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
 
Editorial
PreviousPrevious
Volume 356:2321-2322 May 31, 2007 Number 22
NextNext

Alternative-Pathway Therapy for Hyperammonemia
Vivian E. Shih, M.D.

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
- PDF
-PDA Full Text
-Purchase this article

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

More Information
-Related Article
 by Enns, G. M.
-PubMed Citation
Ammonia is a toxic compound produced in the body from the catabolism of amino acids and protein. Hyperammonemia can damage muscle and brain.1 The body converts ammonia to urea in the liver by means of the urea-cycle enzymes, and the urea so generated is subsequently eliminated in the urine as nitrogenous waste. This essential process is necessary for the maintenance of health.

Metabolic disorders are associated with a defect or deficiency of each of the six enzymes in the urea cycle (Figure 1). These inborn errors of metabolism disrupt the normal processing of ammonia and result in hyperammonemia. . . . [Full Text of this Article]


Source Information

From the Amino Acid Disorder Laboratory, Massachusetts General Hospital, Boston.




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.