Evidence map›Paper›PMID 37280058›Full record

ArticleRheumatology (Oxford, England)2024

The course of cytokine and chemokine gene expression in clinically suspect arthralgia patients during progression to inflammatory arthritis.

Judith W Heutz, Cleo Rogier, Ellis Niemantsverdriet, Susan J F van den Eeden, Pascal H P de Jong, Erik Lubberts, Annemieke Geluk, Annette H M van der Helm-van Mil

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2024. 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
2.5field-weighted citation impact, top 10% 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, 10 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
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

8 authors at 2 institutions in 1 country.

Judith W HeutzDepartment of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands.ORCID 0000-0002-2126-7922
Cleo RogierDepartment of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands.ORCID 0000-0003-3783-7042
Ellis NiemantsverdrietDepartment of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-5781-3817
Susan J F van den EedenDepartment of Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-3845-3019
Pascal H P de JongDepartment of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands.ORCID 0000-0001-6628-6222
Erik LubbertsDepartment of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands.ORCID 0000-0002-3566-040X
Annemieke GelukDepartment of Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-8555-2872
Annette H M van der Helm-van MilDepartment of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands.ORCID 0000-0001-8572-1437
Erasmus MC · NLLeiden University Medical Center · NL

Funding

European Research Council 714312
6 · The paper itself

Abstract

objectivesAutoantibody responses increase years before the onset of inflammatory arthritis (IA) and are stable during transitioning from clinically suspect arthralgia (CSA) to IA. Cytokine and chemokine levels also increase years before IA onset. However, the course in the at-risk stage of CSA during progression to disease or non-progression is unknown. To increase the understanding of processes mediating disease development, we studied the course of cytokine, chemokine and related receptors gene expression in CSA patients during progression to IA and in CSA patients who ultimately did not develop IA.

methodsWhole-blood RNA expression of 37 inflammatory cytokines, chemokines and related receptors was determined by dual-colour reverse transcription multiplex ligation-dependent probe amplification in paired samples of CSA patients at CSA onset and either at IA development or after 24 months without IA development. ACPA-positive and ACPA-negative CSA patients developing IA were compared at CSA onset and during progression to IA. Generalised estimating equations tested changes over time. A false discovery rate approach was applied.

resultsNone of the cytokine/chemokine genes significantly changed in expression between CSA onset and IA development. In CSA patients without IA development, G-CSF expression decreased (P = 0.001), whereas CCR6 and TNIP1 expression increased (P < 0.001 and P = 0.002, respectively) over a 2 year period. Expression levels in ACPA-positive and ACPA-negative CSA patients who developed IA were similar.

conclusionWhole-blood gene expression of assessed cytokines, chemokines and related receptors did not change significantly from CSA to IA development. This suggests that changes in expression of these molecules may not be related to the final process of developing chronicity and may have occurred preceding CSA onset. Changes in gene expression in CSA patients without IA development may provide clues for processes related to resolution.

Indexed as

Arthritis, RheumatoidArthralgiaChemokinesCytokinesGene ExpressionHumansChemokinesCytokineschemokinesclinically suspect arthralgiacytokinesgene expressioninflammatory arthritisMLPA

Identifiers

PMID37280058
PMCPMC10836970
OpenAlexW4379600055

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.