Endocrine Abstracts

JOINT3460

A 65-year-old patient was referred to an endocrinologist due to hypokalemia and arterial hypertension. He had been taking medication for arterial hypertension for more than 30 years and had normal values with amlodipine and perindopril. Hypokalemia was constant in laboratory findings over the years, with potassium levels usually 3.0–3.9 mmol/l. He also had episodes of supraventricular tachycardia a few months ago. Laboratory findings two years ago showed impaired glucose tolerance with FGP 6.7 mmol/l and HbA1c 6.4% then. These findings were checked and now showed that the patient had overt diabetes mellitus with HbA1c 7.1%. Aldosterone level was measured and came convincingly high with suppressed renin angiotensin plasma activity (0.1 ug/l/h) and aldosterone 2131 pmol/l and 1978 pmol/l, respectively, so a confirming test was not needed. Further, an abdominal CT scan was done and showed an adenoma in the right suprarenal gland. The patient refused adrenal vein sampling since he was not interested in surgical treatment, so spironolactone 50 mg was initiated. The patient was not obese, with an ITM of 24 kg/m² and no changes in body weight during the years. Also, there was no family history of diabetes. Since the initiation of spironolactone treatment, hypokalemia withdrew, and the patient noticed normal glucose levels during SMBG with FBG constantly below 7 mmol/l and postprandial BG below 8 mmol/l. After six months, he had definite remission of diabetes with HbA1c 5.7% without any medication. It is known that primary hyperaldosteronism leads to many cardiovascular consequences, but it can be seen in a broad range of phenotypes. It is important to remember that primary hyperaldosteronism is one of the possible endocrine causes of glucose metabolism impairment, which was the case with the patient we presented. Also, although the use of MRA as spirinolactone is connected with development of glucose metabolism impairment the opposite happened in this case.