Liquorice Intoxication Can Lead to Cardiac Arrest!

Abstract

A 45-year-old man was admitted to the Emergency Department with fatigue and muscular weakness. Soon after hospital admission, he developed "torsades de pointe" and was successfully resuscitated. The admission laboratory investigations had revealed a profound hypokalemia (1.65 mmol/L). The patient had a long-term use of alcohol-free "pastis" in an attempt to reduce his chronic ethanol consumption. As the beverage likely contained a significant amount of liquorice, the diagnosis of glycyrrhizin chronic intoxication was suspected. The diagnosis of liquorice-related pseudohyperaldosteronism was assessed by normal plasma aldosterone levels and low plasma renin activity. Intravenous and oral supplementation of potassium was required for 5 days, and the patient had an uneventful follow-up.

Figure 1

Both cortisol and aldosterone bind with equal affinity to mineralocorticoid receptors that are activated predominantly with aldosterone. Type 2 11-β-hydroxysteroid dehydrogenase (11-βHSD) converts cortisol to its inactive form, cortisone, and evokes corticosteroid specificity. By inhibitory effects of Glycyrrhiza glabra and glycyrrhizin on type 2 11-βHSD, the mineralocorticoid receptors are activated by cortisol, leading to accumulation of glucocorticoids with anti-inflammatory and mineralocorticoid properties, hypokalemia, and mineralocorticoid-related hypertension.