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Editor,—We published in 1999, to our knowledge, the first description of diversion colitis appearing to trigger instream ulcerative colitis (Gut1999;44:279–282). We have recently encountered a fourth patient with the same rare condition.
A 66 year old non-smoking white man presented in 1997 with large bowel obstruction. His mother had died of colorectal carcinoma at the age of 71 years. There was no family history of inflammatory bowel disease. An instant barium enema revealed obstruction at the level of the mid-sigmoid colon with radiological features suggestive of sigmoid carcinoma. The patient underwent a Hartmann's procedure with colostomy. The resection specimen showed a Dukes's B carcinoma of the sigmoid colon with no evidence of colitis. The patient then received adjuvant chemotherapy consisting of 12 weeks of infusional 5-fluorouracil. Eighteen months later he had a colonoscopy through the rectal stump and the stoma. The colon proximal to the colostomy looked normal but the rectal stump appeared mildly inflamed. Biopsy samples of the rectal stump were consistent with active colitis and a putative diagnosis of diversion colitis was made. Treatment with steroid enemas was effective. Six months later the patient developed bleeding and mucus discharge through the colostomy for the first time. Stool cultures including analysis for Clostridium difficile were negative. Colonoscopy through the colostomy to the limit of the examination revealed severe, active colitis. The biopsy samples on this occasion were consistent with ulcerative colitis with chronic inflammation in the lamina propria, cryptitis and crypt abscess formation. The patient responded well to treatment with oral corticosteroids and mesalazine.
We have postulated previously that the development of ulcerative colitis may be initiated by inflammation of another aetiology at an anatomically discontinuous site of the bowel. This description of an additional case would support the hypothesis that diversion colitis might be one such trigger for ulcerative colitis. The mechanisms underlying this remain speculative but may involve the recruitment of activated lymphocytes from the diverted colon to the phenotypically similar vascular endothelium of the instream colon.
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