Surgeons, who documented what they had seen and felt in the abdomen of the patient, made the earliest descriptions of Crohn’s disease (CD). Dalziel wrote the first pathology description in 1913. Crohn and his coworkers reinvented what Dalziel had written about and called it by a different name, ‘regional enteritis’. Later others elaborated on the histologic features, at first the lymphoid follicles, later the granulomas. Some thought the latter were comprised of lymphatic endothelial cells and that endothelial plugs obstructed the lymphatics. Tonelli and others recognized that lymphedema was important and caused by obstructions to lymphatic vasculature. Some lymphatics they described contained lymphocyte plugs and others granulomas. Immunohistochemistry (IHC) has now shown that endothelial cells are not the cause of lymphatic obstruction, but rather CD68‐positive macrophages, concluding that the ‘lymphocyte thrombi’ are passive, caught upstream of granuloma‐obstructed lymphatics. Numerous authors recognized that transmural edema was the most significant change in Crohn’s disease and that this was later followed by fibrosis and contracture of the diseased segment. Key descriptive papers spoke of the segmental lymphedema. Most recently, attention has been given to attachments of the intralymphatic CD68+ granulomas to a focal point where endothelial damage occurred, damage suggesting infectious penetration of the mucosa, necrosis of lymphatic endothelium and then granulomatous response, both inside and outside the lymphatics, of submucosa, muscularis, and subserosa. D2‐40 IHC outlines the endothelium, and anti‐CD68 shows the granulomas. IHC adds a valuable perspective when reviewing CD resections.

中文翻译：

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早期病理学家对克罗恩病病理学的理解是错误的，是正确的：历史的观点。

外科医生记录了他们在患者腹部所见和所见，并最早描述了克罗恩病（CD）。Dalziel在1913年写下了第一个病理学描述。Crohn和他的同事们重新发明了Dalziel所写的内容，并用另一个名字“区域性肠炎”来称呼它。后来其他人阐述了组织学特征，首先是淋巴滤泡，后来是肉芽肿。一些人认为后者是由淋巴管内皮细胞组成的，并且内皮塞阻塞了淋巴管。Tonelli等人认识到淋巴水肿很重要，并且是由淋巴管的阻塞引起的。他们描述的某些淋巴管含有淋巴细胞栓塞，而其他肉芽肿则包含。免疫组织化学（IHC）现在显示，内皮细胞不是引起淋巴阻塞的原因，而是CD68阳性的巨噬细胞，认为“淋巴细胞血栓”是被动的，被捕获在肉芽肿阻塞的淋巴管上游。许多作者认识到，透壁水肿是克罗恩病中最显着的变化，其后是纤维化和患病部位的挛缩。关键的描述性论文谈到了节段性淋巴水肿。最近，注意力已经集中在淋巴内CD68 +肉芽肿附着到发生内皮损伤的焦点上，这种损伤表明粘膜感染性渗透，淋巴内皮坏死，然后在淋巴管内外的粘膜下层肉芽肿反应，肌层和浆膜下层。D2-40 IHC概述了内皮，抗CD68则显示了肉芽肿。