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Articles

Treatment with low-dose prednisolone is associated with altered body composition but no difference in bone mineral density in rheumatoid arthritis patients: a controlled cross-sectional study

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Pages 161-168 | Accepted 08 Sep 2010, Published online: 16 Nov 2010
 

Abstract

Objectives: To determine whether low-dose prednisolone affects body composition and bone mineral density (BMD) in patients with rheumatoid arthritis (RA), also considering inflammation and physical disability.

Methods: This cross-sectional study included 100 patients (50 women) with RA with a median (IQR) disease duration of 8 (4–15) years. Fifty patients had been treated with prednisolone (5–7.5 mg) for at least 2 years (the P-group) and 50 patients matched for gender and age had not (the NoP-group). Body composition and BMD were assessed by dual‐energy X-ray absorptiometry (DXA). Disease activity (28-joint Disease Activity Score, DAS28) and physical disability (Health Assessment Questionnaire, HAQ) were assessed.

Results: The total patient group had increased fat mass (FM) and a high trunk:peripheral fat ratio, of which 38% had a fat free mass index (FFMI, kg/m2) below the 10th percentile of a reference population. The P-group had significantly higher FM but similar lean body mass (LBM) and BMD compared with the NoP-group. In multivariate analyses, treatment with prednisolone and a higher HAQ score were significantly and independently associated with higher FM but not with LBM. Higher C-reactive protein (CRP) was independently associated with lower LBM. Higher HAQ score and low weight were significantly and independently associated with lower BMD at femoral neck and lumbar spine.

Conclusions: RA patients treated with low-dose prednisolone had significantly higher FM than patients without prednisolone, an effect that was independent of current inflammation. However, there was no association between prednisolone treatment and muscle mass or BMD. Thus, the net effect of prednisolone on body composition and bone is different in inflammatory diseases such as RA.

Acknowledgements

This work was supported by grants from the Swedish Rheumatism Association, King Gustav V's 80-year Foundation, the Family Erling-Persson Foundation, and the Swedish Research Council and through the regional agreement on medical training and clinical research (ALF) between Stockholm County Council and the Karolinska Institutet. We thank research nurse M. Wörnert for excellent assistance and E. Sandberg and I.-L. Wivall for excellent laboratory work.

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