Vaughan Williams C A, McNeilly A S, Baird D T
Clin Endocrinol (Oxf). 1983 Jul;19(1):9-19. doi: 10.1111/j.1365-2265.1983.tb00737.x.
Twenty women with secondary hypogonadism and four normal women in the early follicular phase of the cycle were treated for 7 days with 10, 50 or 100 micrograms synthetic LHRH administered intramuscularly at 4 h intervals. Concentrations of pituitary and ovarian hormones in plasma were measured at intervals during the treatment period. The episodic pattern of LH secretion and the gonadotrophin responses to acute stimulation with LHRH were evaluated before and after treatment. In normal women the concentrations of gonadotrophins and the LH response to LHRH remained unchanged, whilst the FSH response to LHRH was reduced after treatment. Concentrations of oestradiol rose progressively in response to treatment, indicating follicular development. In hypogonadal subjects with unimpaired pituitary function, treatment with LHRH induced a marked but transient increase in the concentrations of LH and FSH in plasma and a progressive rise in that of oestradiol. The concentration of progesterone was increased in four of the 11 subjects. However, the amplitude of LH pulses and the responses of FSH and LH to LHRH after treatment were suppressed below pretreatment values. Women with hypogonadotrophic hypogonadism and diminished pituitary responses to LHRH exhibited a sustained increase in the concentrations of LH, FSH and oestradiol in plasma to normal follicular phase levels. The amplitude of LH pulses and the LH response to LHRH were increased after treatment but did not reach normal values. The FSH response to LHRH was further reduced after treatment. Treatment of similar subjects with 10 micrograms LHRH induced a small increase in the concentration of gonadotrophins but not of ovarian steroids. These data demonstrate that the effect of chronic treatment with LHRH on women with secondary hypogonadism depends on the level of endogenous gonadotrophins. The dose of LHRH used in hypogonadal women receiving treatment by intermittent injection may require adjusting according to the level of gonadotrophin secretion if an optimal response is to be obtained.
20名继发性性腺功能减退的女性和4名处于月经周期卵泡早期的正常女性，接受了为期7天的治疗，每隔4小时肌肉注射10、50或100微克合成促黄体生成素释放激素（LHRH）。在治疗期间，定期测量血浆中垂体和卵巢激素的浓度。在治疗前后评估促黄体生成素（LH）分泌的脉冲模式以及促性腺激素对LHRH急性刺激的反应。在正常女性中，促性腺激素的浓度以及LH对LHRH的反应保持不变，而治疗后FSH对LHRH的反应降低。雌二醇的浓度随着治疗逐渐升高，表明卵泡发育。在垂体功能未受损的性腺功能减退受试者中，LHRH治疗导致血浆中LH和FSH浓度显著但短暂升高，以及雌二醇浓度逐渐升高。11名受试者中有4名孕酮浓度升高。然而，治疗后LH脉冲的幅度以及FSH和LH对LHRH的反应被抑制到治疗前值以下。伴有低促性腺激素性性腺功能减退且垂体对LHRH反应减弱的女性，血浆中LH、FSH和雌二醇的浓度持续升高至正常卵泡期水平。治疗后LH脉冲的幅度以及LH对LHRH的反应增加，但未达到正常值。治疗后FSH对LHRH的反应进一步降低。用10微克LHRH治疗类似受试者会导致促性腺激素浓度小幅升高，但不会使卵巢甾体激素浓度升高。这些数据表明，LHRH长期治疗对继发性性腺功能减退女性的影响取决于内源性促性腺激素的水平。如果要获得最佳反应，接受间歇性注射治疗的性腺功能减退女性使用的LHRH剂量可能需要根据促性腺激素分泌水平进行调整。
