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Previous Volume 339:1787-1788 December 10, 1998 Number 24 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: Kidney 11-hydroxysteroid dehydrogenase 2 protects against mineralocorticoid excess by oxidatively converting cortisol, which binds to mineralocorticoid receptors as well as does aldosterone, to cortisone. Loss-of-function mutations in the gene for this enzyme cause the syndrome of apparent mineralocorticoid excess, with severe hypertension and hypokalemia.^1,2 Most patients with the syndrome can be treated effectively with mineralocorticoid-receptor antagonists, potassium-sparing diuretics, and dexamethasone. We describe a woman with apparent mineralocorticoid excess who was cured by renal transplantation.

Hypertension was diagnosed in a woman at 19 years of age, and apparent mineralocorticoid excess at 28 years of age because of . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Draper, N., Stewart, P. M (2005). 11{beta}-Hydroxysteroid dehydrogenase and the pre-receptor regulation of corticosteroid hormone action. J Endocrinol 186: 251-271 [Abstract] [Full Text]  
• Ferrari, P., Sansonnens, A., Dick, B., Frey, F. J. (2001). In Vivo 11{beta}-HSD-2 Activity: Variability, Salt-Sensitivity, and Effect of Licorice. Hypertension 38: 1330-1336 [Abstract] [Full Text]