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The Thyrotropin (TSH) Profile in Isolated Gonadotropin Deficiency: A Model to Evaluate the Effect of Sex Steroids on TSH Secretion^*

Population Council New York, New York 10021
the Department of Endocrinology and Metabolism, Shaare Zedek Medical Center and the Hebrew University, Hadassah Medical School Jerusalem, Israel

Address all correspondence and requests for reprints to: I. M. Spitz, M.D., Population Council, 1230 York Avenue, New York, New York 10021.

This study evaluated the effect of estrogens and androgens on TSH secretion in hypogonadal male and female patients with isolated gonadotropin deficiency (IGD). The IGD subjects were clinically euthyroid and had normal circulating levels of thyroid hormones and T₄-binding globulin (TBG). The patients were challenged with TRH (200 µg) in the untreated state, during treatment, and 1 month after cessation of hormonal replacement therapy. For the study, five females were treated with ethinyl estradiol (0.05 mg twice daily) for 21 days; after stopping for 7 days, the treatment schedule was repeated for another two cycles. The remaining female was given a similar regimen with conjugated estrogens (0.625 mg daily). Five males were treated with hCG (5000IU twice weekly) for 3 months; two were treated with hCG and Pergonal. The female patients had significantly decreased basal TSH levels as well as impaired TSH responses to TRH. After 3 months of ethinyl estradiol treatment, there was a rise in TBG, total serum T₄ and T₃ levels and a decrease in T₃ resin uptake; the free T₄ index was unchanged. During estrogen administration, there was no change in basal TSH, but there was an increase in the peak TSH response to TRH, which became identical to that of the controls. Cessation of estrogen was associated with areduction in releasable TSH, and the profile reverted to the pretreatment state. In addition, serum TBG levels, with the associated changes in thyroid hormones, also returned to normal.

The male patients had TSH responses to TRH identical to those of the male controls. After 3 months of hCG treatment, there was a marked rise in serum estradiol as well as testosterone. Serum T₄ was reduced without a change in T₃, T₃ resin uptake,or TBG. Furthermore, there was no alteration in the TSH response to TRH. On the other hand, the administration of ethinyl estradiol (0.1 mg daily for 2 weeks) to two male IGD subjects produced an increase in TBG. This was associated with elevation of serum T₄ and T₃ levels and reduction of T₃ resin uptake. During estradiol administration, there was an increase in the TSH response to TRH.

These data are compatible with the hypothesis that estrogens are required to maintain a normal TSH response to TRH in the female. However, testosterone may counteract the effect of estradiol, which may explain why normal males tend to have a lower TSH response to TRH than females.

^* This work was supported by a grant (to I.M.S.) from the Chief Scientist’s Office, Ministry of Health, Israel.

Received September 27, 1982.

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