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      Glucocorticoid-induced osteoporosis: an update.

      Trends in Endocrinology and Metabolism
      Bone Density, Bone Resorption, Bone and Bones, drug effects, Calcium, administration & dosage, Cushing Syndrome, complications, Diphosphonates, therapeutic use, Female, Fractures, Bone, epidemiology, Glucocorticoids, adverse effects, Humans, Osteoblasts, Osteoclasts, Osteocytes, Osteogenesis, Osteoporosis, chemically induced, drug therapy, Osteoporosis, Postmenopausal, Vitamin D

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          Abstract

          Glucocorticoid-induced osteoporosis occurs in two phases: a rapid, early phase in which bone mineral density is reduced, possibly as a result of excessive bone resorption, and a slower, progressive phase in which bone mineral density declines because of impaired bone formation. Although the indirect effects of glucocorticoids on bone are evident, their direct effects on osteoblasts, osteoclasts and osteocytes are primarily operative in the pathogenesis of glucocorticoid-induced osteoporosis. The management of patients exposed to glucocorticoids includes general health measures, sufficient calcium and vitamin D, and reducing the therapeutic regimen to the minimal effective dose. The gold standard in the pharmacological treatment of glucocorticoid-induced osteoporosis in postmenopausal women involves the use of bisphosphonates, which should be started soon after beginning chronic glucocorticoid therapy. Anabolic and alternative therapeutic strategies are currently under investigation in glucocorticoid-induced osteoporosis.

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