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Nephrology
Published in John D Firth, Professor Ian Gilmore, MRCP Part 1 Self-Assessment, 2017
John D Firth, Professor Ian Gilmore
Liddle’s syndrome is caused by a mutation in the sodium channel (ENaC) in the distal nephron. The mutation keeps the channel open, which has a similar effect to a raised aldosterone level, including increased potassium excretion leading to hypokalaemia. Aldosterone levels are not raised and may be lowered as a result of feedback from sodium and water retention. The condition is sometimes called pseudohyperaldosteronism.
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].