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Endocrine Reviews 18 (1): 135-156
Copyright © 1997 by The Endocrine Society

11ß-Hydroxysteroid Dehydrogenase and the Syndrome of Apparent Mineralocorticoid Excess1

Perrin C. White, Tomoatsu Mune2 and Anil K. Agarwal

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas Texas 75235-9063

I. Introduction
II. Biochemistry of Cortisol Metabolism
III. Mineralocorticoid Receptor Function
A. Actions of aldosterone
B. Structure and function of the mineralocorticoid receptor
C. Hypothesis: 11-HSD protects the mineralocorticoid receptor
IV. Loss of Function of 11-HSD
A. Syndrome of apparent mineralocorticoid excess (AME)
B. Licorice intoxication
C. Ectopic ACTH syndrome
D. Essential hypertension
E. Related conditions
V. Functional Roles of 11-HSD
A. Liver
B. Kidney and other mineralocorticoid target tissues
C. Brain
D. Circulatory system
E. Skin
F. Ovary
G. Placenta
H. Other fetal tissues
VI. The Type I (Liver) Isozyme of 11-HSD
A. Terminology
B. Biochemistry
C. Molecular biology
D. Expression
E. Lack of involvement in the syndromes of AME or 11-reductase deficiency
VII. The Type 2 (Kidney) Isozyme of 11-HSD
A. Biochemistry
B. Molecular biology
C. Expression
D. Mutations in HSD11B2 are detected in all patients with AME
VIII. Summary\.




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