Insights on accelerated skeletal repair in Cushing's disease.
Overview
abstract
Cushing's disease with prolonged exposure to high circulating levels of glucocorticoids is associated with deterioration of the structural integrity of bone, resulting in increased skeletal fragility and fractures. The mechanism of bone repair following successful surgical treatment is poorly understood. A 34-year-old man presented with a tibial fracture and severely low BMD, elevated AM serum cortisol, ACTH, and 24 h urinary free cortisol, which did not suppress with 2 days of high dose dexamethasone. Following transphenoidal resection of a pituitary microadenoma, serum cortisol and ACTH normalized. A repeat DXA at 8 months post-resection showed no change in BMD, however the Trabecular Bone Score (TBS), which reported severe deterioration of trabecular bone architecture at diagnosis, improved to normal. At that time, teriparatide (TPTD) was given for 2 years, which resulted in a 53.9% increase in BMD with only a small improvement in TBS. In this patient, spontaneous recovery of trabecular bone architecture was reflected by the early correction in TBS. Subsequent TPTD treatment was associated with marked improvement in BMD, presumably due to enhanced mineralization. Complete skeletal repair was achieved by this two-step mechanism in a very short time following successful surgical treatment for Cushing's disease.
