This has been shown to inhibit the enzyme in the kidney that lowers the plasma cortisol (by conversion to cortisone which thus maintains mineralocorticoid receptors free for aldosterone). Thus liquorice ingestion can lead to lead to an excess mineralocorticoid action and effects similar to that of hyperaldosteronism e.g. hypokalaemia.
Diagnosis of overconsumption
- liquorice overconsumption should be suspected clinically in patients
presenting with otherwise unexplained hypokalemia and muscle weakness
- a clue is provided when dietary history reveals excessive liquorice intake - note that liquorice is contained in some herbal medicines (2)
- due to its aldosterone-like action, laboratory investigations reveal
hypokalemia and metabolic alkalosis
- creatine phosphokinase (CPK) may be elevated in cases with rhabdomyolysis (due to severe hypokalemia) which may be complicated with acute tubular necrosis
- the inhibition of 11-ß-hydroxysteroid dehydrogenase by liquorice will cause
reduction in the conversion of cortisol to cortisone
- therefore, in conditions causing pseudo-hyperaldosteronism (as licorice excess), the cortisol:cortisone ratio in the peripheral venous plasma is sharply raised. Moreover licorice-induced hypertension is also accompanied by reduction in plasma renin as well as aldosterone level, which is not the case in primary or secondary hyperaldosteronism.
- Omar HR et al. Licorice abuse: time to send a warning message. Ther Adv Endocrinol Metab. 2012 Aug;3(4):125-38
- Yasue H et al. Severe hypokalemia, rhabdomyolysis, muscle paralysis, and respiratory impairment in a hypertensive patient taking herbal medicines containing licorice. Intern Med. 2007;46(9):575-8.
Last reviewed 01/2018