Licorice: Treat or Poison?

Introduction: Patients take many supplements considering them to be safe. Licorice has been used as a sweetener in candies and treats. Furthermore it is used in complimentary medicine for treatment of variety of conditions. Case Description: 64 year old woman with diagnosis of stage 1B HR+ Her2- Left breast IDC, DCIS s/p lumpectomy, completed adjuvant radiation 6 months ago who was recommended by onclology to take anastrozole for 5 years as adjuvant therapy which she refused and instead saw a Chinese traditional practitioner and was started on supplements that included licorice 6 grams/day. She presented to the ED with complaints of L flank pain for one day. Workup of the L flank pain including CT Abd/pelvis, urinalysis, and urine culture did not reveal any abnormalities. However, incidentally found to have severe hypokalemia, K of 1.9 mmol/L,ABG: PH of 7.49 PCO2 of 38mmHg, Bicarbonate of 29 mmol/L, severe HTN and prolonged QTC 509 mS. Serum aldostrone and renin were depressed, her 24 hour urine potassium was 185 mmol/24 HR. She requried admission and recieved total of 700 meq of KCL over 48 hours . Discussion: Pseudo-hyperaldosteronism is a condition that clinically mimics hyperaldosteronism with suppression of plasma renin activity and aldosterone levels. Hypokalemia, metabolic alkalosis, and HTN can be seen in this condition. Dietary causes include prolonged overconsumption of licorice. 11Bhdryoxysteroid dehydrogenase type 2 enzyme is responsible for conversion of cortisol to inactive cortisone.Licorice, specifically glycyrrhizic acid and its hydrolytic product Glycyrrhetinic acid are potent competitive inhibitors of 11-BHSD2 and lead to excess cortisol which avidly binds to the mineralocorticoid receptor resulting in cortisol-induced mineralocorticoid effect of sodium retention and urinary potassium waisting. Glycyrrhizic acid onsumption in excess of 100 to 200 mg daily has been noted to cause clinically significant complications. In addition to electrolyte abnormalities, licorice induced HTN and hypertensive encephalopathy, hypokalemic myopathy manifesting as flaccid paralysis, and QT prolongation and possible torsade de pointes with fatal arrhythmias can be seen. Our patient was asymptomatic ,which in fact put her at higher risk of cardiac complications and sudden death given her prolonged QT findings. Presenting to the ED with non related flank pain potentially saved her life.