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  • Title: [11 beta-Hydroxysteroid dehydrogenase (11-beta-OHSD): physiology and lack of action in pathology].
    Author: Vantyghem MC, Hober C, Racadot A, Lefebvre J.
    Journal: Ann Endocrinol (Paris); 1994; 55(6):271-7. PubMed ID: 7864584.
    Abstract:
    The 11 beta OHSD is an ubiquitous enzyme which inactivates cortisol to cortisone by transforming the hydroxyl group at the 11-carbon to a keto group. Therefore, it confers to mineralocorticoid receptors their selectivity toward their ligand and may constitute an important mechanism of regulation tissue-specific of the access of ligand toward its receptors. More widely the 11 beta OHSD would modulate glucocorticoid activity to their own receptor. There is no possibility to measure directly this enzyme and its deficiency is indirectly evaluated by enhancement of the quotient (THF + alpha THF)/THE after analysis of urinary steroid metabolites. Such enzymatic deficits may be congenital and are observed in childhood where they give an apparent mineralocorticoid excess (AME) syndrome (type 1). Sometimes acquired and reversible, they are due to licorice intoxication, hypothyroidism, chronic alcoholism and may be involved in the genesis of some cases of hypertension.
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