Effect of Testosterone in the Recovery of Spermatogenesis in Hypophysectomized Patients

A group of adult hypophysectomized patients (due to cromophobe adenoma) was studied at different periods of time after operation. All of them showed loss of libido and potentia, low levels of urinary FSH and LH and of testosterone glucoronide. Daily doses of corticoids and thyroid hormone were administered. Testis biopsies were taken before and after each one of the following courses of treatment. The 14 patients were divided into 5 different groups. Group I, comprising 3 patients, was treated first with HMG (Pergonal-500, 3 ampoules per week) combined with HCG (3,000 IU per week). After 16 weeks, HMG continued to be administered, but HCG was discontinued and replaced by testosterone propionate at different weekly doses in each patient (200, 100 or 50 mg) during another 16 weeks. The 3 patients of group II were first administered HMG (similar dose and period of time as above) and then with HMG combined with testosterone (200, 100 or 50 mg, respectively). The 3 patients of group III were first treated with HCG in similar dose and period of time as above, and then with HCG combined with testosterone in similar dose and period of time as above. The 3 patients of group IV were given testosterone alone in similar doses and period of time as above. Finally, the 2 patients of group V were used as controls and no gonadotropins or testosterone treatment were administered during the period of the research. The following was observed: (1) HMG combined with HCG induced restoration of full spermatogenesis, development of mature Leydig cells and regression of preexistent peritubular hyalinosis. HMG alone showed a partial recovery of Leydig cells and of spermatogenesis until spermatid stages. HCG induced development of germinal cells until middle meiosis process and complete development of Leydig cells. (2) When testosterone was added to HMG or to HCG, an inhibitory effect was noted as judged by the regression of spermatogenesis and Leydig cells development, which was accompanied by reappearance of peritubular hyalinosis. The intensity of this inhibitory effect was dose-dependent. When testosterone was given alone, an almost complete atrophy of seminiferous tubules and Leydig cells was present. (3) The probable mechanism of action of testosterone upon the endogenously circulating or exogenously administred gonadotropins is discussed.