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  • Title: Apparent mineralocorticoid excess syndromes.
    Author: Shimojo M, Stewart PM.
    Journal: J Endocrinol Invest; 1995; 18(7):518-32. PubMed ID: 9221270.
    Abstract:
    Apparent mineralocorticoid excess (AME) is a syndrome attributable to congenital deficiency of the enzyme 11 beta-dehydrogenase (11 beta-OHSD) which converts active glucocorticoid cortisol to inactive cortisone. When 11 beta-OHSD activity is impaired, cortisol acts as a potent mineralocorticoid and causes hypertension and hypokalemia with a suppression of the renin-angiotensin-aldosterone system. The increased ratio of urinary cortisol/cortisone metabolites and a prolonged half-life of cortisol are useful for the diagnosis. Dexamethasone and/or potassium sparing diuretics have been used for medication of AME. Licorice ingestion induces a mineralocorticoid excess state, and it seems that this is the result of acquired inhibition of 11 beta-DH by glycyrrhetinic acid. The existence of a second 11 beta-OHSD isoform has been suggested strongly for a long time, and recently, a human 11 beta-OHSD 2 cDNA has been isolated. It appears that 11 beta-OHSD 2 conveys specificity upon the renal MR, and a defect in its activity seems likely to account for the phenotype of AME.
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