Syndromes that Mimic an Excess of Mineralocorticoids
- PDF / 596,936 Bytes
- 5 Pages / 595.276 x 790.866 pts Page_size
- 38 Downloads / 193 Views
REVIEW ARTICLE
Syndromes that Mimic an Excess of Mineralocorticoids Chiara Sabbadin1 • Decio Armanini1
Received: 3 February 2016 / Accepted: 13 May 2016 Ó Springer International Publishing Switzerland 2016
Abstract Pseudohyperaldosteronism is characterized by a clinical picture of hyperaldosteronism with suppression of renin and aldosterone. It can be due to endogenous or exogenous substances that mimic the effector mechanisms of aldosterone, leading not only to alterations of electrolytes and hypertension, but also to an increased inflammatory reaction in several tissues. Enzymatic defects of adrenal steroidogenesis (deficiency of 17a-hydroxylase and 11b-hydroxylase), mutations of mineralocorticoid receptor (MR) and alterations of expression or saturation of 11-hydroxysteroid dehydrogenase type 2 (apparent mineralocorticoid excess syndrome, Cushing’s syndrome, excessive intake of licorice, grapefruits or carbenoxolone) are the main causes of pseudohyperaldosteronism. In these cases treatment with dexamethasone and/or MR-blockers is useful not only to normalize blood pressure and electrolytes, but also to prevent the deleterious effects of prolonged over-activation of MR in epithelial and nonepithelial tissues. Genetic alterations of the sodium channel (Liddle’s syndrome) or of the sodium-chloride co-transporter (Gordon’s syndrome) cause abnormal sodium and water reabsorption in the distal renal tubules and hypertension. Treatment with amiloride and thiazide diuretics can respectively reverse the clinical picture and the renin aldosterone system. Finally, many other more common situations can lead to an acquired pseudohyperaldosteronism, like the expansion of volume due to exaggerated water and/or sodium intake, and the use of drugs, as con-
& Decio Armanini [email protected] 1
Department of Medicine (DIMED), Endocrinology, University of Padua, Via Ospedale 105, 35128 Padua, Italy
traceptives, corticosteroids, b-adrenergic agonists and FANS. In conclusion, syndromes or situations that mimic aldosterone excess are not rare and an accurate personal and pharmacological history is mandatory for a correct diagnosis and avoiding unnecessary tests and mistreatments. Keywords Pseudohyperaldosteronism Aldosterone Mineralocorticoid receptor Hypertension 11 Hydroxysteroid dehydrogenase type 2 Apparent mineralocorticoid excess syndrome Deoxycorticosterone Licorice
1 Introduction Aldosterone is the main mineralocorticoid, whose action is regulated by the renin angiotensin system, by 11-hydroxysteroid dehydrogenase type 2 (HSD2) and by the mineralocorticoid receptor (MR). The epithelial effects of aldosterone are involved in the regulation of electrolyte and water balance and consequently of blood pressure. Several studies have also stressed the non-epithelial effects of aldosterone, playing a central role in the inflammatory processes. These effects are mediated not only by genomic mechanisms, involving the MR and 11-HSD2 (for example in hippocampus, heart, vessels and mononuclear leucocytes) [1], but
Data Loading...
