Endocrine Abstracts

Ingestion of excessive amounts of liquorice may cause significant electrolyte imbalances due to a mimicking of mineralocorticoid excess. A 70-year-old female attended hospital with palpitations and was found to have hypokalaemia. She was documented to have multiple supraventricular ectopic beats coinciding with her feeling of palpitations, This was precipitated by toxic consumption of liquorice, more than 2 kg in 72 h, to celebrate her 70^th birthday. All abnormalities resolved with abstinence from further birthday liquorice. Mineralocorticoids and corticosteroids are structurally similar and bind equally to the Minrealocorticoid Receptor (MR). It is the selective presence of isoform 2 of 11beta-hydroxysteroid dehydrogenase (11BHSD) that downregulates the effect of cortisol in the tissues mentioned above. This enzyme utilizes NAD to oxidize cortisol to the inactive cortisone to prevent MR activation. Isoform 1 of this enzyme is present in all metabolic tissues to conversely reduce cortisone to cortisol to activate Glucocorticoid Receptors. Therefore, the placement and function of 11BHSD is critical to preventing an apparent mineralocorticoid excess from the unopposed effect of cortisol on a non-selective MR. Liquorice root (Glycyrrhiza glabra) contains glycyrrhizic acid (GZA), this molecule directly inhibits type 2 11BHSD. Acceptable safe dosage is 0.2 mg/kg with toxic doses beginning at consumption greater than 2 mg/kg. Given that liquorice contains 0.2% GZA by mass, a 60 kg adult would therefore exceed safety at 6g and reach toxicity at 60 g of liquorice per day. Our patient’s intake therefore exceeded this by a factor of 11. Hypokalaemia has long been associated with an increase in cardiac conduction abnormalities. The resultant hypokalaemia from upregulating the aforementioned pumps then has three major cardiotoxic effects in that it inhibits outward potassium currents in ventricular tissue, it inhibits the cardiac Na+–K+ pump, and the resting membrane potential is elevated with increased threshold for depolarization and hyperpolarized, this generally slows effective wave conduction. The combination of these three effects therefore facilitates re-entry rhythms with resultant tachyarrhythmias. Reports of these are not new, but they are usually in extremis. A case in Turkey linked the ingestion of liquorice to an episode of ventricular fibrillation in a patient with Brugada syndrome. Similarly, a patient from Oman developed recurrent polymorphic ventricular tachycardia episodes however, she was morbidly obese. Our patient was unique in having a structurally normal heart without cardiac risk factors and her rhythm returned to its baseline without intervention, thus, demonstrating the early stages of liquorice-induced cardiotoxicity.