The mineralocorticoid excess associated with the ingestion of liquorice or carbenoxolone (the hemisuccinate derivative of glycyrrhetinic acid ΓÇô the active component of liquorice) was once believed to result as a direct effect of either of these agents on the kidney; however, it is now known that this is not the case and that the condition is due to the inhibition of the enzyme 11b-hydroxysteroid dehydrogenase which converts cortisol to cortisone. This enzyme plays a critical role in aldosterone-selective tissues (such as the kidney) in preventing cortisol from gaining access to the non-specific mineralocorticoid receptor. If it is inhibited or congenitally absent, then the so-called syndrome of apparent mineralocorticoid excess ensues.
