Effect of Acute Increases in Serum Triiodothyronine on TSH and Prolactin Responses to TRH, and Estimates of Pituitary Stores of TSH and Prolactin in Normal Subjects and in Patients with Primary Hypothyroidism
- 1 March 1976
- journal article
- clinical trial
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 42 (3) , 443-458
- https://doi.org/10.1210/jcem-42-3-443
Abstract
Previous investigators have shown that daily administration of TRH to normal individuals leads to diminishing TSH responses, which were believed due to rising serum T3 with subsequent feedback inhibition of the pituitary. Patients with primary hypothyroidism were examined in the present study to test this hypothesis, since their T3 cannot increase after TRH. Bi-daily TRH (100 μg) was given to 4 patients for 3 consecutive days, and repeated on a 4th day following oral T3 (50 μg). TSH and PRL responses were unchanged during these 3 days of serial TRH and were unaltered by T3 administration on the fourth day. In 5 other hypothyroid subjects studied before and during 3 consecutive days of T3 administration, TSH but not PRL responses to TRH appeared to decrease slowly but progressively. These observations led us to re-examine TRH responses in normal subjects given T3, since other workers had reported that 50 μg T3 completely abolished TSH response. Responses to TRH in 11 normals on a control day were compared to those observed 1 hour after oral T3. In spite of marked increases in serum T3, there was no significant difference between the mean TSH responses of the two studies. TRH was administered by continuous infusion (1 μg/min) for 6 hours in 5 normal subjects. PRL and TSH responses peaked within 60 and 180 minutes, respectively, and then plateaued. To ascertain whether this plateau effect was due to increases in T3, similar infusions were given to 5 hypothyroid patients, and a similar pattern of response was observed, suggesting that the plateau phase was not due to increases in serum T3. The total amount of TSH and PRL discharged during TRH infusion was estimated, and served as an index of pituitary content of these hormones. In the 5 normal subjects, total daily net TSH and PRL release averaged 123 mU and 197 μg, respectively. These estimates are consistent with direct analyses by others of PRL and TSH content in the human pituitary. In 5 hypothyroid patients, readily dischargeable TSH and PRL content averaged 640 mU and 307 μg, respectively. We conclude that: 1) acute increases in serum T3 do not suppress TRH-stimulated TSH or PRL secretion in either normal or hypothyroid subjects; 2) the decline and subsequent plateau in TSH and PRL levels during continuing TRH stimulation are related to factors governing de novo synthesis and release, rather than to rising T3 levels; 3) integration of the earily peak TSH and PRL responses to continuous TRH infusion may serve as a useful tool for the estimation of pituitary content of these hormones in vivo.Keywords
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