Kruse K, Sippell W G, Schnakenburg K V
J Clin Endocrinol Metab. 1984 Jan;58(1):12-7. doi: 10.1210/jcem-58-1-12.
Two unrelated boys with congenital adrenal hypoplasia were followed from birth for 20 yr. In spite of continuous treatment with hydrocortisone and fluorocortisone both patients had delayed growth and bone maturation since early childhood and failure of spontaneous puberty. Tests of the hypothalamic-pituitary function showed low basal plasma LH and FSH levels and blunted LH and FSH responses to standard GnRH tests and increased basal and TRH-stimulated PRL levels. Low dose pulsatile GnRH administration for 26 h, mimicking presumed physiological GnRH secretion, induced a continuing rise of plasma FSH in both patients and a slight increase of plasma LH and testosterone in one patient. These results indicate a hypothalamic origin of the gonadotropin deficiency with possible prenatal onset, since both patients had cryptorchidism during infancy. Hypogonadism in patients with adrenal hypoplasia may result from deficient steroid secretion of the hypoplastic fetal adrenals.
两名患有先天性肾上腺发育不全的无血缘关系男孩从出生起接受了20年的跟踪观察。尽管持续接受氢化可的松和氟氢可的松治疗,但两名患者自幼儿期起生长和骨骼成熟均延迟,且青春期自发启动失败。下丘脑 - 垂体功能测试显示基础血浆促黄体生成素(LH)和促卵泡生成素(FSH)水平低,对标准促性腺激素释放激素(GnRH)测试的LH和FSH反应迟钝,基础及促甲状腺激素释放激素(TRH)刺激后的催乳素(PRL)水平升高。模仿假定的生理性GnRH分泌,低剂量脉冲式GnRH给药26小时,使两名患者的血浆FSH持续升高,一名患者的血浆LH和睾酮略有增加。这些结果表明促性腺激素缺乏起源于下丘脑,可能在产前就已发病,因为两名患者在婴儿期均患有隐睾症。肾上腺发育不全患者的性腺功能减退可能是由于发育不全的胎儿肾上腺类固醇分泌不足所致。