FRI0289 Comparison of A Tumor Necrosis Factor Inhibitor, an Interleukin-6 Inhibitor, and Conventional Disease-Modifying Anti-Rheumatic Drugs on Bone Quality in Patients with Rheumatoid Arthritis
Authors: Y. Yonemoto, K. Okamura, T. Kaneko, T. Kobayashi, C. Okura, K. Takagishi
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Recently, attention has been focused on bone quality, independent of bone mineral density (BMD), as a risk factor for fractures. Serum and urine pentosidine and serum homocysteine are typical bone-quality markers, and previous findings indicate that these markers are elevated in patients with rheumatoid arthritis (RA). Recent findings also indicate that the use of biologic agents and methotrexate (MTX) could decrease serum and urine pentosidine levels; however, it is unclear which type of biologic agent would have the greatest effect on improving bone-quality markers. <h3>Objectives</h3> This study compared the effects of both a TNF and an IL-6 inhibitor and conventional disease-modifying anti-rheumatic drugs (DMARDs) on bone quality markers in patients with RA. <h3>Methods</h3> A total of 73 RA patients (10 male, 63 female; median age, 66 years) without renal dysfunction or diabetes were included in this study. Twenty-three patients received TNF-inhibitor, 13 received IL-6 inhibitor, and 37 received conventional DMARDs. Serum pentosidine, serum homocysteine, intact procollagen type I N-terminal propeptide (intact P1NP), tartrate-resistant acid phosphatase type 5b (TRACP-5b), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and matrix metalloproteinase-3 (MMP-3) levels, the disease activity score (DAS)28-ESR, DAS28-CRP, clinical disease activity index (CDAI), and simplified disease activity index (SDAI) scores, and the BMD (lumbar spine and femoral neck) were assessed. We compared these parameters between patients with the TNF-inhibitor (T group), the IL-6 inhibitor (I group), or conventional DMARDs (C group). <h3>Results</h3> No significant differences were observed between groups in serum homocysteine, intact P1NP, TRACP-5b levels, or BMD; however, CRP, ESR, and MMP-3 levels, as well as the DAS28-ESR, DAS28-CRP, CDAI and SDAI scores, were significantly lower in the T and I groups than in the C group. Notably, serum pentosidine levels were significantly lower in the I group than in the T and C groups. <h3>Conclusions</h3> In this study, the levels of serum pentosidine were significantly lower in the I group. These results suggest that biologics, especially in the form of an IL-6 inhibitor, can improve not only disease activity, but also bone quality, in patients with RA. <h3>References</h3> Saito M, et al., Reductions in degree of mineralization and enzymatic collagen cross-links and increases in glycation induced pentosidine in the femoral neck cortex in cases of femoral neck fracture. Osteoporos Int. 2006;17:986-95. Senolt L, et al., Advanced glycation end-product pentosidine is not a relevant marker of disease activity in patients with rheumatoid arthritis. Physiol Res. 2007;56:771-7. Takahashi M, et al., Relationship between pentosidine levels in serum and urine and activity in rheumatoid arthritis. Br J Rheumatol. 1997;36:637-42. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4780