Skeletal Fragility in Endogenous Hypercortisolism.

Skeletal fragility is a frequent complication of endogenous hypercortisolism, and fragility fractures may be the first clinical manifestation of the disease. Fractures involve more frequently the vertebrae and may occur in 30-50% of the patients exposed to glucocorticoid excess, in close relationship with severity and duration of hypercortisolism. Although improvement of bone mineral density was reported after resolution of hypercortisolism, there are patients with persistently high fracture risk after the cure of hypercortisolism, and other patients in whom the resolution of hypercortisolism may take a long time, implying a multistep therapeutic approach. Since vertebral fractures tend to occur early during the natural history of disease, a skeletal-specific approach should be undertaken in these patients; however, the cost-effectiveness of this approach is still largely unknown since data on effectiveness and safety of bone-active drugs in endogenous hypercortisolism are scarce.