Factors associated with changes in volumetric bone mineral density and cortical area in men with ankylosing spondylitis: a 5-year prospective study using HRpQCT.

Bone mineral density DXA high-resolution peripheral quantitative computed tomography other diseases related to bone (ankylosing spondylitis) radiology

Journal

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA
ISSN: 1433-2965
Titre abrégé: Osteoporos Int
Pays: England
ID NLM: 9100105

Informations de publication

Date de publication:
Jan 2022
Historique:
received: 19 10 2020
accepted: 24 06 2021
pubmed: 16 7 2021
medline: 18 1 2022
entrez: 15 7 2021
Statut: ppublish

Résumé

Patients with ankylosing spondylitis (AS) have impaired volumetric bone mineral density (vBMD) assessed with high-resolution peripheral computed tomography (HRpQCT). This first longitudinal HRpQCT study in AS shows that cortical and trabecular vBMD decreased at tibia and that signs of inflammation were associated with cortical bone loss at tibia and radius. Patients with ankylosing spondylitis (AS) have reduced volumetric bone mineral density (vBMD) in the peripheral skeleton assessed with high-resolution peripheral quantitative computed tomography (HRpQCT). The aims were to investigate longitudinal changes in vBMD, cortical area, and microarchitecture and to assess factors associated with changes in vBMD and cortical area in men with AS. HRpQCT of radius and tibia was performed in 54 men with AS at baseline and after 5 years. Univariate and multivariable linear regression analyses were used. At tibia, there were significant decreases exceeding least significant changes (LSC) in cortical and trabecular vBMD, mean (SD) percent change -1.0 (1.9) and -2.7 (5.0) respectively (p<0.001). In multivariable regression analyses, increase in disease activity measured by ASDAS_CRP from baseline to follow-up was associated with decreases in cortical vBMD (β -0.86, 95% CI -1.31 to -0.41) and cortical area (β -1.66, 95% CI -3.21 to -0.10) at tibia. At radius, no changes exceeded LSC. Nonetheless, increase in ASDAS_CRP was associated with decreases in cortical vBMD, and high time-averaged ESR was associated with decreases in cortical area. Treatment with TNF inhibitor ≥ 4 years during follow-up was associated with increases in cortical vBMD and cortical area at tibia, whereas exposure to bisphosphonates was associated with increases in cortical measurements at radius. No disease-related variables or treatments were associated with changes in trabecular vBMD. The findings in this first longitudinal HRpQCT study in patients with AS strengthen the importance of controlling disease activity to maintain bone density in the peripheral skeleton.

Identifiants

pubmed: 34263348
doi: 10.1007/s00198-021-06049-4
pii: 10.1007/s00198-021-06049-4
pmc: PMC8758642
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

205-216

Subventions

Organisme : Västra Götalandsregionen
ID : VGFOUREG-383071
Organisme : Västra Götalandsregionen
ID : VGFOUREG-564511, VGFOUREG-754661
Organisme : Vetenskapsrådet
ID : 2016-02035
Organisme : Vetenskapsrådet
ID : 2017-02229
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF agreement
ID : ALFGBG-141111, ALFGBG-430851, , ALFVLL-640251
Organisme : The Swedish state under the agreement between the Swedish government and the county councils, the ALF agreement
ID : ALFGBG-716051
Organisme : Göteborgs Läkaresällskap
ID : GLS-880811, GLS-498111, GLS-406801

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2021. The Author(s).

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Auteurs

A Deminger (A)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. anna.deminger@vgregion.se.
Department of Rheumatology, Region Västra Götaland, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden. anna.deminger@vgregion.se.

E Klingberg (E)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden.
Department of Rheumatology, Region Västra Götaland, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.

M Lorentzon (M)

Geriatric Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Geriatric Medicine Clinic, Region Västra Götaland, Sahlgrenska University Hospital, Gothenburg, Sweden.
Mary McKillop Institute for Health Research, Australian Catholic University, Melbourne, Australia.

M Hedberg (M)

Section of Rheumatology, Region Västra Götaland, Södra Älvsborg Hospital, Borås, Sweden.

H Carlsten (H)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden.
Department of Rheumatology, Region Västra Götaland, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.

L T H Jacobsson (LTH)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden.

H Forsblad-d'Elia (H)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden.
Department of Rheumatology, Region Västra Götaland, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.
Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, Umeå, Sweden.

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