Corticosteroid induced hyperglycemia

Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur at higher bone mineral density (BMD) values than occur in postmenopausal osteoporosis. The increased risk of fracture has been reported with doses of prednisone or its equivalent as low as to mg daily [ 1 ]. Thus, glucocorticoid-induced bone loss should be treated aggressively, particularly in those already at high risk for fracture (older, prior fragility fracture). In other individuals, clinical risk factor and bone density assessment may help guide therapy. The prevention and treatment of glucocorticoid-induced bone loss will be reviewed here. The clinical features are reviewed separately. (See "Pathogenesis, clinical features, and evaluation of glucocorticoid-induced osteoporosis" .)

In patients on long-term low-dose prednisolone (< mg/day or equivalent), calcium and vitamin D 3 therapy may be sufficient to prevent continuing bone loss and reduce falls. However, patients who continue to lose bone or those at high risk of fracture (previous fragility fracture, bone density < -) should also be offered oral bisphosphonates. Although most clinical trial data are limited to 1-2 years, it is rational to maintain fracture prophylaxis for as long as corticosteroids are taken at a daily dose of more than 5 mg prednisolone or equivalent.

Corticosteroid induced hyperglycemia

corticosteroid induced hyperglycemia

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