An Unusual Case of Licorice-Induced Hypertensive Crisis

Black licorice induced hypertension is an uncommon cause of hypertension in modern times because newer types of licorice rarely use the active ingredients in licorice root in large quantities. However, certain licorices and candies still contain glycyrrhizic acid (GZA) in sufficient quantities to affect blood pressure and cause other health issues.

A 65-year-old woman with previously well controlled hypertension on a single medication presented to the emergency room with acute, symptomatic hypertension with blood pressures running 200s/140s. Despite IV medications, her hypertension remained refractory to treatment. This prompted a hospital admission with treatment using nicardipine in the ICU. Her blood pressure was difficult to control without a short acting antihypertensive medication infusion. She required a seven-day hospitalization (five of which were in the ICU) until her symptoms and hypertension were controlled with a three-drug regimen. Labs were notable for potassium's running on the low side of normal and low levels of both renin (less than 0.6 with normal less than or equal to 0.6-3.0) and aldosterone (1.0 with normal 3-16 ng/dL). Ten days after discharge, she was having symptomatic hypotension and was seen in the clinic. She in fact was eating large amounts of Snaps licorice which uses its original 1930s recipe including licorice granules. Her licorice habit abruptly started six months prior and included a minimum of two to four boxes per day every day.

The patient currently is doing well and is down to only two antihypertensive medications at lower doses. She has given up her licorice habit. Natural licorice is extracted from Glycyrrhiza glabra root containing glycyrrhizin or glycyrrhizic acid (GZA). GZA inhibits the type 2 isoenzyme of 11 beta-hydroxysteroid dehydrogenase (11 β -HSD), which prevents local inactivation of cortisol, specifically in the renal collecting tubules. There is increased availability of cortisol to bind to renal mineralocorticoid receptors resulting in excess mineralocorticoid activity or pseudohyperaldosteronism. The patient may present with findings similar to primary aldosteronism: hypertension with sodium retention, edema, hypokalemia, metabolic alkalosis and low plasma renin activity. Plasma aldosterone levels would be low (in primary aldosteronism it is elevated). Specific testing can be performed, but resolution of symptoms after the patient stops eating licorice strongly suggests the diagnosis.