Response to: Morphological distinction of cortisol‐producing and aldosterone‐producing adrenal cortical adenomas: not only possible but a critical clinical responsibility

Response to: Morphological distinction of cortisol‐producing and aldosterone‐producing adrenal cortical adenomas: not only possible but a critical clinical responsibility
复制标题

DOI:
10.1111/j.1365-2559.2012.04219.x
复制
发表时间:
2012-05
期刊:
影响因子:
6.4
通讯作者:
B. Kusters;M. Peppelman;H. Timmers;J. Lenders;A. Hermus
B. Kusters;M. Peppelman;H. Timmers;J. Lenders;A. Hermus
中科院分区:
医学2区
文献类型:
--
作者:
B. Kusters;M. Peppelman;H. Timmers;J. Lenders;A. Hermus

文献摘要

被引文献

相似文献

通过评估非肿瘤肾上腺皮质的状态,可以在苏木素和伊红(H&E)染色的切片上区分产生醛固酮和产生皮质醇的腺瘤。产生皮质醇的肾上腺皮质腺瘤与非肿瘤性皮质萎缩有关,这是由于下丘脑-垂体轴的负反馈抑制作用(图1)。相反,非肿瘤性肾上腺皮质在含有醛固酮的肾上腺皮质腺瘤的腺体中不萎缩,偶尔表现出增生性变化,特别是在肾小球层(反常增生)(图2)。真实的挑战是区分产生醛固酮的腺瘤和相邻皮质正常的无功能肾上腺皮质腺瘤。由于醛固酮腺瘤的超微结构特征是独特的,这种区别可以通过电子显微镜可靠地进行。产生醛固酮的细胞含有具有板状或板状嵴的线粒体,而产生糖皮质激素的无功能腺瘤细胞含有具有管泡状嵴的线粒体。重要的是,评估非肿瘤性肾上腺皮质是外科病理学家的一项重要功能,可能具有急性临床意义,但它往往被忽视。即使大体上,在一个以皮质腺瘤为主的腺体中发现非肿瘤性肾上腺皮质萎缩,也应该引起外科病理学家的注意,以确定患者是否被诊断为库欣综合征。如果他们没有,及时打电话给相关的临床医生将防止意外的急性阿狄森氏病术后危机。
aldosterone-producing and cortisol-producing adenomas can be distinguished on haematoxylin and eosin (H&E)-stained slides by assessing the status of the nontumorous adrenal cortex. Cortisol-producing adrenal cortical adenomas are associated with atrophy of the non-tumorous cortex due to negative feedback suppression effect of the hypothalamic–pituitary axis (Figure 1). In contrast, the non-tumorous adrenal cortex is not atrophic in glands harbouring an aldosterone-producing adrenal cortical adenoma, and occasionally it exhibits hyperplastic changes, especially in the zona glomerulosa layer (paradoxical hyperplasia) (Figure 2). The real challenge is to distinguish aldosterone-producing adenomas from non-functioning adrenal cortical adenomas that also have a normal adjacent cortex. Because the ultrastructural features of aldosterone-producing adenomas are unique, this distinction can be made reliably by electron microscopy. Aldosterone-producing cells contain mitochondria with lamellar type or plate-like cristae, whereas glucocorticoid-producing and non-functioning adenoma cells contain mitochondria with tubulovesicular cristae. Importantly, assessment of the non-tumorous adrenal cortex is a critical function of the surgical pathologist that can have acute clinical implications, yet it is often overlooked. Even grossly, the identification of atrophy of the non-tumorous adrenal cortex in a gland with a dominant cortical adenoma should prompt the attention of the surgical pathologist to determine whether the patient has been diagnosed with Cushing’s syndrome. If they have not, a timely call to the relevant clinician will prevent the unanticipated postoperative crisis of acute Addison’s disease.