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克罗恩病的早期形态学改变。透射电子显微镜检查结果及其解读:综述

Early morphological changes in Crohn's disease. Transmission electron-microscopic findings and their interpretation: an overview.

作者信息

Schattenfroh S, Bartels M, Nagel E

机构信息

Department of Anesthesiology IV, Medical School of Hannover, FRG.

出版信息

Acta Anat (Basel). 1994;149(4):237-46.

PMID:7976176
Abstract

Recent ultrastructural investigations revealed early epithelial lesions in Crohn's disease, while a specific morphological pattern was not identifiable. An increase in plasma cells, lymphocytes, macrophages, mast cells, eosinophilic and neutrophilic granulocytes, as well as focal edema and inflammation of tissue structures was seen in the lamina propria, submucosa and deeper layers. The results are consistent with the frequent discussion about a pathogenetically significant defect of the mucosal 'barrier function', which consists of mechanical, cellular, humoral, immunological and nonimmunological mechanisms, including different histotopographically defined lines of defense of the epithelium and lamina propria. An intact epithelial layer plays an important role as the first line of defense. It is evident that components of the epithelial barrier (absorptive cells, goblet cells, Paneth cells, M cells) show ultrastructural signs of alteration or injury, while the primary agent or event remains unknown. Another pathomechanism would be a preexisting defect in intestinal 'barrier function'. Such a defect would result in an increased uptake of, or an inadequate immune reaction to, ubiquitously occurring antigens/agents (with genetic predisposition). However, no primary defect of epithelial or inflammatory cells has been definitely identified so far. Direct toxic damage of tissue secondarily introducing the inflammatory changes is also possible. Although the morphological alterations in Crohn's disease are not yet clearly understood and exactly interpreted, transmission electron microscopy has been helpful in defining early lesions and has led to further knowledge about the pathogenesis of this disease.

摘要

最近的超微结构研究揭示了克罗恩病早期的上皮病变,但未发现特定的形态学模式。在固有层、黏膜下层及更深层可见浆细胞、淋巴细胞、巨噬细胞、肥大细胞、嗜酸性粒细胞和中性粒细胞增多,以及组织结构的局灶性水肿和炎症。这些结果与关于黏膜“屏障功能”存在致病意义重大缺陷的频繁讨论相一致,黏膜屏障功能由机械、细胞、体液、免疫和非免疫机制组成,包括上皮和固有层在不同组织学部位定义的不同防线。完整的上皮层作为第一道防线发挥着重要作用。显然,上皮屏障的组成部分(吸收细胞、杯状细胞、潘氏细胞、M细胞)显示出超微结构改变或损伤的迹象,而主要病因或事件仍不清楚。另一种发病机制可能是肠道“屏障功能”预先存在缺陷。这种缺陷会导致对普遍存在的抗原/病原体的摄取增加或免疫反应不足(存在遗传易感性)。然而,到目前为止尚未明确确定上皮细胞或炎症细胞存在原发性缺陷。组织的直接毒性损伤继而引发炎症变化也是可能的。尽管克罗恩病的形态学改变尚未被清楚理解和准确解释,但透射电子显微镜有助于确定早期病变,并使人们对该疾病的发病机制有了进一步了解。

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