Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Clinical Chemistry 55: 1908-1909, 2009; 10.1373/clinchem.2009.133769
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Hortin, G. L.
Right arrow Articles by Winter, W. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hortin, G. L.
Right arrow Articles by Winter, W. E.
(Clinical Chemistry. 2009;55:1908-1909.)
© 2009 American Association for Clinical Chemistry, Inc.


Commentaries

Commentary

Glen L. Hortina, Neil S. Harris and William E. Winter

Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL.

aAddress correspondence to this author at: Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610. E-mail ghortin@pathology.ufl.edu.

The first 20% of the full text of this article appears below.

This case illustrates that initial laboratory results suggestive of SIADH do not rule out other potential causes of hyponatremia, such as hypothyroidism and hypocortisolism. To date, SIADH has been a diagnosis of exclusion, but advances in mass spectrometry offer prospects for accurately measuring ADH in the future.

When analyzers yield low sodium values, an initial priority is to exclude factitious hyponatremia. When sodium is measured by . . . [Full Text of this Article]







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the American Association for Clinical Chemistry.