Endocrine Abstracts

A 58-year-old woman was referred for a short synacthen testing (SST) prior to discontinuing oral prednisolone (up to 10 mg/day), which had been administered for over several years for management of COPD. Her primary team noted features of presumed iatrogenic Cushing’s syndrome, including cervicodorsal fat pad, type 2 diabetes, dyslipidaemia, hypertension, osteopenia, NAFLD and anxiety, and sought to wean her off glucocorticoids to minimise further adverse effects. On examination, she had significant proximal myopathy, increased BMI and marked cervicodorsal fat pad which interfered with her ability to dress unaided. Unexpectedly, she passed the SST [baseline cortisol 211 nmol/l, ACTH 41pg/ml (15-65) and 30-minute post-synacthen cortisol concentration 607 nmol/l (>430 nmol/l)]. She subsequently failed the 1 mg overnight dexamethasone suppression test, (137 nmol/l) and a 48-hour dexamethasone suppression test (171 nmol/l), suggesting endogenous ACTH-dependent hypercortisolaemia. The interpretation of these results was complicated by concomitant carbamazepine use. Investigations were repeated with paired dexamethasone measurements, confirming endogenous cortisol excess. A CRH test supported pituitary-dependent Cushing’s disease and an MRI pituitary was unremarkable. However, 24hr urinary free cortisol and several midnight salivary cortisol concentrations were normal. Her symptom pattern also suggested an element of cyclicity to her Cushing’s. Due to her anaesthetic risk from a respiratory perspective and patient preference, further investigations were paused and a therapeutic trial of metyrapone was commenced. After initial difficulties with glucocorticoid-withdrawal symptoms, ultimately requiring a “block and replace” regime of metyrapone and hydrocortisone, she is doing well, with improved energy, mood, glycaemic control, blood pressure and reduction in facial plethora and cervical adiposity. This case is the exception that proves the rule. Patients with iatrogenic Cushing’s syndrome should be considered to have glucocorticoid-induced adrenal insufficiency unless proven otherwise, both arising from exposure to excess exogenous glucocorticoids. A robust synacthen response in a clinically cushingoid patient on exogenous steroids should prompt consideration of an endogenous source.