Amelioration of Licoricehyphen;Induced Hypokalemic Rhabdomyolysis with DexamethasoneCase Report and Review of the Literature

摘要

The mechanism of licorice-induced hypokalemia and hypertension has been appreciated only recently. The active component of licorice, glycyrrhetinic acid, inhibits 11beta; hydroxysteroid dehydrogenase in the distal nephron, inhibiting the conversion of cortisol to its inactive metabolite cortisone, thus providing cortisol free access to the mineralocorticoid receptor.We describe a 55-year-old woman with a history of daily licorice consumption who developed severe hypokalemia (potassium 1.5 mmol/L) complicated by rhabdomyolysis. Because hypokalemia persisted despite spironolactone and 665 mmol of potassium replacement in less than 48 hours, dexamethasone suppression therapy was prescribed. This resulted in rapid correction of the hypokalemia, and no further potassium supplements were required. The pathophysiology of licorice-induced hypermineralocorticoidism and the rationale for dexamethasone suppression therapy in treating this disorder are reviewed.