Endocrine Abstracts

Cushing’s disease, caused by an ACTH-secreting pituitary adenoma, accounts for up to 80% of endogenous Cushing’s syndrome cases. While trans-sphenoidal surgery is the standard treatment, pituitary MRI identifies surgical targets in only about 60% of patients. We report a 63-year-old woman with a 12-month history of central weight gain, easy bruising, worsening hypertension, recent diagnoses of type 2 diabetes and obstructive sleep apnoea, who was diagnosed with ACTH-dependent Cushing’s syndrome. Laboratory tests revealed a 10-hour post-1 mg dexamethasone cortisol level of 570 nmol/l (< 50 nmol/l), ACTH of 112 ng/L (10-30 ng/l), and a 24-hour urinary free cortisol (UFC) of 236 nmol/l (0-164 nmol/l). Inferior petrosal sinus sampling indicated a central source of ACTH excess. Initial pituitary MRI identified two potential areas of interest. An initial 11C-methionine PET/CT demonstrated tracer uptake within both areas and did not favour one over the other. Medical treatment was initiated to normalise cortisol and enhance ACTH signalling, aiming to better delineate a surgical target on repeat imaging. Initially treated with metyrapone, the patient switched to osilodrostat due to intolerable side effects. After 3 months of eucortisolaemia, her ACTH levels rose to 1091 ng/L (from 353 ng/l), prompting a repeat 11C-methionine PET/CT, which now identified a clear focus of increased tracer uptake in the left inferior pituitary gland. The patient subsequently underwent endoscopic trans-sphenoidal resection of the lesion. Postoperatively, cortisol levels were 51 nmol/l on day 3 and 34 nmol/l on day 11. She is currently on a stable dose of prednisolone (4 mg once daily) and feels well. Histological analysis confirmed a corticotroph pituitary adenoma. This case is the first to utilise 11C-methionine PET/CT before and after cortisol-lowering treatment, suggesting that blocking steroidogenesis may enhance the visibility of corticotroph adenomas through functional imaging.