2-YEAR COMPARISON OF TESTICULAR RESPONSES TO PULSATILE GONADOTROPIN-RELEASING HORMONE AND EXOGENOUS GONADOTROPINS FROM THE INCEPTION OF THERAPY IN MEN WITH ISOLATED HYPOGONADOTROPIC HYPOGONADISM
2-YEAR COMPARISON OF TESTICULAR RESPONSES TO PULSATILE GONADOTROPIN-RELEASING HORMONE AND EXOGENOUS GONADOTROPINS FROM THE INCEPTION OF THERAPY IN MEN WITH ISOLATED HYPOGONADOTROPIC HYPOGONADISM
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DOI：
10.1210/jcem-67-6-1140
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发表时间：
1988-12-01
影响因子：
5.8
通讯作者：
SHERINS, RJ
中科院分区：
文献类型：
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作者：
LIU, L;BANKS, SM;SHERINS, RJ
完全型单纯性低促性腺激素性腺功能减退症（初始平均睾丸体积< 4 mL）的男性需要2年或更长时间的外源性促性腺激素治疗，联合hCG和人绝经期促性腺激素（hMG），以达到最大但低于正常的睾丸大小和精子输出。为了测试脉冲式GnRH治疗（更接近于模拟正常激素刺激）是否会加速或进一步增加睾丸生长，加速精子产生的开始，和/或增加精子产量，我们从治疗开始就对2组可比较的完全性IHH男性给予hCG/hMG或GnRH。（初始睾丸体积，< 4 mL）并且比较它们在治疗的前2小时期间的睾丸反应。5名男性接受脉冲式GnRH治疗，剂量为143-714 ng/kg，每2小时皮下注射，而另外11名男性接受hCG（2000 IU）和hMG（75 IU FSH和75 IU LH）肌肉注射，每周3次。在GnRH治疗的男性中，平均血浆总睾酮和游离睾酮水平在治疗期间上升到正常范围内，但显著低于hCG/hMG治疗的男性（分别为P < 0.01和P < 0.02）。治疗期间的平均血浆雌二醇浓度在正常高值范围内，两组相似。促性腺激素释放激素（GnRH）治疗组的平均血浆FSH水平显著高于hCG/hMG治疗组（P < 0.01），是hCG/hMG治疗组的1.3 ~ 3.2倍。GnRH治疗组的平均睾丸大小与hCG/hMG治疗组无显著差异（P = 0.08）; GnRH和hCG/hMG组2年后的平均睾丸体积分别是治疗前的4.8倍和4.3倍。治疗12个月后，GnRH组中有1名男性产生精子，hCG/hMG组中无受试者产生精子。24个月后，GnRH组的两名男性和hCG/hMG组的八名男性产生了精子。因此，40%的GnRH治疗的平均值和80%的hCG/hMG治疗的男性（p = NS）在治疗2年后产生精子。所有男性的精子浓度均低于500万/mL，两组之间具有可比性（P = NS）。这些结果表明，与hCG/hMG治疗相比，前2年的脉冲式皮下GnRH治疗不会加速或增强睾丸生长，加速精子产生的开始，或显著增加精子产量。
Men with the complete form of isolated hypogonadotropic hypogonadism (initial mean testes volume < 4 mL) require 2 or more yr of exogenous gonadotropin therapy combining hCG and human menopausal gonadotropin (hMG) to achieve maximal, but subnormal, testis size and sperm output. To test whether pulsatile GnRH therapy, which more closely mimicks normal hormonal stimulation, would accelerate or further augment testicular growth, hasten the onset of sperm production, and/or increase sperm output more than occurs during conventional exogenous gonadotropin therapy, we administered either hCG/hMG or GnRH from the inception of therapy to 2 comparable groups of men with complete IHH (initial testicular volume, < 4 mL) and compared their testicular responses during the first 2 hr of therapy. Five men were treated with pulsatile GnRH in doses of 143-714 ng/kg every 2 h, sc. while 11 other men received hCG (2000 IU) and hMG (75 IU FSH and 75 IU LH) im 3 times/week. In the GnRH-treated men, the mean plasma total and free testosterone levels during therapy rose to within the normal range, but were significantly lower (P < 0.01 and P < 0.02, respectively) than those in the hCG/hMG-treated men. The mean plasma estradiol concentrations during therapy were within the high normal range and were similar in the two groups. The mean plasma FSH levels achieved in the GnRH-treated men were significantly (P < 0.01) and 1.3- to 3.2-fold higher than those in the hCG/hMG-treated men. The mean testicular size achieved in the GnRH-treated men was not significantly different form that in the hCG/hMG-treated men (P = 0.08); the mean testicular volumes after 2 yr were 4.8- and 4.3-fold the pretreatment values in the GnRH and hCG/hMG groups, respectively After 12 months of therapy, sperm production had occurred in one man in the GnRH group and in no subject in the hCG/hMG group. After 24 months, two men in the GnRH group and eight men in the hCG/hMG group produced sperm. Thus, 40% of the GnRH-treated mean and 80% of the hCG/hMG-treated men (p = NS) produced sperm after 2 yr of therapy. The sperm concentrations in all men were below 5 million/mL and were comparable in the two groups (P = NS). These results suggest that pulsatile sc GnRH therapy for the first 2 yr does not accelerate or enhance testicular growth, hasten the onset of sperm production, or increase sperm output significantly compared to hCG/hMG therapy.