Gwinup G, Johnson B
Metabolism. 1975 Jun;24(6):777-91. doi: 10.1016/0026-0495(75)90045-1.
Cortisol production is appropriately maintained by a complex control system which involves primarily the hypothalamus, the pituitary, and the adrenal cortices. Very small quantities of ACTH stimulate cortisol production, and maximum stimulation occurs with serum concentrations of only 3 mU/100 ML. Under normal circumstances, cortisol is secreted in bursts about ten times each day and circulates predominately bound to a specific binding protein which is rather completely saturated. Radioimmunoassay of plasma cortisol is now generally available and is the assay method of choice, but because of the episodic nature of its secretion, random values of plasma cortisol must be interpreted with great reservation, and even the comparison of morning and evening values in assessing circadian rhythmicity is not often helpful. Urinary free cortisol determinations provide excellent discrimination between normal function and all forms of hypercortisolism. Although the response of the adrenal cortices to ACTH may be evaluated in a number of different ways, the simplest but most definitive procedure involves continuous intravenous administration over a 48-hr period. Of the various tests which indirectly assess the potential for ACTH secretion, the use of metyrapone is most helpful. In the test of greatest utility, plasma cortisol and 11-desoxycortisol are determined the morning after a single midnight oral dose of 30 mg/kg. The detection of all forms of pathologic hypercortisolism is still best accomplished by the oral administration of dexamethasone. Plasma cortisol can be determined the morning after a single midnight dose of 1 mg, or urinary 17-hydroxycorticosteroids can be determined after 2 days in which 0.5 mg is given at 6-hr intervals. Patients with hypercortisolism of hypothalamic-pituitary origin usually evidence appropriate suppression of urinary steroids if the dose is increased to 2.0 mg every 6 hr for another 48 hr. In patients who do not suppress on this or even higher doses of dexamethasone, the distinction between those with adrenal tumor and those with the ectopic ACTH syndrome can be accomplished most definitively by the assay of plasma ACTH where this determination is available.
皮质醇的分泌由一个复杂的控制系统适当维持，该系统主要涉及下丘脑、垂体和肾上腺皮质。极少量的促肾上腺皮质激素（ACTH）就能刺激皮质醇的分泌，血清浓度仅为3 mU/100 ML时就能产生最大刺激。在正常情况下，皮质醇每天大约以脉冲形式分泌10次，并且主要以与一种特定结合蛋白结合的形式循环，该结合蛋白几乎完全饱和。血浆皮质醇的放射免疫测定法目前已普遍可用，是首选的测定方法，但由于其分泌具有间歇性，血浆皮质醇的随机值必须谨慎解读，即使在评估昼夜节律时比较早晨和晚上的值也常常没有帮助。尿游离皮质醇测定能很好地区分正常功能和各种形式的皮质醇增多症。虽然可以通过多种不同方法评估肾上腺皮质对ACTH的反应，但最简单但最明确的程序是在48小时内持续静脉给药。在各种间接评估ACTH分泌潜能的测试中，使用甲吡酮最有帮助。在最有用的测试中，在午夜单次口服30 mg/kg剂量后第二天早晨测定血浆皮质醇和11-脱氧皮质醇。检测所有形式的病理性皮质醇增多症仍然最好通过口服地塞米松来完成。在午夜单次服用1 mg剂量后第二天早晨测定血浆皮质醇，或者在以6小时间隔给予0.5 mg共2天之后测定尿17-羟皮质类固醇。下丘脑-垂体来源的皮质醇增多症患者，如果将剂量增加到每6小时2.0 mg再持续48小时，通常会出现尿类固醇的适当抑制。对于使用这种剂量甚至更高剂量地塞米松都不被抑制的患者，如果可以进行血浆ACTH测定，那么最明确地区分肾上腺肿瘤患者和异位ACTH综合征患者的方法就是检测血浆ACTH。
