THU0469 Quantifying the treatment with glucocorticoids as a risk factor for the occurrence of osteoporosis and fractures in patients with ra
Authors: E. Wiebe, R. Biesen, K.N. Zeiner, D.C. Freier, S. Hermann, G.-R. Burmester, F. Buttgereit
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Rheumatoid arthritis (RA) is associated with increased systemic bone loss, leading to a high risk for fragility fractures. The etiology of increased fracture risk in RA is multifactorial and comprises next to general risk factors also RA-specific risks, most prominently chronic inflammation, seropositivity and glucocorticoid (GC) use<sup>1</sup>. Yet, there is evidence that GCs may, by adequately suppressing systemic inflammation, also have a positive effect on BMD and fracture risk in RA<sup>2</sup>. <h3>Objectives</h3> The purpose of this study was to investigate the prevalence of osteoporosis and fragility fractures in RA patients and to characterise, among other risk factors, the role of GC dose, cumulative dose (GCCD) and duration as well DMARD treatment on bone health. <h3>Methods</h3> Rh-GIOP is an ongoing prospective observational study collecting and analysing disease- and bone-related data from patients with chronic rheumatic diseases treated with GCs. In this cross-sectional analysis, we evaluated the initial visit of 238 patients with RA. Descriptive analyses were performed, with values displayed as mean/standard deviation and median/range for continuous variables. For subgroup analyses, non-parametric tests were used. <h3>Results</h3> Of 238 patients with RA (79.4% women, mean age: 63.6±12.5 years), 155 were seropositive and 83 seronegative. Seronegative patients were numerically older (66.8±12.1 vs 61.8±12.1 years) and more often in menopause (78.3% vs 61.8%, ns) than seropositive, while the latter had longer disease duration (median: 4.0 vs 11.0 years, p=0.03). Overall, osteoporotic BMD was more frequent at femoral sites, with 21% of patients having T-Scores&lt;−2.5. Osteoporotic BMD was more common in seronegative patients (ns), although no difference in the frequency of fragility fractures (n=18;24.1% vs n=28;23.2%) was found. All patients received GCs (mean dose: 5.0±6.8 mg, mean GCCD 15.1±19.3 g, mean duration 7.7±8.2 years) with seropositive patients having numerically higher GCCD, longer duration of GC therapy and more often current GC doses above &gt;10 g/day. Biological DMARDs were more frequently used in seropositive patients (n=20;24.1% vs n=67;43.2%, p=0.02). Anti-osteoporotic therapies between both groups did not differ. Neither current GC doses nor GCCD nor DMARD therapy had a statistically significant and independent effect on BMD or fragility fractures in either RA group. <h3>Conclusions</h3> Osteoporosis and fragility fractures remain a challenge in the management of RA, being determined by multiple interacting factors. Our data confirm that GCs may not <i>per se</i> increase fracture risk and decrease BMD in RA but rather, that optimal management of disease activity with or without GCs may be beneficial to bone health. Interestingly however, despite higher cumulative GC doses and duration, seropositive RA patients did not have lower BMD or higher prevalence of fragility fractures compared to seronegative patients. Further prospective data is warranted to better characterise the role of GCs and DMARDs in regard to osteoporosis and fracture risk in RA patients. <h3>References</h3> [1] Briot K, et al. "Inflammatory Diseases and Bone Fragility."Osteoporosis International2017December 1;28(12):3301–14. [2] Güler-Yüksel, et al. "Glucocorticoids, Inflammation and Bone."Calcified Tissue International2018January 8. <h3>Disclosure of Interest</h3> E. Wiebe Grant/research support from: Rh-GIOP is supported by a joint funding of Amgen, BMS, Celgene, Generic Assays, GSK, Horizon, medac, Mundipharma, Pfizer and Roche., R. Biesen Grant/research support from: Rh-GIOP is supported by a joint funding of Amgen, BMS, Celgene, Generic Assays, GSK, Horizon, medac, Mundipharma, Pfizer and Roche., K. Zeiner Grant/research support from: Rh-GIOP is supported by a joint funding of Amgen, BMS, Celgene, Generic Assays, GSK, Horizon, medac, Mundipharma, Pfizer and Roche., D. Freier Grant/research support from: Rh-GIOP is supported by a joint funding of Amgen, BMS, Celgene, Generic Assays, GSK, Horizon, medac, Mundipharma, Pfizer and Roche., S. Hermann: None declared, G.-R. Burmester: None declared, F. Buttgereit Grant/research support from: Rh-GIOP is supported by a joint funding of Amgen, BMS, Celgene, Generic Assays, GSK, Horizon, medac, Mundipharma, Pfizer and Roche.