Publication: Pathogenesis of glucocorticoid-induced osteoporosis and options for treatment
Issued Date
2020-01-01
Resource Type
ISSN
17595037
17595029
17595029
Other identifier(s)
2-s2.0-85083768006
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Mahidol University
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SCOPUS
Bibliographic Citation
Nature Reviews Endocrinology. (2020)
Suggested Citation
Pojchong Chotiyarnwong, Eugene V. McCloskey Pathogenesis of glucocorticoid-induced osteoporosis and options for treatment. Nature Reviews Endocrinology. (2020). doi:10.1038/s41574-020-0341-0 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/54490
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Title
Pathogenesis of glucocorticoid-induced osteoporosis and options for treatment
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Abstract
© 2020, Springer Nature Limited. Glucocorticoids are widely used to suppress inflammation or the immune system. High doses and long-term use of glucocorticoids lead to an important and common iatrogenic complication, glucocorticoid-induced osteoporosis, in a substantial proportion of patients. Glucocorticoids mainly increase bone resorption during the initial phase (the first year of treatment) by enhancing the differentiation and maturation of osteoclasts. Glucocorticoids also inhibit osteoblastogenesis and promote apoptosis of osteoblasts and osteocytes, resulting in decreased bone formation during long-term use. Several indirect effects of glucocorticoids on bone metabolism, such as suppression of production of insulin-like growth factor 1 or growth hormone, are involved in the pathogenesis of glucocorticoid-induced osteoporosis. Fracture risk assessment for all patients with long-term use of oral glucocorticoids is required. Non-pharmacological interventions to manage the risk of fracture should be prescribed to all patients, while pharmacological management is reserved for patients who have increased fracture risk. Various treatment options can be used, ranging from bisphosphonates to denosumab, as well as teriparatide. Finally, appropriate monitoring during treatment is also important.