Endocrine Abstracts

A 50-year-old woman was referred with a history of chronic, symptomatic hypokalaemia. She also had hypertension. There was no history of diarrhoea, increased bowel motions, vomiting, or laxatives/diuretic use. She was not diabetic and she did not have menopausal symptoms. Her mother had seven strokes and myocardial infarction. On examination weight is 69.9 kg, height 1.65 m, BP 163/99, pulse 70, heart sounds normal, and examination of the abdomen was unremarkable. ECG was normal. Despite taking potassium supplements, repeat blood tests showed sodium 148 mmol/l, potassium 3.3 mmol/l, magnesium 0.87, creatinine 56, and eGFR >90. Spot urine potassium 25 mmol/l. Primary aldosteronism was suspected. Her renin was undetectable (<1.1 ng/l) and serum aldosterone 772 pmol/l. Saline suppression test showed non-suppressible aldosterone levels. Glucocorticoid-remediable aldosteronism was excluded. MRI failed to show a adrenal lesion. Adrenal vein sampling however confirmed a unilateral, right sided adrenal source for the aldosterone excess and she underwent successful right adrenalectomy. Histology was supportive of the diagnosis. Shortly after the operation she started to experience significant postural dizziness. It was initially thought that this was due to relative suppression of aldosterone secretion by the contralateral gland and so fludrocortisone was started. A short Synacthen test excluded adrenal deficiency. She required increasing doses of fludrocortisone but despite this remained symptomatic. Additionally she experienced headaches, fatigue, cold intolerance, and breathlessness. Therefore a neurocardiogenic process was suspected and she was referred to cardiology. Tilt table test showed her heart rate gradually rose to 138 b.p.m. This was thought to be consistent with a POTs type response. Thus our patient had confirmed primary aldosteronism due to a adrenal adenoma, removal of which helped to unmask POTS. We hypothesise that the excess mineralocorticoid activity from the adenoma hyper secreting aldosterone helped to mask the neurocardiogenic process.