Evidence map›Paper›PMID 39411912›Full record

ArticleACR open rheumatology2025

Circulating Baseline CXCR3

Julia M Scheffler, Christina Drevinge, Catharina Lindholm, Inger Gjertsson, Kristina Lend, Merete Lund Hetland, Mikkel Østergaard, Till Uhlig, Marte Schrumpf Heiberg, Espen A Haavardsholm and 13 more

Abstract read
In one paragraph

Article in ACR open rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Bone Health in Rheumatoid Arthritis: An Update.Current rheumatology reports · 2026
    Review
  2. 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

23 authors.

Julia M SchefflerUniversity of Gothenburg, Gothenburg, Sweden.
Christina DrevingeUniversity of Gothenburg, Gothenburg, Sweden.
Catharina LindholmUniversity of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Inger GjertssonUniversity of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-9301-4844
Kristina LendKarolinska Institute, Karolinska University Hospital, Stockholm, Sweden, and Amsterdam University Medical Center, Amsterdam, the Netherlands.ORCID https://orcid.org/0000-0001-5037-5546
Merete Lund HetlandRigshospitalet, Glostrup, Denmark, and University of Copenhagen, Copenhagen, Denmark.
Mikkel ØstergaardRigshospitalet, Glostrup, Denmark, and University of Copenhagen, Copenhagen, Denmark.
Till UhligDiakonhjemmet Hospital, Oslo, Norway.ORCID https://orcid.org/0000-0002-6881-9552
Marte Schrumpf HeibergDiakonhjemmet Hospital, Oslo, Norway.
Espen A HaavardsholmDiakonhjemmet Hospital and University of Oslo, Oslo, Norway.
Michael T NurmohamedAmsterdam Rheumatology and Immunology Center, Reade, the Netherlands, and Amsterdam University Medical Center, Amsterdam, the Netherlands.ORCID https://orcid.org/0000-0002-6274-1934
Jon LampaKarolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Tuulikki Sokka-IslerUniversity of Eastern Finland, Jyväskylä Central Hospital, Jyväskylä, Finland.
Dan NordströmHelsinki University and University Hospital, Helsinki, Finland.
Kim Hørslev-PetersenDanish Hospital for Rheumatic Diseases, University Hospital of Southern Denmark, Sønderborg, Denmark, and University of Southern Denmark, Odense, Denmark.
Bjorn GudbjornssonLandspitali National University Hospital of Iceland and University of Iceland, Reykjavik, Iceland.
Gerdur GröndalLandspitali National University Hospital of Iceland and University of Iceland, Reykjavik, Iceland.
Ronald van VollenhovenKarolinska Institute, Karolinska University Hospital, Stockholm, Sweden, and Amsterdam University Medical Center, Amsterdam, the Netherlands.
Hans CarlstenUniversity of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Mattias LorentzonUniversity of Gothenburg, Gothenburg, Sweden and Australian Catholic University, Melbourne, Australia.
Anna-Karin Hultgård EkwallUniversity of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Anna RudinUniversity of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Ulrika IslanderUniversity of Gothenburg, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-8493-1739

Funding

Association against RheumatismEmil and Wera Cornells foundationIngaBritt and Arne Lundberg Foundation LU-2018-0008IngaBritt and Arne Lundberg Foundation LU-2020-0010King Gustav V's 80 years' foundationNanna Svartz foundationNovo Nordisk Foundation Center for Basic Metabolic Research 19928Swedish Research Council 2016-01192Swedish Research Council 2019-01035Swedish Research Council 2020-0185The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement ALFGBG-716421The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement ALFGBG-717541The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement ALFGBG-857161The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement ALFGBG-965238
6 · The paper itself

Abstract

objectiveThe high prevalence of osteoporosis in rheumatoid arthritis (RA) is due to inflammation that stimulates differentiation of osteoclasts, a process involving circulating monocytes and T cell-derived factors. The aim of this study was to evaluate relations between circulating monocytes, T cell subsets, and changes in bone characteristics before and after treatment with biological disease-modifying antirheumatic drugs (bDMARDs) in RA.

methodsThirty patients with untreated early RA who met the American College of Rheumatology/EULAR 2010 criteria were included. Data were collected before and 48 weeks after treatment with methotrexate (MTX) together with one of three bDMARDs (abatacept, tocilizumab, or certolizumab pegol). Disease activity was measured using the Clinical Disease Activity Index, swollen or tender joint counts, C-reactive protein levels, and erythrocyte sedimentation rates. Proportions of monocyte and CD4

resultsHR-pQCT revealed an overall decrease in cortical (P = 0.009) and trabecular (P = 0.034) bone mineral density, although a subset of patients showed no bone loss after 48 weeks of treatment. The overall bone loss was not associated with age, body mass index, sex, intraarticular glucocorticoid injections, or baseline disease activity. Loss of trabecular bone volume fraction correlated with high proportions of circulating CXCR3

conclusionMTX together with bDMARDs efficiently reduce disease activity but only prevent bone loss in a subset of patients with RA after 48 weeks of treatment. The correlations of circulating baseline T helper cell and regulatory T cell populations with trabecular bone changes suggest a potential novel role for these cells in systemic bone homeostasis during early RA.

Identifiers

PMID39411912
PMCPMC11667770

What OpenQuestion holds

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Registered trials

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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.