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Concise Publication Free access | 10.1172/JCI107166
1Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016
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1Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016
Find articles by Mitsuma, T. in: JCI | PubMed | Google Scholar
1Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016
Find articles by Hollander, C. in: JCI | PubMed | Google Scholar
Published January 1, 1973 - More info
The relative roles of triiodothyronine (T3) and thyroxine (T4) in modulating pituitary responsiveness to thyrotropin-releasing hormone (TRH) have been assessed. (a) 10 hyperthyroid patients with elevated serum T2 and T4 levels showed no pituitary response to TRH. After 2 wk of propylthiouracil therapy T4 levels had fallen to normal in only five patients while T2 levels were normal in all. Pituitary responsiveness to TRH returned in all patients with normal or high T4 concentrations. (b) Patients with isolated elevations of serum T3 (T3 toxicosis) failed to respond to TRH. TRH responsiveness was restored when T3 levels fell to normal after propylthiouracil therapy. (c) When pituitary responsiveness to TRH was tested 60 min after a single oral dose of 50 μg of T3, which increased serum T3 levels to slightly above the normal range, no rise in thyrotropin (TSH) was seen in six subjects. These findings indicate that T3 elevations alone can rapidly inhibit pituitary responsiveness to TRH.