Circulating Baseline CXCR3


Journal

ACR open rheumatology
ISSN: 2578-5745
Titre abrégé: ACR Open Rheumatol
Pays: United States
ID NLM: 101740025

Informations de publication

Date de publication:
16 Oct 2024
Historique:
revised: 14 08 2024
received: 09 02 2024
accepted: 19 08 2024
medline: 16 10 2024
pubmed: 16 10 2024
entrez: 16 10 2024
Statut: aheadofprint

Résumé

The 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. Thirty 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 HR-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 MTX 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.

Identifiants

pubmed: 39411912
doi: 10.1002/acr2.11742
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : King Gustav V's 80 years' foundation
Organisme : Swedish Research Council
ID : 2016-01192
Organisme : Swedish Research Council
ID : 2019-01035
Organisme : Swedish Research Council
ID : 2020-0185
Organisme : IngaBritt and Arne Lundberg Foundation
ID : LU-2018-0008
Organisme : IngaBritt and Arne Lundberg Foundation
ID : LU-2020-0010
Organisme : Nanna Svartz foundation
Organisme : Emil and Wera Cornells foundation
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement
ID : ALFGBG-716421
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement
ID : ALFGBG-717541
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement
ID : ALFGBG-857161
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement
ID : ALFGBG-965238
Organisme : Novo Nordisk Foundation Center for Basic Metabolic Research
ID : 19928
Organisme : Association against Rheumatism

Informations de copyright

© 2024 The Author(s). ACR Open Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.

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Auteurs

Julia M Scheffler (JM)

University of Gothenburg, Gothenburg, Sweden.

Christina Drevinge (C)

University of Gothenburg, Gothenburg, Sweden.

Catharina Lindholm (C)

University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.

Inger Gjertsson (I)

University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.

Kristina Lend (K)

Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden, and Amsterdam University Medical Center, Amsterdam, the Netherlands.

Merete Lund Hetland (M)

Rigshospitalet, Glostrup, Denmark, and University of Copenhagen, Copenhagen, Denmark.

Mikkel Østergaard (M)

Rigshospitalet, Glostrup, Denmark, and University of Copenhagen, Copenhagen, Denmark.

Till Uhlig (T)

Diakonhjemmet Hospital, Oslo, Norway.

Marte Schrumpf Heiberg (M)

Diakonhjemmet Hospital, Oslo, Norway.

Espen A Haavardsholm (EA)

Diakonhjemmet Hospital and University of Oslo, Oslo, Norway.

Michael T Nurmohamed (MT)

Amsterdam Rheumatology and Immunology Center, Reade, the Netherlands, and Amsterdam University Medical Center, Amsterdam, the Netherlands.

Jon Lampa (J)

Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Tuulikki Sokka-Isler (T)

University of Eastern Finland, Jyväskylä Central Hospital, Jyväskylä, Finland.

Dan Nordström (D)

Helsinki University and University Hospital, Helsinki, Finland.

Kim Hørslev-Petersen (K)

Danish Hospital for Rheumatic Diseases, University Hospital of Southern Denmark, Sønderborg, Denmark, and University of Southern Denmark, Odense, Denmark.

Bjorn Gudbjornsson (B)

Landspitali National University Hospital of Iceland and University of Iceland, Reykjavik, Iceland.

Gerdur Gröndal (G)

Landspitali National University Hospital of Iceland and University of Iceland, Reykjavik, Iceland.

Ronald van Vollenhoven (R)

Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden, and Amsterdam University Medical Center, Amsterdam, the Netherlands.

Hans Carlsten (H)

University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.

Mattias Lorentzon (M)

University of Gothenburg, Gothenburg, Sweden and Australian Catholic University, Melbourne, Australia.

Anna-Karin Hultgård Ekwall (AK)

University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.

Anna Rudin (A)

University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.

Ulrika Islander (U)

University of Gothenburg, Gothenburg, Sweden.

Classifications MeSH