To minimize the risk of glucocorticoid-induced bone loss, should use the smallest possible effective dosage and duration and use topical and inhaled preparations whenever possible. Obtain baseline measurement of bone mineral density (BMD) at the lumbar spine and/or hip when initiating long-term (., exceeding 6 months) glucocorticoid therapy and initiate appropriate preventive therapy. May repeat longitudinal measurements as often as every 6 months to detect possible bone loss. Less frequent (., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.
Thyroid hormone therapy in persons with undiagnosed Addison disease may precipitate an adrenal crisis because the thyroid hormone increases the hepatic clearance of cortisol. In addition, patients with a new diagnosis can have a reversible increase in thyroid-stimulating hormone levels because glucocorticoids inhibit secretion. 25 , 26 Glucocorticoid replacement can result in the normalization of thyroid-stimulating hormone levels less than 30 mIU per L. In individuals with type 1 diabetes mellitus, unexplained hypoglycemia and decreasing insulin requirements may be the initial signs of Addison disease. 27