Aiba M
Acta Pathol Jpn. 1977 Nov;27(6):877-91.
The histochemical activity of alkaline phosphatase (Al-Pase), the induction of which is one of the effects of ACTH on the adrenocortical cells, was examined in 10 adrenocortical tumors causing Cushing's syndrome and in 65 adrenal cortices. All of the compact cells in every gland, and almost all, about half, or a small proportion in the four tumors showed Al-Pase activity. These tumors decreased in steroidogenesis after the administration of dexamethasone. No compact cells exhibited the activity in six tumors, none of which was "dexamethasone-suppressible". Three of the seven attached glands examined were halfway between those of typical Cushing's syndrome and those of other than Cushing's syndrome from the viewpoint of compact/clear cell morphology. All of the tumors that had Al-Pase-positive clear cells increased in steroidogenesis after ACTH administration. These results suggested that Al-Pase activity of tumor cells was also ACTH effect and that a decrease in steroidogenesis of tumors after dexamethasone administration was due not to fluctuations but to suppression of intrinsic ACTH.
碱性磷酸酶(Al-Pase)的组织化学活性在10例导致库欣综合征的肾上腺皮质肿瘤和65个肾上腺皮质中进行了检测,其诱导是促肾上腺皮质激素(ACTH)对肾上腺皮质细胞的作用之一。每个腺体中的所有致密细胞,以及四个肿瘤中几乎所有、约一半或一小部分致密细胞均显示出Al-Pase活性。这些肿瘤在给予地塞米松后类固醇生成减少。六个肿瘤中没有致密细胞表现出活性,其中无一例是“地塞米松可抑制的”。从致密/透明细胞形态学的角度来看,所检查的七个附属腺体中有三个介于典型库欣综合征和非库欣综合征之间。所有具有Al-Pase阳性透明细胞的肿瘤在给予ACTH后类固醇生成增加。这些结果表明,肿瘤细胞的Al-Pase活性也是ACTH的作用,并且地塞米松给药后肿瘤类固醇生成的减少不是由于波动,而是由于内源性ACTH的抑制。