THE PITUITARY-THYROID AXIS IN KLINEFELTER's SYNDROME

Abstract

Conventional thyroid function indices (serum T4 [thyroxine], T3 [triiodothyronine], TSH [thyrotropin] and thyroidal RAIU [radioactive I uptake] before and after TSH) appeared to be normal in most of 25 clinically euthyroid patients with chromatin positive Klinefelter''s syndrome. Administration of TRH [thyrotropin releasing hormone] revealed a decreased TSH reserve in the Klinefelter patients, both off or on testosterone treatment, in comparison to euthyroidal eugonadal male controls. Preliminary data suggest that this blunted TSH response to TRH is not a characteristic of Klinefelter''s syndrome per se but might be caused by the concurrent hypergonadotrophism. Despite the blunted TSH response, the TRH mediated T3 response in the Klinefelter patients was about equal to that in the male controls.