finding corroborates in vitro models of ACPA and RF in immune complex-induced inflammation. These phenotypic associations are independent of classification criteria.

Indexed as

Arthritis, RheumatoidRheumatoid FactorAutoantibodiesHumansImmunoglobulin AImmunoglobulin GImmunoglobulin MInflammationPeptides, CyclicAutoantibodiesImmunoglobulin AImmunoglobulin GImmunoglobulin MPeptides, CyclicRheumatoid FactorAnti-Citrullinated Protein AntibodiesArthritis, RheumatoidAutoantibodiesAutoimmune DiseasesRheumatoid Factor

Identifiers

PMID38049984
PMCPMC10894817
OpenAlexW4389050180

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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.