This study evaluates the clinical efficacy of denosumab for glucocorticoid-induced osteoporosis (GIOP) refractory to previous osteoporosis treatment. Our results show that denosumab significantly increased BMD of the lumbar spine and bilateral hip over the 24-month study period. Denosumab demonstrates potential as a treatment for GIOP refractory to previous therapy.
Introduction: The aim of this study was to evaluate the clinical efficacy and safety of denosumab in patients with rheumatic diseases and glucocorticoid-induced osteoporosis (GIOP) refractory to previous osteoporosis treatment.
Methods: All patients were treated with 60 mg of denosumab subcutaneously every 6 months for 2 years after administration of bisphosphonates or rhPTH was stopped. We assessed bone mineral density (BMD) of the lumbar spine and bilateral hip at baseline, and at 6, 12, 18, and 24 months. We measured serum levels of bone alkaline acid phosphatase (BAP) and tartrate-resistant acid phosphatase (TRACP)-5b at baseline, and at 3, 6, 12, 18, and 24 months.
Results: Fifty-five patients with rheumatic diseases and GIOP were enrolled in this study. All patients were treated with bisphosphonates (n=40), recombinant human parathyroid hormone (n=4), or active vitamin D3 (n=11). Over the 24-month study period, denosumab significantly increased the mean BMD of the lumbar spine and bilateral hip (5.8 ± 0.7%, and 1.3 ± 0.4%, respectively). Additionally, denosumab also significantly reduced the serum levels of TRACP-5b and BAP over this same period (by -38.8 ± 3.5% and -16.3 ± 3.1%, respectively), although these changes in bone turnover markers were not predictive factors of an improvement in BMD values. While three patients developed fragility fractures during the study period, all three had several risk factors for fragility fractures in GIOP.
Conclusions: In conclusion, denosumab is a potential treatment for GIOP in rheumatic diseases, especially in patients refractory to previous therapy, including bisphosphonate therapy.
Keywords: Antiresorptives; Biochemical markers of bone turnover; Corticosteroids; DXA; Osteoporosis.