during maturation leads to impaired or absent spermatogenesis in male rats (53). Furthermore, GH and growth factors, such as insulin-like growth factor-1 (IGF-1), epidermal growth factor (EGF), and transforming growth factor (TGF), influence testicular steroid production and secretion (54-56). In mice, the testicular steroidogenic response to chorionic gonadotropins stimulation was increased by GH and IGF-1 treatment (54), and an effect of GH on Leydig cell function was also shown in prebu-bertal boys (57). Because testosterone secretion by Leydig cells is necessary for sper-matogenesis, a complementary or permissive role of GH in the induction of spermatogenesis by gonadotropins in patients with hypogonadotropic hypogonadism who failed gonadotropin therapy alone has been suggested. Indeed, in an open trial, in three of four patients with hypogonadotropic hypogonadism who remained azoosper-mic during treatment with hCG/hMG for 12 wk, spermatogenesis was induced after GH was added for a further 12 wk. Additionally, serum IGF-1 and testosterone levels rose (58). However, these patients had a pretreatment testicular volume of less than 4 mL, and sperm production may have occurred if gonadotropin treatment had been prolonged without added GH. Further studies of combined gonadotropin/GH treatment of patients with hypogonadotropic hypogonadism who remained azoospermic during gonadotropin treatment confirmed the increase in IGF-1 and testosterone levels, but, although testicular volume increased, spermatogenesis was not induced (59). Similarly, in 11 adult men who were gonadotropin deficient because of surgery for a pituitary lesion, treatment with recombinant GH increased IGF-1 and testosterone levels and seminal plasma volume, but sperm count and motility did not change (60). Taken together, the addition of GH to gonadotropin treatment has no convincing beneficial effect on spermatogenesis in patients with hypogonadotropic hypogonadism and is, therefore, not recommended.
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