The risk of fracture and prevalence of osteoporosis is elevated in patients with idiopathic inflammatory myopathies: cross-sectional study from a single Hungarian center.


Journal

BMC musculoskeletal disorders
ISSN: 1471-2474
Titre abrégé: BMC Musculoskelet Disord
Pays: England
ID NLM: 100968565

Informations de publication

Date de publication:
02 Jul 2020
Historique:
received: 01 11 2019
accepted: 23 06 2020
entrez: 4 7 2020
pubmed: 4 7 2020
medline: 2 4 2021
Statut: epublish

Résumé

The prevalence of osteoporosis and risk of fractures is elevated in rheumatoid arthritis (RA), but we have limited information about the bone mineral density (BMD) and fracture risk in patients with inflammatory myopathies. We intended to ascertain and compare fracture risk, bone mineral density and the prevalence of vertebral fractures in patients with inflammatory myositis and rheumatoid arthritis and to assess the effect of prevalent fractures on the quality of life and functional capacity. Fifty-two patients with myositis and 43 patients with rheumatoid arthritis were included in the study. Fracture Risk was determined using FRAX® Calculation Tool developed by the University of Sheffield. Dual energy X-ray absorptiometry and bidirectional thoracolumbar radiographs were performed to assess BMD and vertebral fractures. Quality of life was measured with Short Form-36 (SF-36) and physical function assessment was performed using Health Assessment Questionnaire (HAQ). We found a significantly elevated fracture risk in RA as compared to myositis patients if the risk assessment was performed without the inclusion of the BMD results. If BMD results and glucocorticoid dose adjustment were taken into account, the differences in fracture risk were no longer significant. The prevalence of osteoporosis was found to be significantly higher in the myositis group (7% vs. 13.5%, p: 0.045), but the fracture prevalence was similar in the two groups (75% vs. 68%). The fracture rates were independently associated with age in the myositis group, and with lower BMD results in the RA patients. The number of prevalent fractures was significantly correlated to poorer physical function in both groups, and poorer health status in the myositis group, but not in the RA group. Our findings suggest that inflammatory myopathies carry significantly elevated risks for osteoporosis and fractures. These higher risks are comparable to ones detected with RA in studies and strongly affect the physical function and quality of life of patients. Therefore further efforts are required to make the fracture risk assessment reliable and to facilitate the use of early preventive treatments.

Sections du résumé

BACKGROUND BACKGROUND
The prevalence of osteoporosis and risk of fractures is elevated in rheumatoid arthritis (RA), but we have limited information about the bone mineral density (BMD) and fracture risk in patients with inflammatory myopathies. We intended to ascertain and compare fracture risk, bone mineral density and the prevalence of vertebral fractures in patients with inflammatory myositis and rheumatoid arthritis and to assess the effect of prevalent fractures on the quality of life and functional capacity.
METHODS METHODS
Fifty-two patients with myositis and 43 patients with rheumatoid arthritis were included in the study. Fracture Risk was determined using FRAX® Calculation Tool developed by the University of Sheffield. Dual energy X-ray absorptiometry and bidirectional thoracolumbar radiographs were performed to assess BMD and vertebral fractures. Quality of life was measured with Short Form-36 (SF-36) and physical function assessment was performed using Health Assessment Questionnaire (HAQ).
RESULTS RESULTS
We found a significantly elevated fracture risk in RA as compared to myositis patients if the risk assessment was performed without the inclusion of the BMD results. If BMD results and glucocorticoid dose adjustment were taken into account, the differences in fracture risk were no longer significant. The prevalence of osteoporosis was found to be significantly higher in the myositis group (7% vs. 13.5%, p: 0.045), but the fracture prevalence was similar in the two groups (75% vs. 68%). The fracture rates were independently associated with age in the myositis group, and with lower BMD results in the RA patients. The number of prevalent fractures was significantly correlated to poorer physical function in both groups, and poorer health status in the myositis group, but not in the RA group.
CONCLUSIONS CONCLUSIONS
Our findings suggest that inflammatory myopathies carry significantly elevated risks for osteoporosis and fractures. These higher risks are comparable to ones detected with RA in studies and strongly affect the physical function and quality of life of patients. Therefore further efforts are required to make the fracture risk assessment reliable and to facilitate the use of early preventive treatments.

Identifiants

pubmed: 32616032
doi: 10.1186/s12891-020-03448-2
pii: 10.1186/s12891-020-03448-2
pmc: PMC7333418
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

426

Subventions

Organisme : Emberi Eroforrások Minisztériuma
ID : ÚNKP-17-2

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Auteurs

Anett Vincze (A)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.

Levente Bodoki (L)

Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.
Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Katalin Szabó (K)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.

Melinda Nagy-Vincze (M)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.

Orsolya Szalmás (O)

Department of Medical Imaging, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

József Varga (J)

Department of Medical Imaging, Division of Nuclear Medicine, University of Debrecen, Debrecen, Hungary.

Katalin Dankó (K)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.

János Gaál (J)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary.
Department of Medicine, Kenézy Gyula University Hospital, University of Debrecen, Debrecen, Hungary.

Zoltán Griger (Z)

Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Móricz Zsigmond út 22, Debrecen, H-4032, Hungary. grigerz@gmail.com.
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, University of Debrecen, Debrecen, Hungary. grigerz@gmail.com.

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