Delemarre-Van de Waal H A
Department of Pediatrics, Free University Hospital, Amsterdam, The Netherlands.
Clin Endocrinol (Oxf). 1993 May;38(5):473-80. doi: 10.1111/j.1365-2265.1993.tb00342.x.
To induce testicular growth including spermatogenesis, 38 patients with hypogonadotrophic hypogonadism were treated with long-term pulsatile GnRH administration.
The group of patients comprised 17 individuals with idiopathic hypogonadotrophic hypogonadism, 11 with Kallmann's syndrome, four with multiple pituitary hormone deficiencies and six with a secondary hypogonadotrophic hypogonadism due to surgical removal of a brain tumour. Thirteen patients (seven with idiopathic hypogonadotrophic hypogonadism and six with Kallmann's syndrome) had undescended testes, of whom six had undergone surgery on both testes and four on one testis. Sixteen of the 17 had previously received androgen therapy and six others had received gonadotrophin treatment, of whom three had long-term treatment to induce testicular development, without success.
GnRH was administered intravenously in a dose of 2-20 micrograms per pulse every 90 minutes. After GnRH discontinuation, hCG treatment was instituted, 1500-3000 IU (i.m.) twice weekly.
During treatment plasma levels of LH, FSH and testosterone increased. In 35 out of the 38 patients plasma testosterone levels increased into the normal adult range. In all patients testicular volume increased. Mean pretreatment testicular volume per patient group ranged from 2.4 to 4.8 ml and increased to 11.5-18.1 ml by the end of treatment. There was a significant difference in the achieved testicular volumes between the patients with Kallmann's syndrome and the brain tumour patients. GnRH treatment mean lasted between 46 and 75 weeks in the different groups. On hCG therapy, testicular development was either maintained or improved. Semen analysis revealed the presence of spermatogenesis in 31 out of the 38 patients (26 patients already on GnRH, and in another five patients on hCG therapy). All three patients pretreated with gonadotrophins as well as three patients with bilateral testicular surgery developed a detectable sperm count. In 19 adolescent patients with growth potential, an adequate height velocity was observed during GnRH treatment.
GnRH is a feasible way to induce testicular growth as well as spermatogenesis in hypogonadotrophic male patients, even in patients in whom gonadotrophin treatment has failed. After GnRH treatment, hCG alone can maintain or even improve testicular development, including spermatogenesis. GnRH treatment may also induce a physiological growth spurt in hypogonadotrophic adolescents.
为诱导睾丸生长包括精子发生，对38例低促性腺激素性性腺功能减退患者进行了长期脉冲式GnRH给药治疗。
该组患者包括17例特发性低促性腺激素性性腺功能减退患者、11例卡尔曼综合征患者、4例多种垂体激素缺乏患者以及6例因脑肿瘤手术切除导致继发性低促性腺激素性性腺功能减退患者。13例患者（7例特发性低促性腺激素性性腺功能减退患者和6例卡尔曼综合征患者）有隐睾，其中6例双侧睾丸均接受过手术，4例单侧睾丸接受过手术。17例患者中有16例之前接受过雄激素治疗，另外6例接受过促性腺激素治疗，其中3例接受过长期治疗以诱导睾丸发育但未成功。
GnRH以每90分钟2 - 20微克/脉冲的剂量静脉给药。停止GnRH治疗后，开始hCG治疗，1500 - 3000 IU（肌肉注射），每周两次。
治疗期间，LH、FSH和睾酮的血浆水平升高。38例患者中有35例血浆睾酮水平升至正常成人范围。所有患者睾丸体积均增大。每个患者组治疗前平均睾丸体积为2.4至4.8毫升，治疗结束时增至11.5 - 18.1毫升。卡尔曼综合征患者和脑肿瘤患者的睾丸体积增量存在显著差异。不同组中GnRH治疗平均持续46至75周。在hCG治疗时，睾丸发育得以维持或改善。精液分析显示38例患者中有31例存在精子发生（26例已接受GnRH治疗，另外5例接受hCG治疗）。所有3例之前接受过促性腺激素预处理的患者以及3例接受双侧睾丸手术的患者精子计数可测。在19例有生长潜力的青少年患者中，GnRH治疗期间观察到足够的身高增长速度。
GnRH是诱导低促性腺激素性男性患者睾丸生长及精子发生的可行方法，即使是促性腺激素治疗失败的患者。GnRH治疗后，单独使用hCG可维持甚至改善睾丸发育，包括精子发生。GnRH治疗还可能诱导低促性腺激素性青少年出现生理性生长突增。
