Liquorice-induced sodium retention. Merely an acquired condition of apparent mineralocorticoid excess? A case report.

Excessive ingestion of liquorice may result in sodium retention, hypertension, hypokalemia, and suppression of renin and aldosterone. Similarities between liquorice-induced effects and congenital apparent mineralocorticoid excess have recently been emphasized, as in both conditions, reduced activity of the enzyme 11 beta-hydroxysteroid dehydrogenase type 2 allows cortisol to act as a potent mineralocorticoid. We report a case of generalized edema without any increase in blood pressure, with biochemical and hormonal features of apparent mineralocorticoid excess, in a young woman who had been ingesting substantial amounts of liquorice for several years. Liquorice-induced wide-spread edema without hypertension in our patient, as well as in a few other cases previously reported, and the more common occurrence of edema associated with hypertension challenge the current explanation of liquorice syndrome as a purely acquired apparent mineralocorticoid excess. Indeed, in both congenital apparent and true mineralocorticoid excess, edema is typically absent, as a result of the sodium escape phenomenon. As pressure-natriuresis may be an essential mechanism accounting for the sodium escape phenomenon, some component of liquorice could partially or completely oppose the circulatory response that converts liquorice-induced sodium retention into blood pressure elevation. In patients with unexplained generalized edema and hypokalemia without hypertension, liquorice ingestion should be carefully investigated and the renin-aldosterone system should be assayed.