Bone mineral density in rheumatoid arthritis patients 1 year after adalimumab therapy: arrest of bone loss
- 1Division of Clinical Immunology and Rheumatology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
- 2Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
- 3Department of Nuclear Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
- P P Tak, Division of Clinical Immunology and Rheumatology, Academic Medical Centre, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;
- Accepted 31 March 2008
- Published Online First 13 April 2008
Objective: To explore the effects of anti-tumour necrosis factor (TNF)α antibody therapy on bone mineral density (BMD) of the lumbar spine and femur neck in patients with rheumatoid arthritis (RA).
Methods: A total of 50 patients with active RA (DAS28⩾3.2) who started adalimumab (40 mg subcutaneously/2 weeks) were included in an open label prospective study. All patients used stable methotrexate and were allowed to use prednisone (⩽10 mg/day). The BMD of the lumbar spine and femur neck was measured before and 1 year after start of treatment.
Results: Disease activity at baseline (28-joint Disease Activity Score (DAS28)) and disease duration were inversely correlated with femoral neck BMD and lumbar spine BMD (p<0.05). Mean BMD of lumbar spine and femur neck remained unchanged after 1 year of adalimumab therapy (+0.3% and +0.3%, respectively). Of interest, a beneficial effect of prednisone on change in femur neck BMD was observed with a relative increase with prednisone use (+2.5%) compared to no concomitant prednisone use (−0.7%), (p = 0.015).
Conclusion: In contrast to the progressive bone loss observed after conventional disease-modifying antirheumatic drug therapy, TNF blockade may result in an arrest of general bone loss. Consistent with previous observations, the data also suggest that the net effect of low-dose corticosteroids on BMD in RA may be beneficial, possibly resulting from their anti-inflammatory effects.
Competing interests: PPT is a member of the advisory board of Abbott and has received honoraria for lectures. The study sponsors had no involvement in the study design, the collection, analysis and interpretation of the data, writing the report, or the decision to submit the paper for publication.
Funding: DMG was supported by the Dutch Arthritis Association. This study was supported by Abbott Laboratories.
Ethics approval: The protocol was approved by the Medical Ethics Committee of the Academic Medical Centre, University of Amsterdam. All patients gave written informed consent.