Endocrine Abstracts

Systemic glucocorticoid (GC) treatment has profound direct and indirect effects on the skeleton (1). At tissue level, GCs exhibit biphasic effects on osteoblast maturation, function, and lifespan. Osteoclast activity and survival is promoted through sclerostin and RANKL. Renal and gut calcium handling is adversely affected as is the sex hormone and GH axes. Secondary hyperparathyroidism contributes to the net loss of bone mass and degradation of architecture. Use is prevalent in the older age groups. In 2023, 9% of the Danish population aged 80 or older filled a prescription for sGCs compared with 3% for age 25-44 and 0.2% of those under 18. There is a general understanding that GCs shift the fracture threshold towards fractures occurring with minor BMD reduction. New data will be discussed. It is difficult to obtain unbiased data on BMD trajectories during sGC exposure because of entanglement of DXA referral and treatment intent, i.e. DXA monitoring also reflects a plan to intervene beyond a certain BMD threshold. BMD trajectories show considerable variation among GC users both in the short and the longer term with some patients experiencing little or no bone loss even with high doses (2). Fracture risk is particularly elevated with exposure to high GC doses, less so with intermittent dosing or lower daily doses. The impact of inhaled GCs is controversial; higher dosing flags a patient subgroup with more pronounced pulmonary disease, which in itself marks higher risk of fractures. There is a certain lack of data in younger adults and of evidence based guidelines in this age group. Clinical management guidelines across countries and societies show marked discrepancy in intervention thresholds and paths but good agreement in terms of choice of medications despite limited fracture data.Reference1. Herath M, Clin Endocrinology 2022; 96: 460-74. 2. Hansen BB, JCEM 2024 (online)