Pseudohyperaldosteronism due to mumijo consumption during pregnancy: a licorice-like syndrome
Published in Gynecological Endocrinology, 2018
Konstantinos Stavropoulos, Alexandros Sotiriadis, Dimitrios Patoulias, Konstantinos Imprialos, Roxani Dampali, Vasileios Athyros, Konstantinos Dinas
Pseudohyperaldosteronism is defined as the presence of clinical picture of hyperaldosteronism with suppression of renin and aldosterone levels, with well documented endogenous and exogenous causes. Inhibition of 11-hydroxysteroid dehydrogenase type 2 (11-HSD2), a high affinity NAD+-dependent unidirectional oxidase, leads to impaired inactivation of cortisol to cortisone and accumulation of cortisol [5]. Cortisol and aldosterone have similar affinity to the mineralocorticoid receptor (MR), but, as normal levels of cortisol are 100- to 1000-fold higher than those of aldosterone in plasma, it is easily induced that in cases of 11-HSD2 deficiency, cortisol levels are excessive, leading to much higher mineralocorticoid activity [6]. Cortisol binds to MR mainly in distal and cumulative nephron tubule, mediating water and sodium reabsorption, potassium loss, and consequently leading to hypertension, hypokalemia, and suppression of renin angiotensin aldosterone axis [7].