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

Citation
M. Raithel et al., Pathobiology of dysplasia in chronic inflammatory bowel disease: Current recommendations for surveillance of dysplasia, Z GASTROENT, 39(10), 2001, pp. 861
Citations number
88
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
ZEITSCHRIFT FUR GASTROENTEROLOGIE
ISSN journal
00442771 → ACNP
Volume
39
Issue
10
Year of publication
2001
Database
ISI
SICI code
0044-2771(200110)39:10<861:PODICI>2.0.ZU;2-C
Abstract
Patients with ulcerative colitis and Crohn's disease bear an about 10- and 4-fold increased risk, respectively, for developing colorectal carcinoma. A part from typical locations of colorectal carcinoma in the sigmoid colon an d rectum other locations were also often observed, e.g. right hemicolon or multifocal distribution. Histologically colorectal neoplasms frequently pre sent as mucinous adenocarcinoma (signet-ring cell carcinoma). The risk for neoplasm depends on extension, severity, duration and therapeutic responsiv eness 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 d ysplasia. Since there are no reliable biological markers available to date, surveillance-programs continue to rely on the discovery of dysplasia (uneq uivocal intraepithelial neoplasia). Detection of dysplasia by colonoscopy a chieves 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 b iopsies should be done every 10 cm from mucosa free of inflammation. Additi onally, every fine or discrete alteration of the mucosal surface should be recorded. Multiple biosies should also be taken from such minimal lesions a s 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 macrosc opically suspect areas bear the highest risk of cancer (non-adenoma like dy splasia), followed by multiple high-grade lesions without a macroscopic les ion, and multiple low-grade dysplasias. Detection of single dysplastic lesi ons in flat mucosa should be followed by a control endoscopy after 2-6 mont hs, and if dysplasia is seen again, colectomy is recommended.