• Shih-Hua Lin, Sung-Sen Yang, Tom Chau, and Mitchell L Halperin.
• Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Nationa Defense Medical Center, Taipei, Taiwan. l521116@ndmctsgh.edu.tw
• Am. J. Med. Sci. 2003 Mar 1; 325 (3): 153-6.

AbstractLong-term licorice ingestion is a well-known cause of secondary hypertension and hypokalemia. Nevertheless, its initial presentation with a very severe degree of hypokalemia and paralysis is exceedingly rare. We report an elderly Asian man who presented to the emergency department with marked muscle weakness that progressed to paralysis. His blood pressure was 160/96 mm Hg. The major biochemical abnormalities were hypokalemia (plasma K+ concentration, 1.8 mmol/L) and metabolic alkalosis (HCO - 3 , 36 mmol/L). His renal potassium excretion was higher (transtubular potassium gradient of 9). Plasma renin activity and aldosterone concentration were suppressed and cortisol concentration was normal. A detailed history revealed that he had ingested tea flavored with 100 g of natural licorice root containing 2.3% glycyrrhizic acid daily for 3 years. Note that renal potassium wasting and hypertension persisted for 2 weeks after discontinuing licorice consumption along with KCl supplement and spironolactone. Long-term licorice ingestion should be kept in mind as a cause of paralysis with an extreme degree of hypokalemia to avoid missing this recognizable and curable medical disorder.

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