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Vertebral Deformities in Rheumatoid Arthritis
A Comparison With Population-Based Controls
Ragnhild E. Ørstavik, MD;
Glenn Haugeberg, MD;
Petter Mowinckel, MS;
Arne Høiseth, MD, PhD;
Till Uhlig, MD, PhD;
Jan A. Falch, MD, PhD;
Johan I. Halse, MD, PhD;
Eugene McCloskey, MD, PhD;
Tore K. Kvien, MD, PhD
Arch Intern Med. 2004;164:420-425.
Background Previous studies have shown an increased prevalence of osteoporosis in rheumatoid arthritis (RA), but the extent of osteoporotic fractures is not clarified. The aim of this study was to compare the prevalence of vertebral deformities in a representative, population-based cohort of female patients with RA with that in matched controls, and to examine the relationship between deformities and RA, bone mineral density (BMD), and corticosteroid use.
Methods Female patients (mean age, 63.0 years; range, 50.7-73.6 years) were recruited from a county register of patients with RA. Population controls were matched for age, sex, and residential area. Participants had thoracolumbar radiographs taken according to a standardized procedure, and BMD was measured at the hip and spine (L2-L4).
Results The overall number of vertebral deformities was substantially higher in the RA group compared with controls (147 vs 51, applying the morphometric criteria), with a highly significant difference between patients and controls regarding the presence of multiple deformities measured morphometrically (11.2% vs 4.8%; odds ratio, 2.60; 95% confidence interval, 1.21-6.04) and moderate or severe deformities measured semiquantitatively (17.3% vs 10.0%; odds ratio, 2.00; 95% confidence interval, 1.11-3.74). In Poisson regression analysis, vertebral deformities were independently associated with RA, BMD, and long-term corticosteroid use.
Conclusions Vertebral deformities are markedly increased in patients with RA compared with controls, especially regarding severe and multiple deformities. A diagnosis of RA was associated with vertebral deformities independently of BMD and long-term corticosteroid use. These findings have important implications for prevention of established osteoporosis in RA.
From the Oslo City Department of Rheumatology, Oslo, Norway (Drs Ørstavik, Haugeberg, Uhlig, and Kvien and Mr Mowinckel); Centrum Institute of Radiology, Oslo (Dr Høiseth); Department of Internal Medicine, Aker Hospital, Oslo (Dr Falch); Clinic of Osteoporosis, Oslo (Dr Halse); and World Health Organization Collaborating Centre for Metabolic Bone Diseases, Sheffield, England (Dr McCloskey). The authors have no relevant financial interest in this article.
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