Evidence map›Paper›PMID 35532073›Full record

ArticleRheumatology (Oxford, England)2022

Anti-citrullinated protein antibody specificities and pulmonary fibrosis in relation to genetic loci in early rheumatoid arthritis.

Mikael Brink, Lotta Ljung, Monika Hansson, Johan Rönnelid, Rickard Holmdahl, Karl Skriner, Guy Serre, Lars Klareskog, Solbritt Rantapää-Dahlqvist

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
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 6 institutions in 3 countries.

Mikael BrinkDepartment of Public Health and Clinical Medicine/Rheumatology, University Hospital, Umeå.ORCID 0000-0001-7675-3488
Lotta LjungDepartment of Public Health and Clinical Medicine/Rheumatology, University Hospital, Umeå.ORCID 0000-0001-8999-0925
Monika HanssonRheumatology Unit, Department of Medicine, Karolinska Institute at Karolinska University Hospital, Stockholm.
Johan RönnelidDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala.ORCID 0000-0003-1186-3226
Rickard HolmdahlMedical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Solna, Stockholm, Sweden.ORCID 0000-0002-4969-2576
Karl SkrinerDepartment of Rheumatology and Clinical Immunology, Charite Universitätsmedizin, Berlin, Germany.ORCID 0000-0002-5415-270X
Guy SerreInstitut Toulousain des Maladies Infectieuses et Inflammatoires, UMR 1291 Inserm, 5051 CNRS, Université de Toulouse, Toulouse, France.
Lars KlareskogRheumatology Unit, Department of Medicine, Karolinska Institute at Karolinska University Hospital, Stockholm.
Solbritt Rantapää-DahlqvistDepartment of Public Health and Clinical Medicine/Rheumatology, University Hospital, Umeå.ORCID 0000-0001-8259-3863
Umeå University · SEKarolinska University Hospital · SECentre National de la Recherche Scientifique · FRCharité - Universitätsmedizin Berlin · DEKarolinska Institutet · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesPulmonary manifestations in RA are common comorbidities, but the underlying mechanisms are largely unknown. The added value of a multiplex of ACPA and genetic risk markers was evaluated for the development of pulmonary fibrosis (PF) in an inception cohort.

methodsA total of 1184 patients with early RA were consecutively included and followed prospectively from the index date until death or 31 December 2016. The presence of 21 ACPA fine specificities was analysed using a custom-made microarray chip (Thermo Fisher Scientific, Uppsala, Sweden). Three SNPs, previously found related to PF were evaluated, rs2609255 (FAM13A), rs111521887 (TOLLIP) and rs35705950 (MUC5B). ACPA and genetic data were available for 841 RA patients, of whom 50 developed radiologically defined PF.

resultsIn unadjusted analyses, 11 ACPA specificities were associated with PF development. In multiple variable analyses, six ACPA specificities were associated with increased risk of PF: vimentin (Vim)60-75, fibrinogen (Fib)β62-78 (72), Fibα621-635, Bla26, collagen (C)II359-369 and F4-CIT-R (P < 0.01 to P < 0.05). The number of ACPA specificities was also related to PF development (P < 0.05 crude and adjusted models). In multiple variable models respectively adjusted for each of the SNPs, the number of ACPA specificities (P < 0.05 in all models), anti-Vim60-75 (P < 0.05, in all models), anti-Fibβ62-78 (72) (P < 0.001 to P < 0.05), anti-CII359-369 (P < 0.05 in all models) and anti-F4-CIT-R AQ4 (P < 0.01 to P < 0.05), anti-Fibα621-635 (P < 0.05 in one) and anti-Bla26 (P < 0.05 in two) were significantly associated with PF development.

conclusionThe development of PF in an inception cohort of RA patients was associated with both presence of certain ACPA and the number of ACPA specificities and risk genes.

Indexed as

Antibody SpecificityAnti-Citrullinated Protein AntibodiesArthritis, RheumatoidPulmonary FibrosisAutoantibodiesGenetic LociGTPase-Activating ProteinsHumansAnti-Citrullinated Protein AntibodiesAutoantibodiesFAM13A protein, humanGTPase-Activating ProteinsACPA specificitiesautoantibodiesgenetic locipulmonary fibrosisRA

Identifiers

PMID35532073
PMCPMC9729003
OpenAlexW4229454835

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.