ABSTRACT
The proliferation of drugs with unique modes of action for treating osteoporosis has been most welcome. Fear of complications, even though rare, associated with long-term bisphosphonates (BPs) changed prescribing patterns. The BPs are stored in bone for years. Drugs not stored in bone; for example, abaloparatide, teriparatide, denosumab, and romosozumab have expanded our armamentarium for treating osteoporosis but have brought new challenges. Bone accrued during treatment with the last 3 drugs, and perhaps abaloparatide, is lost rapidly after their withdrawal due to rebound increase in bone resorption. Treatment with these drugs must be followed by administration of an antiresorptive agent. The article by Kendler et al. (1) in this issue of JCEM reports alendronate preserves bone accrued during administration of denosumab.
Subject(s)
Bone Density Conservation Agents , Osteoporosis , Alendronate , Bone Density , Denosumab , Diphosphonates , Humans , Osteoporosis/drug therapy , TeriparatideSubject(s)
Absorptiometry, Photon , Bone Density , Breast Neoplasms/complications , Osteosclerosis/diagnosis , Bone Neoplasms/diagnosis , Bone Neoplasms/secondary , Breast Neoplasms/pathology , Carcinoma/diagnosis , Carcinoma/secondary , Female , Humans , Middle Aged , Osteosclerosis/etiology , Time FactorsABSTRACT
Excess glucocorticoids, whether endogenous or exogenous, can cause osteoporosis and fractures. Even low doses of oral glucocorticoids and mild endogenous hypercortisolism may be associated with bone loss. Patients treated with glucocorticoids, however, often are not evaluated and treated for this problem. Patients on chronic glucocorticoids or initiating these drugs should have their bone density measured and appropriate laboratory studies. They should be treated with adequate calcium and vitamin D, and antiresorptive therapy (particularly bisphosphonates) should be considered.
