Foster C M, Hopwood N J, Beitins I Z, Mendes T M, Kletter G B, Kelch R P
Department of Pediatrics, University of Michigan Medical School, Ann Arbor.
J Pediatr. 1992 Oct;121(4):528-32. doi: 10.1016/s0022-3476(05)81139-4.
We hypothesized that prepubertal girls with gonadotropin deficiency would produce less follicle-stimulating hormone (FSH) in response to synthetic gonadotropin-releasing hormone (GnRH) than would gonadotropin-sufficient children. To test this hypothesis, we performed 103 GnRH tests serially in 21 children who had idiopathic hypopituitarism with growth hormone deficiency. We tried to predict whether puberty would occur in the 17 girls with bone ages of 8 years or less. Of these 17 girls, 4 failed to have spontaneous secondary sexual characteristics by age 16 1/2 years, and 12 had spontaneous complete pubertal development. One girl had incomplete pubertal maturation with partial gonadotropin deficiency; her results were combined with those of the girls who had no spontaneous pubertal development. With increasing bone age, the girls with complete pubertal development had a decrease in the increment of FSH released in response to GnRH, although basal gonadotropin concentrations did not change. For GnRH tests performed at bone ages of 8 years or less, basal luteinizing hormone (LH) values did not differ between girls with complete puberty and those with absent or incomplete puberty. However, basal FSH and the incremental response of LH and FSH to GnRH were greater in those with complete puberty. Only two girls with prepubertal bone ages at the time of testing, who subsequently had complete puberty, had incremental FSH responses to GnRH that were less than 5 IU/L. Individual incremental LH responses to GnRH did not discriminate well between groups. None of the girls with adrenocorticotropic hormone deficiency, either originally or subsequently, had spontaneous puberty, but 4 of 12 girls with thyrotropin deficiency, either originally or subsequently, had complete puberty. We conclude that a significant increase in GnRH-stimulated FSH suggests that spontaneous pubertal development will occur in girls with idiopathic hypopituitarism. However, a low FSH response to GnRH may not be diagnostic of gonadotropin deficiency.
我们假设，与促性腺激素水平正常的儿童相比，患有促性腺激素缺乏症的青春期前女孩对合成促性腺激素释放激素（GnRH）产生的促卵泡生成素（FSH）会更少。为了验证这一假设，我们对21名患有特发性垂体功能减退伴生长激素缺乏症的儿童连续进行了103次GnRH测试。我们试图预测17名骨龄为8岁或更小的女孩是否会进入青春期。在这17名女孩中，4名在16.5岁时未出现自发性第二性征，12名有自发性完全性青春期发育。一名女孩青春期发育不完全，伴有部分促性腺激素缺乏；她的结果与那些没有自发性青春期发育的女孩的结果合并。随着骨龄增加，完全性青春期发育的女孩对GnRH反应释放的FSH增量有所下降，尽管基础促性腺激素浓度没有变化。对于在骨龄8岁或更小的时候进行的GnRH测试，完全性青春期发育的女孩与青春期缺失或不完全的女孩之间，基础促黄体生成素（LH）值没有差异。然而，完全性青春期发育的女孩的基础FSH以及LH和FSH对GnRH的增量反应更大。在测试时骨龄处于青春期前且随后进入完全性青春期的女孩中，只有两名对GnRH的FSH增量反应小于5 IU/L。个体对GnRH的LH增量反应在不同组之间没有很好的区分度。最初或随后患有促肾上腺皮质激素缺乏症的女孩均无自发性青春期，但最初或随后患有促甲状腺激素缺乏症的12名女孩中有4名进入了完全性青春期。我们得出结论，GnRH刺激的FSH显著增加表明特发性垂体功能减退的女孩会出现自发性青春期发育。然而，对GnRH的FSH反应低可能不能诊断为促性腺激素缺乏。
