Pathogenesis of diversion colitis

This week’s discussions included the causes of diversion colitis.


Tominaga K, et al. Diversion colitis and pouchitis: A mini-review. World J Gastroenterol. 2018 Apr 28;24(16):1734-1747.

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“The basic mechanisms underlying diversion colitis are still unclear. Glotzer hypothesized that it might be the result of bacterial overgrowth, the presence of harmful bacteria, nutritional deficiencies, toxins, or disturbance in the symbiotic relationship between luminal bacteria and the mucosal layer[2]. Reportedly, concentrations of carbohydrate-fermenting anaerobic bacteria and pathogenic bacteria are reduced in de-functioned colons[5,23,53] and these reports indicate that the overgrowth of anaerobic bacteria or a pathogenic bacterium is unlikely to be an important etiological factor. On the other hand, there is an increase of nitrate-reducing bacteria in patients with diversion colitis[7] and nitrate-reducing bacteria produce nitric oxide (NO) which plays a protective role in low concentrations, but at higher levels it becomes toxic to the colonic tissue[54]. Thus, it has been suggested that increases in nitrate-reducing bacteria may result in toxic levels of NO, leading to the diversion colitis.” (Tominaga, 2018, p. 1739)


Kabir SI, et al. Pathophysiology, clinical presentation and management of diversion colitis: a review of current literature. Int J Surg. 2014 Oct;12(10):1088-92.

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“Recently ischaemia has been proposed as a cause of diversion colitis [15]. Levels of Short Chain Fatty Acids (SCFA) in de-functioned colon have been found to be low [13]. It is suggested that shortage of SCFA may lead to an increase in arteriolar resistance and present with features of ischaemia. This vasodilatory effect of SCFA may be a result of synthesis of Nitric Oxide (NO). SCFA provide the exogenous substrate for NO production with the help of micro flora in the colon and NO has vasodilatory effect on the vasculature [16]. However the exact role of NO is still being investigated and to date no studies have been carried out to elucidate the role of NO in the pathogenesis of diversion colitis.” (p. 1742)


Wald A. (2016). Other Diseases of the Colon and Rectum. In: Feldman M, Friedman LS,  Brandt LJ. (Eds.), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 10th ed. (pp. 2301-2303).

Full-text for Emory users.

“Although SCFA deficiency has been widely accepted as the cause of diversion colitis, other observations suggest that SCFA deficiency may not be the entire etiologic explanation. First, studies in children indicate that SCFA enemas are not universally successful in treating diversion colitis. Second, in germ-free rodents with surgical diversion and in patients receiving long-term parenteral nutrition or elimination diets (circumstances in which luminal SCFA concentrations are low), mucosal atrophy occurs rather than inflammation. 39 Third, inflammation does not occur in urinary colon conduits, from which the fecal stream has been diverted, and urine does not contain measurable SCFAs. 40 Finally, in a prospective randomized double-blind study of 13 patients with diversion colitis, butyrate enemas given for 14 days provided no improvement in either endoscopic or histologic parameters. 41 In a subsequent study by the same group, administration of SCFAs did not affect the bacterial population in the excluded colon. 42 Other luminal elements besides SCFA deficiency must play a role, but the nature of such factors is unknown.”


Eggenberger JC, Farid A. Diversion Colitis. Curr Treat Options Gastroenterol. 2001 Jun; 4(3):255-259.

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“The pathogenesis of diversion colitis remains uncertain. Some authors believe that it is due to an alteration of bacterial flora within the excluded large bowel, more specifically a reduction in the total number of bacteria and an absolute reduction in the number of strict anaerobes [8]. However, considerable clinical data implicate a luminal nutrient deficiency of short-chain fatty acids. The majority of biochemical fuels required by the
colonocyte for cellular metabolism are supplied by luminal short-chain fatty acids (primarily acetate, propionate, and butyrate) derived from the anaerobic bacterial fermentation of starch and proteins [9••].

An elegant study by Harig et al. [10••] provides support for this theory. They reported both clinical and endoscopic improvement in patients with diversion colitis after irrigation of the excluded segment with short-chain fatty acid solutions. Subsequent experience by Guillemot et al. [11] failed to show improvement, perhaps due to the relatively short (2-week) course of treatment employed. Unfortunately, neither theory fully explains the wide variation in clinical, endoscopic, or histologic features of diversion colitis.” (Eggenberger, 2001, p. 255-256)


More PubMed results on diversion colitis.

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