KLINEFELTERS-SYNDROME - EFFECTS OF ESTROGEN ON GROWTH-HORMONE, PROLACTIN AND THYROTROPIN RELEASE, AND ON THYROTROPIN AND PROLACTIN RESPONSES TO THYROTROPHIN-RELEASING HORMONE

In 4 normal men and 8 patients with Klinefelter's syndrome the effects of oestradiol-17β (15 μg/kg daily for 8-13 days) on serum levels of pituitary hormones were investigated. Control levels of gonadotrophins in the Klinefelter patients were significantly higher than in the normal males, whereas serum testosterone (T) levels were lower. Oestradiol induced a decrease in serum gonadotrophin concentrations in both the control subjects and the Klinefelter patients, whereas a testosterone suppression was observed in the normal subjects, but not in the Klinefelter patients. Control serum growth hormone (hGH), and prolactin (hPRL) levels were of comparable magnitude in both groups and significantly increased during oestradiol administration. Serum thyrotrophin (TSH) levels were normal before and during oestrogen treatment. Basal serum oestradiol levels were within the normal male range, and were increased during treatment. Prolactin and thyrotrophin responsiveness to TRH stimulation was examined in Klinefelter patients before and during oestrogen administration. Before treatment, hPRL responses to TRH were higher than those observed in normal men. During oestrogen treatment hPRL responses to TRH were significantly increased when compared to those observed before and during treatment. These studies indicate that in patients with Klinefelter's syndrome pharmacological doses of oestrogen induce different effects on the hypothalamic-pituitary axis, as regards the release of gonadotrophins, prolactin, thyrotrophin, and growth hormone, similar to those observed in normal men. This fact supports the conclusion that in Klinefelter's syndrome the abnormality in the pituitary-gonadal feedback mechanism is selectively confined to the testosterone feedback control of gonadotrophin secretion. Finally, in patients with Klinefelter's syndrome, oestrogen is capable of inducing a significant increase of the hPRL response to TRH stimulation.