Assuntos
Tumor de Células de Leydig/complicações , Puberdade Precoce/etiologia , Neoplasias Testiculares/complicações , Adolescente , Hormônio Liberador de Gonadotropina/sangue , Transtornos do Crescimento/etiologia , Humanos , Tumor de Células de Leydig/sangue , Tumor de Células de Leydig/patologia , Masculino , Neoplasias Testiculares/sangue , Neoplasias Testiculares/patologia , Testosterona/sangueAssuntos
Neoplasias das Glândulas Suprarrenais/complicações , Ginecomastia/etiologia , Neoplasias das Glândulas Suprarrenais/diagnóstico por imagem , Neoplasias das Glândulas Suprarrenais/metabolismo , Neoplasias das Glândulas Suprarrenais/patologia , Estradiol/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , RadiografiaRESUMO
The response of LH to exogenously administered estrogens was evaluated in a 63-year-old patient affected by complete testicular feminization syndrome (CTFS) with very low testosterone (T) levels, before and after gonadectomy. Prior to gonadectomy a durative fall in gonadotropin levels was observed after estrogen administration, without observing of an estrogenic positive feed-back (EPF) from LH. After gonadectomy, following an initial decrement in both gonadotropins, the characteristic. LH peak was seen, 48 h after E2B (Estradiol Benzoate) administration. This observation, together with the very low T levels that we found in this patient, prompted us to construe that absence of EPF in males is not due, as previously believed, to a direct inhibitory action of T or E2, deriving from T aromatization, on the hypothalamus, but by a still unknown gonadal factor. The hypothesis that this factor has a tubular origin is formulated and discussed.