Cancer in inflammatory bowel disease

被引:2
作者
Steven H Itzkowitz [1 ]
机构
[1] Division of Gastroenterology Department of Medicine Mount Sinai School of Medicine New York City NY 10029 United States
关键词
Colon cancer; Inflammatory bowel disease; Dysplasia; Chemoprevention; Colonoscopy; Genomic instability;
D O I
暂无
中图分类号
R735.3 [肠肿瘤]; R574 [肠疾病];
学科分类号
1002 ; 100201 ; 100214 ;
摘要
Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer (CRC). Many of the molecular alterations responsible for sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also play a role in colitis-associated colon carcinogenesis. Colon cancer risk in inflammatory bowel disease increases with longer duration of colitis, greater anatomic extent of colitis, the presence of primary sclerosing cholangitis, family history of CRC and degree of inflammation of the bowel. Chemoprevention includes aminosalicylates, ursodeoxycholic acid, and possibly folic acid and statins. To reduce CRC mortality in IBD, colonoscopic surveillance with random biopsies remains the major way to detect early mucosal dysplasia. When dysplasia is confirmed, proctocolectomy is considered for these patients. Patients with small intestinal Crohn’s disease are at increased risk of small bowel adenocarcinoma. Ulcerative colitis patients with total proctocolectomy and ileal pouch anal- anastomosis have a rather low risk of dysplasia in the ileal pouch, but the anal transition zone should be monitored periodically. Other extra intestinal cancers, such as hepatobiliary and hematopoietic cancer, have shown variable incidence rates. New endoscopic and molecular screening approaches may further refine our current surveillance guidelines and our understanding of the natural history of dysplasia.
引用
收藏
页码:378 / 389
页数:12
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