Endocrine Abstracts

Background: Prolonged ingestion of licorice has been known to cause hypokalemia and resistant hypertension amongst other disturbances. This is due to glycyrrhizin that inhibits the 11-β-hydroxysteroid dehydrogenase enzyme type 2 which results into increased plasma cortisol levels that stimulate the mineralocorticoid receptors resulting into apparent mineralocorticoid excess.

Case report: A 45-year-old woman resident in an iodine sufficient area, heavy smoker, was referred by her cardiologist to a tertiary endocrine center due to uncontrolled hypertension, for the past 4-5 years, with maximum systolic blood pressure of 200 mmHg, a transient paresthesia episode and hypokalemia. She denied any headaches, sweating, tremors or pallor, but was affirming rapid heartbeats. Physical examination revealed normal body mass index, regular heart rhythm with H r=80/min, blood pressure of 145/80 mmHg in clinostatism with 140/80 mmHg in orthostatism and no reddish-purple striae. Biochemical assessment revealed moderate anemia, moderate hypokalemia (K= 2.9 mmol/l), eunatremia (Na= 142 mmol/l). The ECG showed flattened T-waves. After 30 mEq KCl iv and oral potassium supplementation her K levels increased to 3.2 mmol/l). Hormonal assessment revealed a low-renin hypertension: mineralocorticoid axis after 2 h of standing and 5-15 minutes of sitting showed plasma aldosterone at the lower limit of normal (29.3 pg/ml) and suppressed direct plasma renin (= 1.92 pg/ml - 4 days after stopping beta blocker treatment), with aldosterone/renin ratio= 1.52 ng/dl/ng/l (non-diagnostic for primary aldosteronism). Glucocorticoid axis, plasma catecholamines (plasma metanephrines= 33.7 pg/ml, plasma normetanephrines= 82 pg/ml), thyroid function, PTH and IGF1 levels were normal. Abdominal ultrasound was unremarkable, however the native computed tomography revealed right adrenal hyperplasia. Upon a thorough dietary history, the patient stated that she was ingesting, for the past 20 years, licorice based candies in excessive amounts (around 160 grams/day). She was discharged with oral potassium supplementation, 10 mg of Amlodipine daily and the indication to withdraw all licorice candies ingestion.

Follow-up: One month after licorice withdrawal, serum potassium level was normal (4.5 mmol/l) without any supplements and blood pressure normalized.

Conclusion: This case highlights the importance of dietary history in patients with hypertension, hypokalemia and hormonal picture of pseudohyperalodsteronism. Apparent mineralocorticoid excess due to increased licorice ingestion should be considered for differential diagnosis of secondary hypertension.