Abstract

BackgroundPatients with rheumatoid arthritis (RA) who have muscle weakness and stiff or painful joints might be at increased risk of falls and fractures.ObjectivesThe present study prospectively investigates correlations between decreasing doses of glucocorticoid (GC) and the incidence of clinical fractures in patients with RA based on the ten-year findings of the TOMORROW study (UMIN000003876) that started in 2010.MethodsWe evaluated anthropometric parameters, bone mineral density, disease activity, RA medication, and the incidence of clinical fractures over a period of ten years in 202 patients with RA (mean age, 58.6 years; mean disease duration, 14.0 years). We also investigated the effects of GC doses on the incidence of clinical fractures over the same period in patients with RA using multivariate regression analysis.ResultsThe incidence of clinical fractures for ten years in patients with RA was 0.036/person-year. There were 89 patients (44.1%) treated with GC at least once during ten years. The incidences of clinical fractures in patients with RA treated with and without GC during ten years were 0.052 and 0.026/person-year, respectively. After adjusting for fracture risk factors including age, sex, smoking, and body mass index, cox proportional hazard model revealed that GC dose of ≥ 2 mg/day at baseline was a significant risk factor for clinical fractures (Hazard ratio [HR]:2.430; 95%CI, 1.040-5.675, p=0.040). Although the risk for clinical fractures did not decrease by just reducing the dose of GC (HR:4.505; 95%CI, 0.589-34.457, p=0.147), it was significantly lower if the dose of GC could be reduced to zero during ten years (HR:0.407; 95%CI, 0.194-0.857, p=0.018).ConclusionMedication with even low dose of GC are apparently significantly associated with an increased frequency of clinical fractures among patients with RA. However, if the dose of GC was reduced to free during ten years, the clinical fracture risk could become lower. We concluded that we should decrease the dose of GC to free after controlling disease activity of RA.Disclosure of InterestsNone declared

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