BACKGROUND: Men with acquired hypogonadotropic hypogonadism (AHH) who desire restoration of fertility are treated with exogenous gonadotropin. However, gonadotropin (Gn) therapy does not always restore testicular function. It is unknown whether the therapeutic responses to Gn therapy correlate with their testicular histological findings. Thus, we analyzed factors influencing testicular dysfunction and therapeutic responses in AHH. METHODS: Of 21 men with AHH, 11 had no postmeiotic germ cells and were classified as the severe spermatogenic failure group. These were compared with the other 10 patients who had postmeiotic germ cells and comprised the mild spermatogenic failure group. RESULTS: Testicular volume and tubular diameter were significantly smaller, and the basement membrane and tunica propria were significantly thicker in the severe failure group. The gonadotropin basal level and response to exogenous gonadotropin-releasing hormone, and the testosterone response to exogenous human chorionic gonadotropin were significantly lower in the severe failure group of patients. Also, the recovery of spermatogenesis and testosterone secretory potentials was poor in the cases with a duration between diagnosis and treatment of 2 years or more. CONCLUSION: Longer periods without treatment may be responsible for irreversible testicular dysfunction in AHH. Gn therapy should be initiated very soon after the diagnosis of AHH if fertility is desired.
BACKGROUND:Men with acquired hypogonadotropic hypogonadism (AHH) who desire restoration of fertility are treated with exogenous gonadotropin. However, gonadotropin (Gn) therapy does not always restore testicular function. It is unknown whether the therapeutic responses to Gn therapy correlate with their testicular histological findings. Thus, we analyzed factors influencing testicular dysfunction and therapeutic responses in AHH. METHODS: Of 21 men with AHH, 11 had no postmeiotic germ cells and were classified as the severe spermatogenic failure group. These were compared with the other 10 patients who had postmeiotic germ cells and comprised the mild spermatogenic failure group. RESULTS: Testicular volume and tubular diameter were significantly smaller, and the basement membrane and tunica propria were significantly thicker in the severe failure group. The gonadotropin basal level and response to exogenous gonadotropin-releasing hormone, and the testosterone response to exogenous human chorionic gonadotropin were significantly lower in the severe failure group of patients. Also, the recovery of spermatogenesis and testosterone secretory potentials was poor in the cases with a duration between diagnosis and treatment of 2 years or more. CONCLUSION: Longer periods without treatment may be responsible for irreversible testicular dysfunction in AHH. Gn therapy should be initiated very soon after the diagnosis of AHH if fertility is desired.