The relationship between intestinal hyperplasia and carcinogenesis

Abstract

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.