Excessive consumption of licorice causes the syndrome of apparent mineralocorticoid excess. It manifests as hypertension, hypokalemia, and metabolic alkalosis. Licorice contains glycyrrhetinic acid, a substance that inhibits 11ß-hydroxysteroid dehydrogenase. This enzyme normally functions to convert cortisol to cortisone. This is important because cortisol avidly binds the mineralocorticoid receptor in the collecting tubules of the kidney, mimicking aldosterones effects (ie, salt retention, potassium excretion). Cortisone is unable to bind the receptor. In patients in whom this enzyme is inhibited, cortisol is not converted to cortisone, inducing a syndrome that presents similarly to mineralocorticoid excess. Aldosterone levels in this situation are suppressed and therefore do not cause hypertension. Dihydrotestosterone and progesterone are not metabolized by 11ß-hydroxysteroid dehydrogenase and have no effect on the mineralocorticoid receptor.
1. Brewster UC, Setaro JF, Perazella MA. The renin-angiotensin-aldosterone system: cardiorenal effects and implications of renal and cardiovascular disease states. Am J Med Sci 2003;326:1524.
2. Cruz DN, Perazella MA. Hypertension and hypokalemia: unusual syndromes. Connecticut Med 1997;61:6775.
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