Evidence map›Paper›PMID 38053459›Full record

ArticleRMD open2023

Antibodies against advanced glycation end-products and malondialdehyde-acetaldehyde adducts identify a new specific subgroup of hitherto patients with seronegative arthritis with a distinct clinical phenotype and an HLA class II association.

Michelle D van den Beukel, Tineke J van Wesemael, Anna Titia W Hoogslag, Nicole V Borggreven, Tom Wj Huizinga, Annette Hm van der Helm-van Mil, René Em Toes, Diane van der Woude, Leendert A Trouw

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

Article in RMD open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. 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 1 institution in 2 countries.

Michelle D van den BeukelImmunology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-7433-1887
Tineke J van WesemaelRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-3101-0530
Anna Titia W HoogslagRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-3051-9052
Nicole V BorggrevenImmunology, Leiden University Medical Center, Leiden, The Netherlands.
Tom Wj HuizingaRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-7033-7520
Annette Hm van der Helm-van MilRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-8572-1437
René Em ToesRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-9618-6414
Diane van der WoudeRheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-8121-5879
Leendert A TrouwImmunology, Leiden University Medical Center, Leiden, The Netherlands l.a.trouw@lumc.nl.ORCID 0000-0001-5186-2290
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn rheumatoid arthritis (RA) around two-thirds of patients are autoantibody positive for rheumatoid factor, anti-citrullinated protein antibodies and/or anti-carbamylated protein antibodies. The remaining seronegative subgroup of patients is clinically heterogeneous and thus far, biomarkers predicting the disease course are lacking. Therefore, we analysed the value of other autoantibodies in RA directed against malondialdehyde-acetaldehyde adducts (MAA) and advanced glycation end-products (AGE).

methodsIn sera of 648 patients with RA and 538 patients without RA from the Leiden Early Arthritis Clinic, anti-MAA and anti-AGE IgG antibody levels were measured using ELISA. Associations between genetic risk factors, acute phase reactants, radiological joint damage, remission and anti-PTM positivity were investigated using regression, correlation and survival analyses.

resultsAnti-AGE and anti-MAA were most prevalent in RA (44.6% and 46.1% respectively) but were also present in non-RA arthritis patients (32.9% and 30.3% respectively). Anti-AGE and anti-MAA antibodies were associated with HLA-DRB1*03 within seronegative RA (OR=1.98, p=0.003, and OR=2.37, p<0.001, respectively) and, for anti-AGE also in non-RA arthritis patients (OR=2.34, p<0.001). Presence of anti-MAA antibodies was associated significantly with markers of inflammation, erythrocyte sedimentation rate and C reactive protein, in all groups independent of anti-AGE. Interestingly, the presence of anti-AGE and anti-MAA antibodies was associated with radiological progression in patients with seronegative RA, but not evidently with sustained drug-free remission.

conclusionsAnti-AGE and anti-MAA were present in around 45% of RA patients and 30% of non-RA arthritis patients, and although not specific for RA, their presence associated with HLA, inflammation and, for RA, with clinical outcomes especially in patients with seronegative RA.

Indexed as

AcetaldehydeArthritis, RheumatoidAutoantibodiesHumansInflammationMaillard ReactionMalondialdehydePhenotypeAcetaldehydeAutoantibodiesMalondialdehydeAnti-Citrullinated Protein AntibodiesArthritisArthritis, RheumatoidAutoantibodies

Identifiers

PMID38053459
PMCPMC10693877
OpenAlexW4389219558

What OpenQuestion holds

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LicenceCC BY-NC
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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.