ECE2020 ePoster Presentations Adrenal and Cardiovascular Endocrinology (58 abstracts)
1Endocrinology, Diabetes and Nutrition Diseases Department, Elias University Hospital, Bucharest, Romania; 2Elias’ Endocrinology Department, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
Background: Hypokalemia can be caused by decreased intake of potassium or by excessive loss of potassium in the urine or through the gastrointestinal tract. Severe and life-threatening hypokalemia is defined by levels below 2.5 mEq/l and can be associated with muscle weakness, cramping, headaches, palpitations, polydipsia and polyuria. Periodic paralysis is a very rare presentation in Caucasians.
Case presentation: A 50-year-old Caucasian man, without previous medical history, presented in the emergency department for quadriparesis with predominantly brachial diparesis and hypertensive crisis (220/100 mmHg). Native cerebral computed tomography (CT) was normal. However, biochemical testing revealed severe hypokalemia (1.4 mEq/l), hypernatremia (149.2 mmol/l), high creatine-kinase (5273 U/l), lactate dehydrogenase (2185 U/l) and transaminases (ALT = 106 U/l, AST = 191 U/l), low eGFR (60.24 ml/min per 1.73 m2) , a raising troponin (from 0.94 ng/ml up to 1.45 ng/ml) and elevated inflammatory markers. Arterial blood gas revealed metabolic alkalosis (pH = 7.56, HCO3- = 36.7 mmol/l). Clinically, he presented with brachial motor deficit, hyporeflexia of the lower limbs, orthopnea, dyspnea and bilateral leg edema. Potassium supplementation was started both intravenously and orally and the patient was transferred to our Endocrinology department, with the suspicion of primary aldosteronism (PA). The patient admitted a long history of high blood pressure, which he had neglected and had never sought medical advice. Plasma aldosterone concentration to direct renin concentration ratio (ARR) confirmed the suspicion (plasma aldosterone = 32.3 ng/dl; direct renin = 0.8 µUI/ml; ARR = 40.3). Consequently, an abdominal non-contrast CT was performed, which showed bilateral adrenal macroadenomas (14/13 mm on the right gland and 12/10 mm on the left gland). Since adrenal venous sampling is not available in our center, we started medical therapy with Spironolactone (150 mg/day, which was gradually reduced to 50 mg/day). Because the patient presented signs of left ventricular dysfunction, we also added Furosemide (40 mg/day). For further blood pressure control an ACE inhibitor, a calcium channel blocker and clonidine were also introduced. Six-month follow-up showed good control of blood pressure and potassium level, occasional paresthesia in the upper limbs and symmetrical gynecomastia.
Conclusion: Hypokalemic paralysis is a rare form of presentation and the suspicion of PA may be easily overlooked, as it mimics hypokalemic periodic paralysis, polymyositis, Guillan-Barre syndrome. Screening for PA is recommended for any case with spontaneous or diuretic induced hypokalemia and hypertension. Disease control can be obtained with spironolactone, however, the unpleasant side effects in men may lead to low compliance to treatment.