Yotsumoto S, Aizawa T, Kotani M, Yamada T
J Clin Endocrinol Metab. 1979 Apr;48(4):660-3. doi: 10.1210/jcem-48-4-660.
In a middle-aged woman with virilizing adenoma, 2 mg dexamethasone increased urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids, whereas 8 mg dexamethasone increased urinary excretion only of 17-KS. With discontinuation of dexamethasone, 17-KS excretion returned to the predexamethasone level. Dexamethasone depressed the basal level of cAMP synthesis and basal testosterone production by the normal adrenal tissue in vitro. Dexamethasone also depressed the increase of cAMP produced by ACTH in the normal tissue. In contrast, dexamethasone increased basal cAMP synthesis and stimulated testosterone secretion in the tumor tissue. ACTH and dexamethasone were additive in their effects on cAMP and testosterone in the tumor tissue. It is suggested that dexamethasone acted directly on the adrenal tumor to stimulate steroid secretion in this patients.
在一名患有男性化腺瘤的中年女性中，2毫克地塞米松增加了17-酮类固醇（17-KS）和17-羟皮质类固醇的尿排泄量，而8毫克地塞米松仅增加了17-KS的尿排泄量。停用 地塞米松后，17-KS排泄量恢复到地塞米松治疗前的水平。地塞米松在体外可抑制正常肾上腺组织中环磷酸腺苷（cAMP）合成的基础水平和基础睾酮生成。地塞米松还可抑制促肾上腺皮质激素（ACTH）在正常组织中所引起的cAMP增加。相比之下，地塞米松可增加肿瘤组织中的基础cAMP合成并刺激睾酮分泌。ACTH和地塞米松对肿瘤组织中cAMP和睾酮的作用具有相加性。提示地塞米松直接作用于肾上腺肿瘤以刺激该患者的类固醇分泌。
