help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cobb, W. E.
Right arrow Articles by Jackson, I. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cobb, W. E.
Right arrow Articles by Jackson, I. M.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*LIOTHYRONINE
Medline Plus Health Information
*Pituitary Disorders

Journal of Clinical Endocrinology & Metabolism, Vol 52, 324-329, Copyright © 1981 by Endocrine Society

ARTICLES

Growth hormone secretory status is a determinant of the thyrotropin response to thyrotropin-releasing hormone in euthyroid patients with hypothalamic-pituitary disease

WE Cobb, S Reichlin and IM Jackson

To assess the influence of endogenous GH secretion on the TSH and T3 responses to TRH administration in patients with hypothalamic-pituitary disease, we analyzed tests in a selected group of 26 euthyroid patients with hypothalamic-pituitary disease and in 15 normal controls. Basal TSH levels and the TSH response to TRH were significantly greater in GH- deficient patients (group 1) than in patients with normal anterior pituitary function and unimpaired GH reserve (group II). However, the T3 response to TRH was significantly less in group 1 than in group II patients. In acromegaly (group III), the TSH response to TRH was blunted, while basal and stimulated T3 levels were no different compared to control levels. These findings suggest that endogenous GH depresses the TSH response to TRH while enhancing the thyroid secretion of T3 in response to the evoked TSH released.


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
K. H. Darzy and S. M. Shalet
Circadian and Stimulated Thyrotropin Secretion in Cranially Irradiated Adult Cancer Survivors
J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6490 - 6497.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
Y. Debaveye, B. Ellger, L. Mebis, E. Van Herck, W. Coopmans, V. Darras, and G. Van den Berghe
Tissue Deiodinase Activity during Prolonged Critical Illness: Effects of Exogenous Thyrotropin-Releasing Hormone and Its Combination with Growth Hormone-Releasing Peptide-2
Endocrinology, December 1, 2005; 146(12): 5604 - 5611.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
S. Porretti, C. Giavoli, C. Ronchi, G. Lombardi, M. Zaccaria, D. Valle, M. Arosio, and P. Beck-Peccoz
Recombinant Human GH Replacement Therapy and Thyroid Function in a Large Group of Adult GH-Deficient Patients: When Does L-T4 Therapy Become Mandatory?
J. Clin. Endocrinol. Metab., May 1, 2002; 87(5): 2042 - 2045.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
D. T. Wyatt, N. Gesundheit, and B. Sherman
Changes in Thyroid Hormone Levels during Growth Hormone Therapy in Initially Euthyroid Patients: Lack of Need for Thyroxine Supplementation
J. Clin. Endocrinol. Metab., October 1, 1998; 83(10): 3493 - 3497.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1981 by The Endocrine Society