垂体组织病理学

I. Doniach
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引用次数: 24

摘要

垂体前叶促肾上腺皮质激素的细胞质分泌颗粒在三色染色中呈嗜碱性,在糖蛋白组织化学染色中呈周期性酸-希夫阳性,这是由于它们含有前体蛋白proopiomelanocorticotrophin (POC)的16000 n端糖基化片段。颗粒对抗ACTH, β-内啡肽和POC n端片段的抗体表现出阳性的免疫细胞化学反应。一小部分促皮质细胞还含有免疫反应性α - msh。免疫细胞化学显示皮质促生成物约占垂体前叶细胞的15-20%,呈单细胞或成团排列。它们分布在正中楔和神经中枢的前部、侧面和后部,神经中枢常被嗜碱性嗜皮质细胞“侵入”。α - msh亚群主要分布在发育初期的中间叶,并在人胎儿垂体的前部分布。克鲁克细胞透明化与病理维持的高糖血症和糖类固醇治疗有关。超微结构显示透明化是由于直径7 - 8nm的中间细胞质丝的大量积累,而通常只有少量。这种变化与不同程度的分泌颗粒损失有关。在未经治疗的阿狄森氏病中,促皮质细胞的数量显著增加,其中许多排列在扩张的肺泡中形成微结节。绝大多数垂体依赖性库欣病病例和所有纳尔逊综合征病例都与嗜碱性或憎色性腺瘤有关。这些细胞与抗acth、β-内啡肽和n端POC呈阳性免疫细胞化学反应。在超微结构上,憎色性腺瘤细胞含有稀疏的分泌颗粒,通常比嗜色性腺瘤小。只有很少的垂体依赖性库欣病报告发现是由于免疫细胞化学证实的皮质增生伴或不伴皮质腺瘤。少数病例的腺瘤细胞显示克鲁克透明化,其中一例与大ACTH的分泌有关,这种现象在异位ACTH分泌肿瘤中更为常见。据报道,有一组因促皮质腺瘤引起的病例,其过量的ACTH分泌通过多巴胺激动剂溴隐肽治疗而减少,这表明肿瘤细胞起源于中部促皮质腺瘤的一个亚群。一个令人困惑的发现是,免疫反应性皮质性腺瘤的发病率与任何临床或生化库欣病的证据无关。这些在手术切除的物质以及死后脑垂体中都有发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Histopathology of the pituitary

The cytoplasmic secretory granules of corticotrophs in the anterior pituitary are basophil in trichrome stains and periodic acid-Schiff positive in the histochemical stain for glycoprotein due to their content of the glycosylated 16000 N-terminal fragment of the precursor protein proopiomelanocorticotrophin (POC). The granules show a positive immunocytochemical reaction to antibodies raised against ACTH, β- endorphin and N-terminal fragments of POC. A small subset of corticotrophs contains immunoreactive αMSH in addition. Immunocytochemistry shows the corticotrophs to constitute about 15–20% of the anterior pituitary cells arranged both singly and in clumps. They are distributed in the median wedge and anteriorly, laterally and posteriorly adjacent to the pars nervosa which is often ‘invaded’ by corticotroph basophils. The αMSH subset is prominent in the rudimentary intermediate lobe and is scattered anteriorly in the pituitary of the human fetus. Crooke cell hyalinization is associated with pathologically maintained hypercortisolaemia and with glucosteroid therapy. The hyalinization is demonstrated in ultrastructure to be due to massive accumulation of intermediate cytoplasmic filaments 7–8 nm in diameter that are normally present in only small number. The change is associated with a varying degree of loss of secretory granules.

In untreated Addison's disease there is a marked increase in the number of corticotrophs, many of which are arranged in distended alveoli to form micronodules. The vast majority of cases of pituitary-dependent Cushing's disease and all cases of Nelson's syndrome are associated with a basophil or chromophobe adenoma. These give a positive immunocytochemical reaction with anti-ACTH, β-endorphin and N-terminal POC. In ultrastructure the cells of the chromophobe adenomas are seen to contain sparse secretory granules that are usually smaller than those in the chromophil adenomas. There are only very few reports of pituitary-dependent Cushing's disease found to be due to immunocytochemically confirmed corticotroph hyperplasia with or without a corticotroph adenoma. A few cases have been described in which the adenoma cells show Crooke's hyalinization, associated in one example with secretion of a big ACTH found more typically in ectopic ACTH-secreting tumours. A group of cases due to corticotroph adenoma has been reported whose excessive ACTH secretion is reduced by treatment with the dopamine agonist bromocriptine, in which it is suggested that the tumour cells arise from a subset of corticotrophs of pars intermedia origin. A puzzling finding has been the incidence of immunoreactive corticotroph adenomas that are not associated with any evidence of clinical or biochemical Cushing's disease. These have been noted in surgically resected material as well as in postmortem pituitaries.

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