AT A GLANCE

A new study published in The Journal of Clinical Endocrinology & Metabolism suggests romosozumab could be used to manage glucocorticoid-induced osteoporosis (GIOP).

“[The] Wnt/β-catenin signaling pathway is one of the pathogenic mechanisms of GIOP. We previously reported the potential of inhibiting sclerostin as a treatment for GIOP,” explain study authors Kawazoe et al., who subsequently designed a new study to compare the efficacy of romosozumab (ROMO), a monoclonal antibody against sclerostin, with existing therapies for GIOP.

For study purposes, patients with rheumatic diseases who had not previously received treatment for osteoporosis and who were newly being treated with prednisolone ≥15 mg/day were randomly assigned to receive ROMO (n = 11), denosumab (DMAb) (n = 14), or bisphosphonates (BPs) (n = 14). Subsequently, the authors assessed the bone mineral density (BMD) of the lumbar spine, femoral neck, and total hip every 6 months and bone turnover markers every 3 months for 12 months.

According to the authors, patients who received ROMO showed the greatest median percent change in lumbar spine BMD from baseline at 12 months (8.6% vs. 3.3% [DMAb] vs. −0.4% [BPs]). Among bone-formation markers, the authors add, serum levels of bone alkaline phosphatase were slightly elevated in the ROMO group. Further, although serum levels of N-terminal propeptide of type I procollagen and osteocalcin were decreased in all three groups, these changes were smaller in the ROMO group. Finally, serum levels of bone-resorption markers and a urine bone-quality marker were decreased in all groups.

“Treatment with ROMO significantly increased lumbar spine BMD in glucocorticoid-treated patients, suggesting that ROMO is effective for GIOP,” conclude the authors.

Reference

1.     Kawazoe M, Kaneko K, Masuoka S, et al. Comparison of efficacy of romosozumab with denosumab and risedronate in patients newly initiating glucocorticoid therapy. J Clin Endocrinol Metab. 2025;110(8):e2778–e2786.