This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Kenneth D. Burman, MD

JAMA. 1996;275(9):723-724.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

There have been significant advances in our understanding of thyroid pathophysiology as well as in our ability to measure thyroid-stimulating hormone (TSH), total and free triiodotriiodo- (T₃), and thyroxine (T₄).¹ The thyroid gland normally produces approximately 90 µg of T₄ and 40 µg of T₃ daily; all of circulating T₄ is derived from direct thyroidal secretion, whereas about 85% of T₃ comes from extra thyroidal conversion of T₄ to T₃, with only about 15% of T₃ being produced by direct thyroidal secretion. Over 99% of circulating T₄ and T₃ are bound to serum-binding proteins, and it is only the small unbound fraction that is biologically active. Thyroxine is mainly a prohormone, and T₃ is responsible for most if not all of the biological activity attributable to thyroid hormone. In many clinical situations, including systemic illness, surgery, and . . . [Full Text PDF of this Article]

Author Affiliations
From the Endocrinology Division, Washington Hospital Center, and the Endocrine Division, George Washington University Medical Center, Washington, DC.

Footnotes
Reprint requests to Chief, Endocrine Section, Washington Hospital Center, Washington, DC 20010 (Dr Burman).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?