Endocrine Abstracts

A 75-year-old female presented with 12kg weight loss and malaise, 18 months after a diagnosis of type 2 diabetes mellitus. Abdominal CT scanning demonstrated bilateral adrenal masses and her symptoms responded rapidly to empirical treatment with dexamethasone. CT guided biopsy demonstrated adrenal hyperplasia.

Centripetal weight distribution and proximal myopathy were prominent, and serum cortisol failed to suppress following standard 48h low dose (662nmol/L) and high dose (559nmol/L) dexamethasone suppression tests. Plasma ACTH levels were low but measureable (8 - 11ng/L). Inferior petrosal sinus sampling (IPSS) demonstrated a central to peripheral gradient of 13 to 1 after CRH and the patient underwent transsphenoidal surgery. Hypercortisolism persisted (0900 cortisols 529 and 652nmol/L), and no adenoma was identified histologically.

A marked variability in 0900 serum cortisol values was noted (232 - 695 nmol/L) and sequential salivary cortisols were measured to explore the possibility of cyclical Cushing's syndrome. 0900 Salivary cortisol values were low/normal (mean 12.7nmol/L) with higher levels at 2200 (mean 16.0nmol/L; p=0.096). Timed UFC measurements (sequential 3h measurements over 24h on three occasions) indicated a progressive rise from 14nmol/h (0600 to 0900) to 25nmol/h (1200-1500); with the highest levels recorded at 2100-2400 (28nmol/h). Repeat CT demonstrated bilateral nodular adrenal enlargement (right 5cm). Food dependent Cushing's was suspected, and following a test meal, serum cortisol rose from 197 (baseline) to a peak of 704nmol/L. The cortisol rise was greater than that observed after 1mcg CRH (peak 414nmol/L), 1mcg synthetic ACTH (peak 647nmol/L), or after no meal (peak 278nmol/L). Bilateral adrenalectomy was performed and histology revealed macronodular hyperplasia.

Food-dependent Cushing's should be considered where low early morning cortisol levels are identified with a reversed circadian rhythm. Incomplete ACTH suppression may have led to a false positive IPSS localisation. The initial features of hypoadrenalism may have reflected reduced cortisol release due to a hypocaloric diabetic diet.