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[慢性炎症性肠病发育异常的病理生物学:发育异常监测的当前建议]

[Pathobiology of dysplasia in chronic inflammatory bowel disease: Current recommendations for surveillance of dysplasia].

作者信息

Raithel M, Weidenhiller M, Schwab D, Müller S, Hahn E G

机构信息

Medizinische Klinik I mit Poliklinik, Universität Erlangen-Nürnberg, Erlangen.

出版信息

Z Gastroenterol. 2001 Oct;39(10):861-75. doi: 10.1055/s-2001-17870.

Abstract

Pathobiology of dysplasia in chronic inflammatory bowel disease: Current recommendations for surveillance of dysplasia. Patients with ulcerative colitis and Crohn's disease bear an about 10- and 4-fold increased risk, respectively, for developing colorectal carcinoma. Apart from typical locations of colorectal carcinoma in the sigmoid colon and rectum other locations were also often observed, e. g. right hemicolon or multifocal distribution. Histologically colorectal neoplasms frequently present as mucinous adenocarcinoma (signet-ring cell carcinoma). The risk for neoplasm depends on extension, severity, duration and therapeutic responsiveness of chronic colonic inflammation, and it seems pathogenetically to be similar in ulcerative colitis and Crohn's disease. Colorectal carcinoma in inflammatory bowel disease arises from epithelial dysplasia. Since there are no reliable biological markers available to date, surveillance-programs continue to rely on the discovery of dysplasia (unequivocal intraepithelial neoplasia). Detection of dysplasia by colonoscopy achieves 70-85 % sensitivity.Endoscopic surveillance should start after 8 years of disease's duration in pancolitis, after 10-12 years in left- sided colitis and after 12 years in Crohn's disease of the colon, with regular intervals every 1-2 years. 3-5 biopsies should be done every 10 cm from mucosa free of inflammation. Additionally, every fine or discrete alteration of the mucosal surface should be recorded. Multiple biosies should also be taken from such minimal lesions as well as from more macroscopically suspicious areas like plaques, nodular lesions or stenosis. The clinical consequence of a positive screening for dysplasia is colectomy because of an assumed risk of cancer of about 40-70 %. Dysplasia in macroscopically suspect areas bear the highest risk of cancer (non-adenoma like dysplasia), followed by multiple high-grade lesions without a macroscopic lesion, and multiple low-grade dysplasias. Detection of single dysplastic lesions in flat mucosa should be followed by a control endoscopy after 2-6 months, and if dysplasia is seen again, colectomy is recommended.

摘要

慢性炎症性肠病发育异常的病理生物学

当前发育异常监测的建议。溃疡性结肠炎和克罗恩病患者发生结直肠癌的风险分别增加约10倍和4倍。除了乙状结肠和直肠这些结直肠癌的典型发病部位外,其他部位也经常被观察到,例如右半结肠或多灶性分布。组织学上,结直肠肿瘤常表现为黏液腺癌(印戒细胞癌)。肿瘤发生风险取决于慢性结肠炎症的范围、严重程度、持续时间和治疗反应性,在溃疡性结肠炎和克罗恩病中其发病机制似乎相似。炎症性肠病中的结直肠癌源于上皮发育异常。由于目前尚无可靠的生物学标志物,监测方案仍依赖于发育异常(明确的上皮内瘤变)的发现。通过结肠镜检查检测发育异常的敏感性为70 - 85%。全结肠炎患者在患病8年后应开始内镜监测,左侧结肠炎患者在患病10 - 12年后开始,结肠克罗恩病患者在患病12年后开始,每隔1 - 2年定期进行。应从无炎症的黏膜每隔10厘米取3 - 5块活检组织。此外,黏膜表面的每一处细微或离散改变都应记录下来。对于微小病变以及肉眼更可疑的区域如斑块、结节性病变或狭窄处,也应取多块活检组织。发育异常筛查呈阳性的临床后果是因假定约40 - 70%的癌症风险而行结肠切除术。肉眼可疑区域的发育异常患癌风险最高(非腺瘤样发育异常),其次是无肉眼可见病变的多个高级别病变以及多个低级别发育异常。在平坦黏膜中检测到单个发育异常病变后,应在2 - 6个月后进行对照内镜检查,如果再次发现发育异常,则建议行结肠切除术。

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