RESUMO
Aims: To discuss the likelihood of severe hypokalaemia as a cause of reversible diabetes. Presentation of the Case: A 46 year old patient presented to the Accident and Emergency unit (A&E) with a history of polyuria and polydipsia of recent onset. He was severely hyperglycaemic (glucose = 40 mmol/L, HbA1c = 11%), hypokalaemic (serum potassium < 2.0 mmol/L) and hypertensive [Blood Pressure (BP) = 180/115]. Conn's syndrome was confirmed by finding a raised serum aldosterone (1650 pmol/L; normal value < 440 pmol/L), suppressed renin (< 0.2 ng/ml/h; normal range: 0.2-2.5 ng/ml/h) and a left sided adrenal tumour (2.0 x 2.0 cm) on CT scanning. He was managed initially with IV potassium and insulin (initially 100 units daily) together with oral potassium, spironolactone 100 mg daily, lisinopril 20 mg daily and amlodipine 10 mg daily. After six days his potassium was 3.4 mmol/L and the IV potassium infusion was stopped. Twelve days later his fasting blood glucose, serum potassium and BP's were normal and the insulin and antihypertensive medications, apart from spironolactone, were stopped. He was discharged on spironolactone alone for four months during which time his blood glucose, blood pressure, and serum potassium levels remained normal and his HbA1c had fallen from 11.0 to 5.2%. He then underwent successful laparoscopic adrenalectomy and his serum aldosterone came down to 127pmol/L (within normal range). Histology confirmed the diagnosis of a Conn’s tumour. Conclusion: Although hyperaldosteronism per se predisposes to diabetes we suspect that this patient’s rapidly reversible hyperglycaemia resulted primarily due to a failure of insulin secretion as a result of his severe potassium depletion.