Linked Life Data

233400

Source:http://linkedlifedata.com/resource/pubmed/id/233400

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1981-3-27
pubmed:abstractText
The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adrenocorticotropic Hormone, http://linkedlifedata.com/resource/pubmed/chemical/Cosyntropin, http://linkedlifedata.com/resource/pubmed/chemical/Hydrocortisone, http://linkedlifedata.com/resource/pubmed/chemical/Thyroid Hormones, http://linkedlifedata.com/resource/pubmed/chemical/Thyrotropin, http://linkedlifedata.com/resource/pubmed/chemical/Thyrotropin-Releasing Hormone, http://linkedlifedata.com/resource/pubmed/chemical/Thyroxine, http://linkedlifedata.com/resource/pubmed/chemical/Thyroxine-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Triiodothyronine, http://linkedlifedata.com/resource/pubmed/chemical/Triiodothyronine, Reverse, http://linkedlifedata.com/resource/pubmed/chemical/Zinc, http://linkedlifedata.com/resource/pubmed/chemical/adrenocorticotropin zinc
pubmed:status
MEDLINE
pubmed:issn
0001-5989
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-94
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1979
pubmed:articleTitle
Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH.
pubmed:publicationType
Journal Article