Biological Heterogeneity in Susceptibility to Glucocorticoid-Induced Bone Loss: Short- and Long-Term Hip BMD Trajectories.

Context: Glucocorticoids (GCs) are widely used for their anti-inflammatory and immunosuppressive properties. Their effect on bone health is predominantly negative by decreasing bone formation and increasing risk of fractures.
Objective: This work aimed to quantify the short- and long-term changes in total hip bone mineral density (THBMD) after initiating systemic GC treatment in previously GC treatment-naive adults without bone protective agents.
Methods: An observational study was conducted using THBMD data from dual-energy x-ray absorptiometry (DXA). Individuals were stratified by sex and tertiles of GC exposure. Individuals not GC-exposed served as a reference group. Routine-care DXA scans were obtained from the main public hospitals servicing the Island of Funen in Denmark. A total of 15 099 adults underwent routine DXA at Odense University Hospital between 2006 and 2021. Data were enriched with Danish national registers. Intervention included systemic GCs (observational data). The short-term outcome included annualized THBMD changes between first 2 DXA scans. The long-term outcome included greater than 5% annualized THBMD loss over a 10-year follow-up.
Results: Strong associations between GC exposure and THBMD loss was found for both outcomes, with larger losses in the middle and upper tertiles of GC exposure. The risk of experiencing greater than 5% annualized THBMD loss was elevated, especially in the first 2 years of initiating GC treatment. There is significant heterogeneity in THBMD responses, with approximately 1 in 5 patients experiencing no nominal bone loss despite receiving upper tertile levels of GC exposure.
Conclusion: The findings confirm the association between initial GC exposure and significant bone loss. The heterogeneity in individual responses emphasizes the need for early monitoring and personalized approaches in managing bone health for patients undergoing GC treatment.
(© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.)