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Significant loss of bone mass in patients with early, active ankylosing spondylitis: A followup study
Author(s) -
Gratacós J.,
Collado A.,
Pons F.,
Osaba M.,
Sanmartí R.,
Roqué M.,
Larrosa M.,
MúñozGómez J.
Publication year - 1999
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199911)42:11<2319::aid-anr9>3.0.co;2-g
Subject(s) - medicine , ankylosing spondylitis , femoral neck , erythrocyte sedimentation rate , spondylitis , surgery , gastroenterology , urology , osteoporosis
Objective To analyze whether inflammatory disease activity plays a substantial role in the loss of bone mass observed in ankylosing spondylitis (AS) patients who have not yet developed ankylosis. Methods A longitudinal cohort study of 34 patients with early AS (duration <10 years) without ankylosis was conducted. The mean followup was 19 months. Loss of bone mass in defined regions of the lumbar spine and femoral neck was analyzed by dual x‐ray absorptiometry. Patients were grouped according to biologic parameters of disease activity (erythrocyte sedimentation rate or C‐reactive protein level). Group 1 consisted of 14 patients with active disease; group 2 comprised 20 patients with inactive disease. Serum levels of interleukin‐6 (IL‐6) and of hormones (sex, thyroid, and calciotropic), vertebral mobility (Schober test), daily physical activity, and treatment administered were recorded every 6 months for all patients. Results At the end of the followup period, patients with active AS showed a significant reduction in bone mass in the lumbar spine (mean 1.01 gm/cm 2 at study entry versus 0.961 gm/cm 2 at followup [ P = 0.005]) and femoral neck (0.849 gm/cm 2 versus 0.821 gm/cm 2 [ P = 0.015]), which represented losses of 5% and 3%, respectively. In contrast, no significant reduction in bone mass was observed in patients with inactive AS. As expected, serum IL‐6 levels were significantly higher in patients with active AS than in those with inactive disease (mean ± SD 8.3 ± 9 pg/ml versus 2.8 ± 5 pg/ml [ P = 0.008]). No significant differences were observed between the 2 groups in any of the other variables analyzed. Conclusion The observation that loss of bone mass in AS occurred only in patients with persistent active disease strongly suggests that inflammatory activity of the disease itself plays a major role in the pathophysiology of the early bone mineral disorders observed in these patients.

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