Winer R L, Rajudin M M, Skowsky W R, Parker L N
Metabolism. 1982 Mar;31(3):269-73. doi: 10.1016/0026-0495(82)90063-4.
A common endocrine defect in uremia is gonadal dysfunction with decreased testosterone production. Since gonadal and adrenal tissues share androgen biosynthetic pathways, we studied the stimulated adrenal androgen response in uremic patients. In contrast to the delayed or subnormal gonadal response to hCG reported by others, the adrenal response of androgens, as well as cortisol and aldosterone, to cosyntropin stimulation was unimpaired. In summary, the secretory reserve capacity of the adrenal gland for androgen, glucocorticoids and mineralocorticoids in uremia was studied with cosyntropin stimulation and found to be wall preserved.
尿毒症常见的内分泌缺陷是性腺功能障碍，睾酮生成减少。由于性腺和肾上腺组织共享雄激素生物合成途径，我们研究了尿毒症患者受刺激后的肾上腺雄激素反应。与其他人报道的对人绒毛膜促性腺激素（hCG）的性腺反应延迟或低于正常水平相反，雄激素以及皮质醇和醛固酮对促肾上腺皮质激素刺激的肾上腺反应未受损。总之，通过促肾上腺皮质激素刺激研究了尿毒症患者肾上腺对雄激素、糖皮质激素和盐皮质激素的分泌储备能力，发现其保存完好。
