Acid Colitis Research Articles

Short chain fatty acids in inflammatory bowel disease. The effect of bacterial fermentation of blood

Short chain fatty acids in inflammatory bowel disease. The effect of bacterial fermentation of blood

Comparison of parenteral nutrition and enteral feeding with pectin in experimental colitis in the rat

The effect of a pectin-supplemented enteral diet on experimental colitis was compared with parenteral nutrition and with a pectin-free enteral diet. Forty-five rats had feeding catheters placed into either the stomach (IG, n = 31) or the superior vena cava (IV, n = 14) and then received acetic acid (colitis) or saline (control) enemas. After the enema, all rats received the same diet, either IG or IV, for 6 d except for 15 rats (IGP, 9 colitis and 6 controls), which had 1% pectin added to the diet. At the end of the feeding period the IGP group had significantly less colonic inflammation and/or necrosis than either IV (p less than 0.03) or IG (p less than 0.04) groups. Nitrogen balance, serum albumin, total iron-binding capacity and body weight did not differ significantly among dietary regimens. Thus, the degree of bowel injury in experimental colitis was decreased when animals were fed a pectin-supplemented enteral diet and this effect was independent of nutritional status.

Short chain fatty acids in inflammatory bowel disease. The effect of bacterial fermentation of blood

An in vitro faecal incubation system was used to investigate how blood added to faeces influences short chain fatty acid (SCFA) production. The result was a change in SCFA pattern from one largely dominated by acetate and propionate to a pattern less dominated by these two acids but with greater amounts of longer and branched SCFA (butyrate, isobutyrate, valerate and isovalerate). Patients with active ulcerative colitis revealed variable concentrations of SCFA in their individual stool specimens, 66% of the samples being outside the 95% confidence interval set by a control group and without any specific trend. The SCFA concentrations were normal in patients with Crohn's disease of the colon. The study concludes that the changes in SCFA pattern seen elsewhere in studies on ulcerative colitis could be due to bacterial fermentation of blood either in the colon or in the stools after passing. It cautions against using faecal concentrations in this disease without due regard to the phenomenon of dilution or pollution of the colonic chymus by colonic effusion of blood.

The value of 5-aminosalicylic acid in inflammatory bowel disease for patients intolerant or allergic to sulphasalazine.

The use of sulphasalazine in inflammatory bowel disease is often limited by intolerance or allergy. In previous studies 5-aminosalicylic acid (5ASA), the active ingredient of sulphasalazine, coated with an acrylic resin, has been shown to be as effective as sulphasalazine in maintaining remission. In this study coated 5ASA was given to 37 patients intolerant or allergic to sulphasalazine. Thirty-three patients have tolerated 5ASA satisfactorily, and most experienced improved control of their disease. Four patients reported similar side effects with sulphasalazine and 5ASA.

Metabolism of Arachidonic Acid in Acetic Acid Colitis in Rats: Similarity to Human Inflammatory Bowel Disease

We recently reported that human inflammatory bowel disease mucosa contains large amounts of leukotriene B4, a potent chemotactic agent formed from arachidonic acid through the lipoxygenase pathway. To more fully evaluate the role of arachidonic acid metabolites in the mediation of intestinal inflammation, we studied arachidonate metabolism in an animal model: acetic acid colitis in the rat. Incubation of acetic acid colitis mucosa with arachidonic acid resulted in the production of leukotriene B4 and a series of monohydroxy fatty acids, all products of the lipoxygenase pathway, plus much smaller amounts of cyclooxygenase products including prostaglandin E2. All of these metabolities were made in significantly greater quantities by mucosa from acetic acid-treated rats than by controls. The pattern of arachidonate metabolism in acetic acid colitis was strikingly similar to that in human inflammatory bowel disease. Moreover, the concentration of leukotriene B4 in acetic acid-treated mucosa was almost identical to that in human inflammatory bowel disease mucosa and was 50 times greater than that in normal rat colonic mucosa. These data indicate that lipoxygenase products, including leukotriene B4, may be important mediators of intestinal inflammation in a wide variety of inflammatory conditions. Moreover, the similarities in the metabolism of arachidonate by human inflammatory bowel disease and by acetic acid colitis may allow the use of this model, and perhaps other animal models of intestinal inflammation, in the screening of potential therapeutic agents for inflammatory bowel disease.