The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Correspondence
PreviousPrevious
Volume 340:1121-1122 April 8, 1999 Number 14
NextNext

Adrenal Lymphocytic Infiltration and Adrenocortical Tumors in a Patient with 21-Hydroxylase Deficiency

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

 Sign up for free e-toc
 

This Article
-Full Text
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
To the Editor: Congenital adrenal hyperplasia due to 21-hydroxylase deficiency results in deficient production of cortisol and aldosterone, chronic stimulation of the adrenal cortex by corticotropin, and overproduction of androgens. Cortisol-replacement therapy often fails to normalize corticotropin and androgen secretion, and high doses may be needed.1 Adrenocortical tumors, including cancers, are rare in patients with 21-hydroxylase deficiency but have been reported in patients with large adrenal glands and presumably inadequate cortisol therapy.2

A 16-year-old girl with 21-hydroxylase deficiency was evaluated for hirsutism and primary amenorrhea. She had a muscular habitus, hyperpigmentation, and a low voice. Physical examination revealed a beard, . . . [Full Text of this Article]

References


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.