KLINEFELTER'S SYNDROME: EFFECTS OF OESTROGEN ON GROWTH HORMONE, PROLACTIN AND THYROTROPHIN RELEASE, AND ON THYROTROPHIN AND PROLACTIN RESPONSES TO THYROTROPHIN-RELEASING HORMONE

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Abstract
In 4 normal men and 8 patients with Klinefelter''s syndrome the effects of estradiol-17.beta. (15 .mu.g/kg daily for 8-13 days) on serum levels of pituitary hormones were investigated. Control levels of gonadotropins in the Klinefelter patients were significantly higher than in the normal males, whereas serum testosterone (T) levels were lower. Estradiol induced a decrease in serum gonadotropin concentrations in the control subjects and the Klinefelter patients, whereas a T suppression was observed in the normal subjects, but not in the Klinefelter patients. Control serum growth hormone (GH), and prolactin (PRL) levels were of comparable magnitude in both groups and significantly increased during estradiol administration. Serum thyrotropin (TSH) levels were normal before and during estrogen treatment. Basal serum estradiol levels were within the normal male range, and were increased during treatment. PRL and TSH responsiveness to TRH [thyrotropin releasing hormone] stimulation was examined in Klinefelter patients before and during estrogen administration. Before treatment, PRL responses to TRH were higher than those observed in normal men. During estrogen treatment PRL responses to TRH were significantly increased when compared to those observed before treatment. TSH responses to TRH were normal both before and during treatment. In patients with Klinefelter''s syndrome pharmacological doses of estrogen induce different effect on the hypothalamic-pituitary axis, as regards the release of gonadotropins, PRL, TSH and GH, similar to those observed in normal men. In Klinefelter''s syndrome the abnormality in the pituitary-gonadal feedback mechanism is selectively confined to the T feedback control of gonadotropin secretion. Finally, in patients with Klinefelter''s syndrome, estrogen is capable of inducing a significant increase of the PRL response to TRH stimulation.