Background & Objectives
Glucocorticoid-induced osteoporosis is the most common form of secondary osteoporosis, and 0.5–1% of the overall U.S. population receives prolonged treatment (i.e., three months or longer) with glucocorticoids for various inflammatory rheumatic musculoskeletal diseases (iRMDs). Such patients are at risk of fractures, both because they are exposed to glucocorticoids and because their inflammatory status causes the loss of bone mineral density.
The negative effects of glucocorticoids on bone depend on dose and treatment duration. What remains unclear is whether a safe dose exists, especially for patients with iRMDs. Adami et al. undertook this study to determine the effects of glucocorticoid doses on bone health in iRMD patients.
Methods
The researchers conducted a longitudinal cohort study on women with iRMDs. Bone mineral density and fractures were assessed prospectively and compared to a matched cohort without inflammatory rheumatic musculoskeletal diseases. Kaplan-Meier curves with log rank test were made for rheumatic disease patients (stratified for glucocorticoid use and dose) and the matched cohort. Multivariable Cox regression survival models were also employed to analyze the effect of glucocorticoids on fracture.
Results
A total of 884 women with inflammatory rheumatic musculoskeletal diseases and 1,766 controls (matched for age, T score and 10-year fracture risk) were included in the study and followed for up to six years. In brief, rheumatoid arthritis represented the most common disease (53.8%). No patients were receiving anti-osteoporosis medications at baseline. The vast majority of patients did not receive anti-osteoporosis treatment during the follow-up.
Bone mineral density decreased significantly in all patients receiving glucocorticoids who were not receiving anti-osteoporosis treatment. Anti-osteoporosis treatment, largely bisphosphonates, prevented bone loss only in patients receiving less than 5 mg/day of a prednisone equivalent. Fracture incidence was higher in patients with iRMDs compared with controls, but only glucocorticoid doses less than or equal to 5 mg/day were associated with a significantly higher risk of fracture.
Conclusion
Glucocorticoid doses as low as 2.5 mg/day were associated with bone mineral density loss in patients with iRMDs, but this effect was preventable. Bone mineral density loss in patients receiving less than or equal to 5 mg/day was not totally prevented by anti-osteoporosis medications currently used in clinical practice, resulting in a higher risk of fracture.
This study suggests that it may be beneficial to start anti-osteoporosis medications in patients with iRMD who are taking even very low doses of glucocorticoids.
For complete details, including source material, refer to the full study.
