J Korean Soc Endocrinol.  2005 Apr;20(2):179-182.

A Case of Licorice Induced Hypokalemic Paralysis with Rhabdomyolysis

• Hong HI
• Han KH
• Hwang JW
• Kim YD
• Shim MS
• Kim JY

Abstract

Prolonged ingestion of licorice can cause hypermineralocorticoidism, with sodium retention, potassium loss and hypertension. Nevertheless, its initial presentation with a very severe degree of hypokalemic paralysis and rhabdomyolysis are exceedingly rare. We describe a patient who experienced hypokalemic paralysis and rhabdomyolysis after licorice ingestion. The patient's initial blood pressure was 160/80mmHg. The major biochemical abnormalities included; hypokalemia(K+ 1.3mEq/L), metabolic alkalosis, with a pH of 7.64, and urine myoglobin > 3000ng/mL. The plasma rennin activity and aldosterone level were suppressed. The 24 hour urine cortisol concentration was normal. The patients, over a 1 month period, had ingested 500g of licorice boiled in water. After quitting the licorice, the hypokalemia and muscle paralysis gradually improved and blood pressure returned to normal

MeSH Terms

Aldosterone
Alkalosis
Blood Pressure
Chymosin
Eating
Glycyrrhiza*
Glycyrrhizic Acid
Humans
Hydrocortisone
Hydrogen-Ion Concentration
Hypertension
Hypokalemia
Myoglobin
Paralysis*
Plasma
Potassium
Rhabdomyolysis*
Sodium
Water
Aldosterone
Chymosin
Glycyrrhizic Acid
Hydrocortisone
Myoglobin
Potassium
Sodium
Water

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