A New Cause of Glycyrrhizic Acid-Induced Apparent Mineralocorticoid Excess (AME) Syndrome with Hyperadrenergic Symptoms

Introduction: AME is caused by genetic or drug-induced inhibition of renal 11Beta-hydroxysteroid dehydrogenase-2(11βDSH-2) inactivating conversion of cortisol to cortisone, leading to major cortisol activation of the renal mineralocorticoid receptor (MR). Acquired AME can occur due to the ingestion of glycyrrhizic acid(GA), found in licorice root and chewing tobacco.However, the brain contains 11βDSH-1 which can affect the level of brain catecholamines We present a new cause for AME from Advanced Liver Support supplements who also presented with never before reported hyperadrenergic symptoms associated with AME which we believe are due to the additional brain effects of 11BDSH-1 inhibition. Case Description: A 65-year-old female developed accelerated hypertension, hypokalemia, metabolic alkalosis and adrenergic symptoms 4 months after daily ingestion of 4 tablets/day of Advanced Liver Support, Advanced BioNutritionals (Nacros, Georgia). Each pill contained 250 mg of GA. She had a BP 220/120 mmHg with episodes of palpitations, sweating & tremors. Her Na was 141 mmol/L, K 3.1 mmol/L, Cl 101 mmol/Land HCO3 30 mmol/L. Fasting free catecholamines were normal, plasma renin activity was reduced at 0.437 ng/mL/hr & serum aldosterone level was less than 1 ng/dL. Cessation of the liver supplement resulted in complete resolution of her hypertension, adrenergic symptoms & abnormal lab values within a few days, and her two blood pressure medications were discontinued. She has been followed for a year without reoccurrence of hypertension. Discussion: GA is increasingly found in unregulated nutritional supplements and has the potential to induce a reversable syndrome of AME. Numerous other health supplements containing GA are available, which clinicians must consider in cases of AME. Acquired AME differs from genetic AME due to GA inhibition of both 11βDSH-1 and 2 enzymes. 11βDSH-2 inhibition increases local renal and CNS cortisol levels, while 11βDSH-1 inhibition increases pituitary hypothalamic tract mediated catecholamine release which can be responsible for additional hyperadrenergic effects of drug- induced AME.