Endocrine Abstracts

Primary hyperaldosteronism (PHA), accounts for 5–10% of all hypertensive patients and is associated with increased cardiovascular risk. However, making the diagnosis is not always straightforward.

A 50-year-old male was admitted with an acute myocardial infarct. He was markedly hypertensive (BP 190/100 mmHg) and hypokalemic. He was commenced on beta-blockers and an Angiotensin converting enzyme inhibitor (ACEI). Plasma aldosterone concentration was 290 pmol/l (ref 100–800), renin <0.2 pmol/ml per h (ref 0.5–3.1), plasma renin aldosterone ratio (PRA) > 4150. Potassium at time of the test was 3.0 mmol/l (ref 3.5–5.0). However careful review of the notes confirmed that he had received three doses of i.v. beta-blockers prior to these samples being taken. Even a single dose of beta-blocker can suppress renin rendering the renin:aldosterone ratio uninterruptible. Formal diagnosis therefore had to be delayed for 2 months until it was felt safe to discontinue the ß-blockers, which confirmed the diagnosis. He was re-admitted three weeks later with flash pulmonary oedema with no evidence of myocardial ischaemia or renal artery stenosis and symptoms resolved within hours. Abdominal computed tomography (CT) showed a left adrenal 1.5 cm nodule. Prior to planned surgery he had arterial venous sampling, which showed higher aldosterone production from the right adrenal vein (173 000 compared to Lt adrenal 2930). The aldosterone to cortisol ratio of 24.5 was diagnostic of a right aldosterone producing adenoma.

This case illustrates a number of factors that can confound the diagnosis of Conn’s syndrome. Firstly the use of beta-blockers makes diagnosis difficult. Secondly it illustrates the value of adrenal vein sampling in confirming functionality, even when a lesion is seen on CT. Thirdly it highlights that flash pulmonary oedema should be considered as a possible presentation of Conn’s syndrome.