Pseudohyperaldosteronism Due to Licorice: A Practice-Based Learning from a Case Series.

Pseudohyperaldosteronism (PHA) is characterized by hypertension, hypokalemia, and a decrease in plasma renin and aldosterone levels. It can be caused by several causes, but the most frequent is due to excess intake of licorice. The effect is mediated by the active metabolite of licorice, glycyrrhetinic acid (GA), which acts by blocking the 11-hydroxysteroid dehydrogenase type 2 and binding to the mineralocorticoid receptor (MR) as an agonist. The management of licorice-induced PHA depends on several individual factors, such as age, gender, comorbidities, duration and amount of licorice intake, and metabolism. The clinical picture usually reverts upon licorice withdrawal, but sometimes mineralocorticoid-like effects can be critical and persist for several weeks, requiring treatment with MR blockers and potassium supplements. Through this case series of licorice-induced PHA, we aim to increase awareness about exogenous PHA, and the possible risk associated with excess intake of licorice. An accurate history is mandatory in patients with hypertension and hypokalemia to avoid unnecessary testing. GA is a component of several products, such as candies, breath fresheners, beverages, tobacco, cosmetics, and laxatives. In recent years, the mechanisms of action of licorice and its active compounds have been better elucidated, suggesting its benefits in several clinical settings. Nevertheless, licorice should still be consumed with caution, considering that licorice-induced PHA is still an underestimated condition, and its intake should be avoided in patients with increased risk of licorice toxicity due to concomitant comorbidities or interfering drugs.

Adipose tissue in cortisol excess: What Cushing's syndrome can teach us?

Endogenous Cushing's syndrome (CS) is a rare condition due to prolonged exposure to elevated circulating cortisol levels that features its typical phenotype characterised by moon face, proximal myopathy, easy bruising, hirsutism in females and a centripetal distribution of body fat. Given the direct and indirect effects of hypercortisolism, CS is a severe disease burdened by increased cardio-metabolic morbidity and mortality in which visceral adiposity plays a leading role. Although not commonly found in clinical setting, endogenous CS is definitely underestimated leading to delayed diagnosis with consequent increased rate of complications and reduced likelihood of their reversal after disease control. Most of all, CS is a unique model for systemic impairment induced by exogenous glucocorticoid therapy that is commonly prescribed for a number of chronic conditions in a relevant proportion of the worldwide population. In this review we aim to summarise on one side, the mechanisms behind visceral adiposity and lipid metabolism impairment in CS during active disease and after remission and on the other explore the potential role of cortisol in promoting adipose tissue accumulation.