Bone loss occurs in Inflammatory Rheumatic Musculoskeletal Diseases (iRMD) patients treated with low dose glucocorticoids, but is prevented by anti-osteoporosis medications.

Abstract

The negative effects of glucocorticoids (GCs) on the bone depend on dose and treatment duration. However, it is unclear whether a safe dose exists, especially for patients with inflammatory rheumatic musculoskeletal diseases (iRMDs). We conducted a longitudinal cohort study on women with iRMD. Bone mineral density and fractures were assessed prospectively and compared to a matched cohort. Kaplan-Meier curves with log-rank test were made for iRMD (stratified for glucocorticoid use and dosage) and matched cohort respectively. Multivariable Cox regression survival models were also employed to analyze the effect of GCs on fracture. 884 women with iRMD and 1,766 controls (age, T-score, and 10-year fracture risk matched) were included in the study and followed for up to 6 years. BMD levels decreased significantly in all GCs users not receiving anti-osteoporosis treatment (-4.26% p 0.0011, -4.23% p 0.0422, -2.66% p 0.0006 for ≥5 mg/day, 2.5 mg to 5 mg and 0 to 2.5 mg/day of prednisolone, respectively). Anti-osteoporotic treatment (largely bisphosphonates) prevented bone loss only in patients receiving less than 5 mg/day of prednisone. Fracture incidence was greater in patients with iRMD compared to controls but only GC doses above 5 mg/day were associated with significantly higher risk of fracture. GC doses as low as 2.5 mg/day were associated with BMD loss in iRMD but this effect was preventable. BMD loss in patients taking ≥5 mg/day was not totally prevented by anti-osteoporotic medications currently used in clinical practice, resulting in higher risk of fracture. This article is protected by copyright. All rights reserved.