Licorice-induced hypokalemic myopathy in a 59-year-old female patient

Introduction: 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is considered to protect the mineralocorticoid receptor (MR) by inactivating cortisol to cortisone, and by that generating specificity to the MR for aldosterone. 11β-HSD2 can be inhibited by several substances, for example licorice, leading to a mineralocorticoid excess syndrome including hypertension and hypokalemia.

Case: A 59-year old female patient presented to the emergency department with progredient tetraparesis. The clinical examination showed a flaccid paresis and areflexia of all extremities. Biochemical studies revealed severe hypokaliemia (1,3 mmol/l, reference range 3,6 – 4,8 mmol/l). The patient's electrocardiogram was normal. Intravenous potassium substitution was initiated. Endocrine diagnostic showed the constellation of hyporeninemic hypoaldosteronism. Further anamnesis revealed an excessive daily consumption of licorice sweets (at least 100 gram daily). After two days, intravenous potassium substitution was changed to oral substitution. Serum potassium remained stable after quitting the licorice intake, the tetraparesis was regressive. Cardiac arrhythmia did not occur. The patient was advised to avoid licorice intake and to undergo close monitoring of electrolyte levels in the next few weeks.

Conclusion: Licorice contains glycyrrhetinic acid which inhibits renal 11β-HSD2. Therefore, excessive licorice consumption can lead to pseudohyperaldosteronismus with severe hypokalemia and hypertension, leading to serious complications as seen in our patient. Studies have indicated that a daily licorice intake over 60 – 70 g should be avoided.