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Experimental colonic carcinogenesis after gastric surgery

Peptic ulcer surgery may predispose to the subsequent development of colorectal cancer. This experimental study has investigated the effects of gastric operations on colonic cell proliferation, bile acid excretion and carcinogenesis. Male Sprague‐Dawley rats (n = 705) underwent sham operation, Polya partial gastrectomy or vagotomy and pyloroplasty. The carcinogen azoxymethane was administered weekly for 6 weeks thereafter (total dose 60 mg kg−1). When the animals were killed 24 weeks after operation, colons were examined for mucosal mass, crypt cell production rate (CCPR) and tumour yield; faeces were assayed for contents of neutral steroids and bile acids (both total and individual). Morphometric indices and mucosal DNA content were similar in all three groups. Polya gastrectomy reduced: (1) CCPR throughout the colon (by 42–65 per cent, P< 0·002); (2) the number of rats with colorectal tumours (26 per cent versus 63 per cent, P<0·05); (3) faecal levels of neutral steroids and bile acids, notably hyodeoxycholic acid (P<0·01). Although vagotomy and pyloroplasty increased caecal CCPR, there were no consistent differences in faecal steroids and no alteration in tumour yield after the operation. These results fail to support clinical studies suggesting that gastric surgery predisposes to colonic carcinogenesis. Indeed, Polya partial gastrectomy exerts a protective effect, probably by inhibiting colonic cell proliferation.