The Hidden Liquorice: Apparent Mineralocorticoid Excess Caused by Inadvertent Exposure to Liquorice Root Extract

ABSTRACT Objective: Excessive consumption of liquorice can cause endocrine symptoms of apparent mineralocorticoid excess (AME). This is usually caused by excessive consumption of liquorice-containing sweets and native liquorice root, but various chemical compounds in liquorice may also be used in many other products where they are considered additives and are therefore not explicitly declared. Methods: We here report a 21-year-old patient who presented with severe edema; spells of dizziness, headaches, and peripheral paraesthesia; and general and muscular fatigue. Results: Blood samples showed low serum potassium (2.3–3.1 mmol/L [ref 3.5–4.6]) requiring potassium supplementation (40 mmol × 2 daily) and high normal sodium (142–147 mmol/L [ref 137–145]). Measurement of 24-hour urinary steroid metabolite excretion raised the suspicion of AME. Additional blood tests showed undetectable serum concentrations of aldosterone (<38 pmol/L [ref 50–360]) and renin (<2 × 10-3 IU/L [ref 6–60]). Pituitary function (thyroid hormones, prolactin, insulin-like growth factor-1, insulin-like growth factor-binding protein 3) was normal. No obvious endocrine cause of AME could be established, and the patient re-evaluated her personal dietary products. Liquorice root was present in several herbal teas and sugar-free chewing gum that had been consumed daily in large amounts. Cessation of usage of these products resulted in complete resolution of AME-related symptoms, so inadvertent excessive intake of liquorice was assumed to be the cause. Conclusions: Our case report reveals other potential sources of liquorice besides sweets, including industrial sweeteners and flavoring agents that could potentially cause clinical symptoms. Clinicians should thus extend their medical history-taking to a broader range of consumer products when AME is suspected. Abbreviations: ACTH adrenocorticotropic hormone AME apparent mineralocorticoid excess 11-βHSD2 11-β-hydroxysteroid dehydrogenase 2 ER estrogen receptor GZA glycyrrhizinic acid MR mineralocorticoid receptor