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Volume 39, Issue 2, Pages 116-122 (October 2009)


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Effect of Tumor Necrosis Factor Alpha Inhibition on Bone Density and Turnover Markers in Patients with Rheumatoid Arthritis and Spondyloarthropathy

Cheryl Barnabe, MD, FRCPCCorresponding Author Informationemail address, David A. Hanley, MD, FRCPC

published online 01 July 2008.

Objectives

Anti-tumor necrosis factor-α (TNFα) therapy has proven efficacious in improving both disease activity and focal bone erosions in patients with rheumatoid arthritis (RA) and spondyloarthopathies. We review the current literature reporting on the effect of anti-TNFα on bone density as measured by dual energy radiograph absorptiometry at the lumbar spine and hip, as well as markers of bone turnover and resorption, in patients using anti-TNFα for rheumatic disease indications.

Methods

A PubMed search, as well as manual search of related articles and references of articles retrieved, was performed to identify all studies pertaining to the effect of anti-TNFα therapy on bone mineral density (BMD) and bone turnover markers.

Results

In RA, 4 studies (238 patients) showed a stabilization or increase of BMD at the spine (up to 2.8%) or hip (up to 13.1%), with only 1 negative study in 48 patients (decline of 3.2% at the spine and 2.7% at the hip). In spondyloarthopathies, 3 studies (75 patients) all demonstrated an increase in BMD at the lumbar spine (3.2-3.6%) and at the hip (1.8-2.2%). Changes in markers of bone formation and bone resorption were heterogeneous but in general represented a modest increase in formation and decline in resorption.

Conclusions

In general, anti-TNFα therapy has a beneficial effect on bone density and bone turnover markers. Retrieved studies were heterogeneous with regards to patients studied, underlying risks for osteoporosis, and supplemental therapy, which may limit the findings of the true effect of anti-TNFα therapy on bone.

 Resident, Division of Rheumatology, Department of Medicine, University of Calgary, Calgary, Alberta, Canada

 Professor, Departments of Medicine, Community Health Sciences, and Oncology, Division of Endocrinology and Metabolism, University of Calgary, Calgary, Alberta, Canada

Corresponding Author InformationAddress reprint requests to Cheryl Barnabe, MD, FRCPC, University of Calgary, Division of Rheumatology, 1301 3350 Hospital Dr NW, Calgary, Alberta, Canada T2N 2T9

 Cheryl Barnabe has no conflicts of interest to disclose.

 David Hanley claims Amgen as support, clinical trials of Denosumab; and serves on the Canadian advisory board.

PII: S0049-0172(08)00084-X

doi:10.1016/j.semarthrit.2008.04.004


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