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Low-Dose Prednisone Induces Rapid Reversible Axial Bone Loss in Patients with Rheumatoid Arthritis: A Randomized, Controlled Study

Roland F. J. M. Laan, MD; Piet L. C. M. van Riel, MD; Levinus B. A. van de Putte, MD; Leon J. Th. O. van Erning, PhD; Martin A. van't Hof, PhD; and J. Albert M. Lemmens, MD
[+] Article and Author Information

From the University Hospital Nijmegen, the Netherlands. Requests for Reprints: Roland F.J.M. Laan, MD, Department of Rheumatology, University Hospital Nijmegen, PO Box 9101, 6500 HB Nijmegen, the Netherlands. Grant Support: By the Program for the Stimulation of Health Research, and by the Dutch League against Rheumatism.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;119(10):963-968. doi:10.7326/0003-4819-119-10-199311150-00001
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Objective: To determine the effects of a short course of a low dose of a glucocorticoid agent on bone mass.

Design: Double-blind, placebo-controlled, randomized study.

Setting: Outpatient clinic of a university hospital.

Patients: Forty patients with active rheumatoid arthritis.

Intervention: All patients started receiving intramuscular gold salts. In addition, they were randomly allocated to receive either prednisone or placebo. The initial dose was 10 mg/d, which was tapered between weeks 12 and 20. Thereafter, patients were followed for an additional 24 weeks.

Measurements: Lumbar bone mineral density was measured with dual-energy, quantitative computed tomography in a trabecular and a cortical region of interest.

Results: Despite favorable effects on disease activity and functional capacity, trabecular bone mineral density decreased in the prednisone-treated patients between baseline and week 20 (mean change, 8.2%; 95% CI, 12.7% to 3.7%; P = 0.001). Little change was found in the placebo-treated patients (P > 0.2), and the prednisone group had a greater mean bone loss than the placebo group (9.5%; CI, 3.4% to 15.6%; P = 0.003). After discontinuation of prednisone, an increase was found in trabecular bone mineral density between weeks 20 and 44 (mean change, 5.3%; CI, 0.7% to 9.9%; P = 0.03). Little change was found after withdrawal of placebo (P > 0.2). The mean improvement in the prednisone group was 6.8% (CI, 0.8% to 12.8%; P = 0.03) greater than for placebo. In both treatment groups, cortical bone mineral density did not change markedly in either period (P 0.2).

Conclusions: Low doses of glucocorticoid agents cause marked vertebral trabecular bone loss in the initial months of therapy in patients with active rheumatoid arthritis. After discontinuation of treatment, this bone loss seems to be (partially) reversible.

Figures

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Figure 1.
Mean changes in lumbar, trabecular bone mineral density during and after low-dose prednisone treatment in a subset of patients who did not use prednisone between weeks 20 and 44.

The change (mean SE) in bone mineral density was measured using dual-energy, quantitative computed tomography. The prednisone dose was 10 mg/d from week 0 to 12 and was tapered between weeks 12 and 20.

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Figure 2.
Changes in lumbar, trabecular bone mineral density in individual patients receiving low-dose prednisone or placebo between weeks 0 and 20.

Patients who used prednisone in the second part of the study (between weeks 20 and 44) are indicated with a dashed line. squares = men; circles = premenopausal women; diamonds = postmenopausal women.

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