Funder J W
Baker Medical Research Institute, Victoria, Australia.
Endocrinol Metab Clin North Am. 1995 Sep;24(3):613-21.
Apparent mineralocorticoid excess is a congenital syndrome of sodium retention and hypertension with suppressed renin and aldosterone and normal cortisol levels. Patients with the syndrome have, however, highly abnormal levels of urinary cortisol to cortisone metabolites, indicating a reduced or absent activity of 11 beta-hydroxysteroid dehydrogenase 2, the enzyme responsible for conversion of cortisol to receptor-inactive cortisone. Very recently, the gene for 11 beta-hydroxysteroid dehydrogenase 2 was cloned, and mutations leading to absent or markedly reduced enzyme activity were found in 10 or 11 patients to date.
表观盐皮质激素增多症是一种先天性钠潴留和高血压综合征,伴有肾素和醛固酮受抑制且皮质醇水平正常。然而,该综合征患者尿中皮质醇与可的松代谢产物的水平异常高,这表明11β - 羟类固醇脱氢酶2的活性降低或缺失,该酶负责将皮质醇转化为无受体活性的可的松。最近,11β - 羟类固醇脱氢酶2的基因被克隆,迄今为止在10或11例患者中发现了导致酶活性缺失或显著降低的突变。