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


     


Clinical Chemistry 54: 1246, 2008; 10.1373/clinchem.2008.108290
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 Web of Science
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
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Burman, K. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Burman, K. D.
Related Collections
Right arrow Clinical Case Studies
(Clinical Chemistry. 2008;54:1246.)
© 2008 American Association for Clinical Chemistry, Inc.


Clinical Case Studies

Commentary

Kenneth D. Burman

Endocrine Section, Washington Hospital Center, and Department of Medicine, Georgetown University, Washington, DC.

Address correspondence to the author at: Section of Endocrine, Washington Hospital Center, 110 Irving Street, NW, Room 2A-72, Washington, DC 20010-2975. Fax 202-877-6588; e-mail kenneth.d.burman@medstar.net

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

Discordant measurements of serum triiodothyronine (T4),1 thyroxine (T3), and thyroid-stimulating hormone (TSH) should always raise suspicions for unusual conditions. The clinical condition of the patient is especially relevant and should help guide further laboratory investigation. In the vast majority of instances, when a patient has authentic clinical hyperthyroidism with an increased T4 or T3, serum TSH should be low or undetectable (i.e., <0.01 mIU/L). Van Der Watt et al. nicely describe the possible causes of an increased serum free T4 (FT4) with a normal FT3 and TSH. I would like to emphasize several specific circumstances. A TSH-secreting pituitary tumor can mediate hyperthyroidism although serum TSH is low or normal (1). TSH bioactivity depends on proper glycosylation of the TSH molecule, and this may be altered in patients with a TSH-secreting pituitary tumor or a nonfunctional pituitary tumor (1). In . . . [Full Text of this Article]







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the American Association for Clinical Chemistry.