Effect of defunction on cytokinetics and cancer at colonic suture lines

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Abstract
An intestinal suture line potentiates experimental carcinogenesis in its vicinity, probably due to adaptive hyperplasia. By contrast, a defunctioning colostomy causes distal hypoplasia, and fewer tumours develop. Male Sprague-Dawley rats (n = 160) were used to study adaptation (assessed by a stathmokinetic technique) and carcinogenesis (induced by azoxymethane) at an end-to-end anastomosis that was raised in either functioning or defunctioned left colon. Controls had no procedure and other rats had proximal colostomy alone. Defunction had a profound antitropic effect on the colon, reducing bowel length and weight and crypt cell production rate (CCPR) by 22–56 per cent. Anastomotic CCPR was increased by a factor of 2–6 over controls: mean(s.e.m.) values of 12·71(2–85) versus 4·87(0·41) cells/crypt/h (P<0·01), but defunction reduced this by 76per cent to a mean(s.e.m.) value of 3·00(0·52) cells/crypt/h below that in the intact colon. In the left colon, 39–50 per cent of tumours were sited at the anastomosis. Compared with controls there were 77 per cent fewer tumours in defunctioned colon, but they still favoured the site of anastomosis. Neoplasms at the colostomy site accounted for 74–77 per cent of all right-sided tumours. Anastomosis and defunction have powerful but contrasting effects on colonic adaptation and carcinogenesis; when combined they tend to cancel each other out.