A 72 year-old man was admitted to hospital in May 2021 with bilateral pitting leg oedema, worsening hypertension (BP 202/89mmHg, compared to 138/86mmHg on enalapril and felodipine in 2020) and severe hypokalaemia (potassium 2.3mmol/L, sodium 145mmol/L).

He described a one-month history of increasing leg swelling and estimated 5kg weight gain.  He did not have proximal myopathy, Cushingoid facies, bruising, thinned skin or striae.  He had seen his GP three weeks prior, at which time serum potassium was normal (5.1mmol/L) and he had been commenced on bendroflumethiazide 5mg daily without improvement in oedema.

Initial management included oral and intravenous potassium replacement, and spironolactone 100mg daily.  Serum potassium normalised after seven days and blood pressure improved to 160/78mmHg.

Initial investigation results included undetectable plasma aldosterone (<103pmol/L) and low plasma renin concentration (5.5mIU/L, normal 4.2-59.7), suggesting non-aldosterone mediated hypervolaemia.   Plasma cortisol was elevated with loss of diurnal variation (1673nmol/L at 0853hrs, 1534nmol/L at 1525hrs), and Cushing’s syndrome (CS) was confirmed on 24-hour urine collection (total cortisol 13,584nmol, normal <380).

Further investigation revealed an unusual underlying cause for CS, which will be discussed further.  This presentation will also address the unusual clinical presentation, in which typical phenotypic features of CS were absent.  Finally, the major management dilemma posed in treating CS in this case will be discussed, with a review of the relevant literature, along with questions raised by unique interactions between treatment given for CS and treatment given for its underlying cause.