Krieger D T, Luria M
J Clin Endocrinol Metab. 1977 Feb;44(2):361-8. doi: 10.1210/jcem-44-2-361.
The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease. TRF administration was associated with a mean increment of 267 pg/ml in plasma ACTH concentrations in patients with Nelson's syndrome, and of 42 pg/ml in patients with Cushing's disease. The increment in plasma cortisol concentrations in the latter group was 12 mug%. No ACTH or cortisol response was observed in normal subjects. Patients with Cushing's disease or Nelson's syndrome exhibited significantly greater increments in plasma ACTH concentrations in response to vasopressin administration (P less than .05, P less than .02 respectively) than did normal subjects; the increment in cortisol concentration was also greater, (P less than .05), in patients with Cushing's disease than in normal subjects. No significant difference was present between patients with Cushing's disease and Nelson's syndrome with regard to the magnitude of the ACTH response to vasopressin administration. In contrast, the increment in plasma cortisol and plasma ACTH concentrations following insulin induced hypoglycemia was significantly less in patients with Cushing's disease than seen in normal subjects, (P less than .001, P less than .05 respectively); while this stimulus was associated with a significantly greater increment in plasma ACTH concentrations in patients with Nelson's syndrome as compared to that seen in normal subjects, (P less than .01) and in patients with Cushing's disease (P less than .01). These findings indicate that pituitary function in patients with Nelson's syndrome is not autonomous and suggest the possibility that altered central nervous regulatory mechanism might play a role in the etiology of the pituitary tumors which are frequently associated with this syndrome. The TRF induced rise in plasm cortisol and ACTH concentrations in patients with Cushing's disease and Nelson's syndrome suggests the possibility of altered hypothalamic or pituitary receptors in such patients.
对5例纳尔逊综合征患者和12例未经治疗的库欣病患者测定了血浆促肾上腺皮质激素（ACTH）和/或皮质醇浓度对促甲状腺激素释放因子（TRF）、血管加压素和胰岛素给药的反应。给予TRF后，纳尔逊综合征患者血浆ACTH浓度平均升高267 pg/ml，库欣病患者平均升高42 pg/ml。后一组患者血浆皮质醇浓度升高12 μg%。正常受试者未观察到ACTH或皮质醇反应。与正常受试者相比，库欣病或纳尔逊综合征患者给予血管加压素后血浆ACTH浓度升高更显著（分别为P<0.05，P<0.02）；库欣病患者皮质醇浓度升高也更显著（P<0.05）。库欣病患者和纳尔逊综合征患者对血管加压素给药的ACTH反应幅度无显著差异。相比之下，库欣病患者胰岛素诱导低血糖后血浆皮质醇和血浆ACTH浓度的升高显著低于正常受试者（分别为P<0.001，P<0.05）；而与正常受试者相比，该刺激与纳尔逊综合征患者血浆ACTH浓度的显著升高有关（P<0.01），与库欣病患者相比也显著升高（P<）。这些发现表明，纳尔逊综合征患者的垂体功能并非自主的，并提示中枢神经调节机制改变可能在常与此综合征相关的垂体肿瘤病因中起作用。TRF诱导库欣病和纳尔逊综合征患者血浆皮质醇和ACTH浓度升高，提示此类患者下丘脑或垂体受体可能发生改变。
