Williamson R C, Rainey J B
Scand J Gastroenterol Suppl. 1984;104:57-76.
Conditions that potentiate colorectal carcinogenesis have in common the ability to increase cell proliferation in colonic crypts. Since compensatory hyperplasia of the shortened gut involves large bowel as well as small bowel, postoperative adaptation might promote the development of bowel cancer. This hypothesis was tested in Sprague-Dawley or Fischer rats given parenteral azoxymethane (50-160 mg/kg). Resection and bypass of a third or more of the small intestine consistently enhance colorectal carcinogenesis; so does pancreatobiliary diversion to mid small bowel. Partial colectomy has little effect on adaptation or carcinogenesis, but colonic defunction reduces mucosal mass and tumour yields. Bile acids are cocarcinogenic when instilled per rectum but not in colon sequestered as a Thiry-Vella fistula. Most intestinal anastomoses and stomas are favoured sites for tumour development. Postoperative hyperplasia plays a cocarcinogenic role in this experimental model. Patients with operations such as ileal resection and jejunoileal bypass should be screened for evidence of hyperplasia or dysplasia in the large intestine.
增强结直肠癌发生的条件通常具有增加结肠隐窝细胞增殖的能力。由于缩短肠道的代偿性增生涉及大肠和小肠，术后适应性变化可能会促进肠癌的发展。在给予肠外注射氧化偶氮甲烷（50 - 160 mg/kg）的斯普拉格-道利大鼠或费希尔大鼠中对这一假说进行了验证。切除和旁路三分之一或更多的小肠会持续增强结直肠癌的发生；胰胆管转流至小肠中部也会如此。部分结肠切除术对适应性变化或癌症发生影响不大，但结肠去功能化会减少黏膜质量和肿瘤发生率。经直肠注入胆汁酸具有促癌作用，但通过蒂里-韦拉瘘管隔离在结肠时则不然。大多数肠道吻合口和造口是肿瘤发生的有利部位。在这个实验模型中，术后增生起到促癌作用。对于接受回肠切除术和空肠回肠旁路术等手术的患者，应筛查大肠增生或发育异常的证据。
