Takahara J, Hosogi H, Yunoki S, Hashimoto K, Uneki T
Endocrinol Jpn. 1976 Dec;23(6):451-6. doi: 10.1507/endocrj1954.23.451.
Hypothalamic pituitary adrenal function was studied in 14 patients with anorexia nervosa. Although basal plasma cortisol levels in the morning were elevated in most cases, basal plasma ACTH levels were not suppressed. Oral administration of 1 mg dexamethasone 10 hr before blood sampling failed to suppress plasma ACTH and cortisol levels in most patients with anorexia nervosa. Apparent biological half-life of exogenous cortisol was prolonged in all 4 patients with anorexia nervosa tested. The cortisol response to insulin-induced hypoglycemia and exogenous ACTH appeared to be blunted in these patients. It is concluded that anorexia nervosa has dysfunctions of hypothalamic pituitary adrenal axis, especially an abnormal feedback mechanism on ACTH secretion.
对14例神经性厌食症患者的下丘脑-垂体-肾上腺功能进行了研究。尽管大多数病例中早晨基础血浆皮质醇水平升高,但基础血浆促肾上腺皮质激素(ACTH)水平并未受到抑制。在采血前10小时口服1毫克地塞米松未能抑制大多数神经性厌食症患者的血浆ACTH和皮质醇水平。在接受测试的所有4例神经性厌食症患者中,外源性皮质醇的表观生物半衰期均延长。这些患者对胰岛素诱导的低血糖和外源性ACTH的皮质醇反应似乎减弱。结论是神经性厌食症存在下丘脑-垂体-肾上腺轴功能障碍,尤其是对ACTH分泌的异常反馈机制。