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SAT-284 Licorice Root Tea and Hypokalemia

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Abstract Disclosure: H.D. Nguyen: None. Introduction: The differential diagnosis of hypokalemia is broad. However, licorice consumption is often not on this list. Case: A 64-year-old healthy woman who was referred… Click to show full abstract

Abstract Disclosure: H.D. Nguyen: None. Introduction: The differential diagnosis of hypokalemia is broad. However, licorice consumption is often not on this list. Case: A 64-year-old healthy woman who was referred to the endocrine clinic for evaluation of hypokalemia and hypernatremia. She had no personal or family history of hypertension, diabetes mellitus, hyperlipidemia, cardiovascular disease, or fungal infection. Medications included vitamin D 1000 IU daily, polyethylene glycol 3350, simethicone, and bisacodyl prn. On physical exam, blood pressure 136/84, heart rate 79, height 175cm, weight 66kg, BMI 21.5. She exhibits no facial plethora, moon facie, central obesity, abdominal bruits, or purple abdominal striae. Bilateral lower extremity is notable for mild non-pitting pretibial and ankle edema. Laboratory studies showed serum sodium (sNa) 146-148 mmol/L (normal range 136-145), serum potassium (sK) 3.1-3.4 mmol/L (normal range 3.5 -5.1), HCO3 33-35 mmol/L (normal range 22-29), plasma aldosterone concentration (PAC) <1.0ng/dL, plasma renin activity (PRA) <0.167ng/ml/hr. Two years prior, sNa 140-142, sK 3.8-4.9. Upon further questioning, she revealed she had been consuming licorice root tea daily for the past two years to control indigestion and constipation. As excessive licorice root consumption was a differential diagnosis for these laboratory abnormalities, she was asked to undergo repeated testing after stopping licorice root for two weeks. Repeated blood work two and four weeks later showed sNa 137-139, sK 4.3-4.6, HCO3 24-28, PAC 1.5-8ng/dl, PRA 0.265 - 1.307 ng/ml/hr. Discussion: Licorice root contains glycyrrhizic acid, which can inhibit 11-beta-hydroxysteroid dehydrogenase type 2, an enzyme responsible for converting bioactive cortisol to inactive cortisone. Hence, excessive consumption of licorice root can lead to elevated serum cortisol level. Cortisol has mineralocorticoid activity and can bind to the ambivalent mineralocorticoid receptors, causing increased renal sodium reabsorption and potassium excretion, leading to hypernatremia, hypokalemia, fluid retention, and hypertension. Excessive cortisol activity at mineralocorticoid receptors also results in suppressed plasma renin and aldosterone levels. Other differential diagnoses for hypokalemia with low renin and aldosterone levels include hypercortisolism, syndrome of apparent mineralocorticoid excess, activating mutation of mineralocorticoid receptor, treatment with triazole antifungals such as itraconazole, deoxycorticosterone producing tumors, congenital adrenal hyperplasia, and Liddle syndrome. These diagnoses usually require further investigation. A thorough history inquiring about possible licorice root consumption can help prevent unnecessary work up. Conclusion: Licorice root consumption should be on the differential diagnoses of unexplained hypokalemia. Presentation: Saturday, July 12, 2025

Keywords: consumption; history; root; licorice root; hypokalemia

Journal Title: Journal of the Endocrine Society
Year Published: 2025

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