The patient’s at-home BP readings following discontinuation of the tea after 5, 6, and 7 days were 111/72mmHg, 104/78mmHg, and 102/67mmHg, respectively. Based on these improved readings, her lisinopril dose was reduced to 20mg/day and at an appointment 1-month after discontinuing the tea, her BP was 129/85mmHg (at-home ranges: 100–130/60–80). The patient was taken off all medication after lab work confirmed normal levels of sodium, potassium, ionized calcium, PTH, and normalized free cortisol. 

In the setting of hypernatremia, hypokalemia, and low plasma renin, the syndrome of AME may appear similar to primary aldosteronism, however “the finding of low aldosterone is what distinguishes AME from primary aldosteronism.” Both genetic and acquired forms of AME exist, with the genetic form being the result of an autosomal recessive mutation in the 11-β-HSD2 gene and the acquired form resulting from chronic licorice consumption, in which the active ingredient (glycyrrhizic acid) produces an inhibitory effect on this gene. Another diagnosis that could be considered in this patient is Liddle syndrome, however urinary cortisol levels help differentiate between this condition and AME (normal levels in Liddle syndrome, elevated levels in AME).

Reports of AME associated with licorice consumption date back to the 1960s, however these days, pure forms of glycyrrhizic acid are rarely found in the U.S. In 2015, the FDA even mandated specific limits of glycyrrhizin content in food and most licorice flavoring found now is artificial. Interestingly, the patient’s elevated PTH and kidney stones may have been tied to her licorice consumption as well, since upon discontinuation her PTH normalized. This phenomenon may have to do with the isoflavins found in licorice which in previous studies have been implicated in modulating bone metabolism resulting in elevated PTH. 

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In this case, conducting a thorough interview of the patient’s dietary habits led to the discovery of licorice tea as the probable cause of resistant hypertension in an otherwise healthy individual. The authors conclude that “although the diagnosis of acquired AME as the source of resistant hypertension remains a rare diagnosis, it should continue to be considered as its diagnosis simply requires thorough questioning during the clinical interview.”


1. Apostolakos, J. M. and Caines, L. C. (2016), Apparent Mineralocorticoid Excess Syndrome: A Case of Resistant Hypertension From Licorice Tea Consumption. The Journal of Clinical Hypertension. doi: 10.1111/jch.12841