# Non-Specific Tissue Inflammatory Evidence Found In IBS Group



## Mike NoLomotil (Jun 6, 2000)

FINDINGS SECONDARY TO THE PURPOSE OF THE STUDY: In this study, the investigators set out to better differentiate the colonoscopic findings of "mucosal abnormalities" associated with portal hypertension; in so doing they used a control group of 224 patients with IBS who had been "scoped" and compared the tissue biopsy findings of each, yielding the expected finidings in the portal hypertensives of substantial inflammatory damage confusable with colitis.HOWEVER additional findings in the IBS group of a predominance of non-specific inflammatory evidence (infiltrate, edema, and vascular ectasia-vascular swelling) were noted (the control group, with "colitis-like symptoms"). This is another finding consistent with the presence of intravascular inflammatory responses in the gut microcirculation, and the ectasia and extravasation of fluid (edema) associated with abnormal-release of immunologic mediators.The finidngs also serve to further differentiate the tissue and vascular inflammatory response of "inflammatory" bowel disease ("colitis") from the reactions seen in reactive gut disease ("irritable bowel syndrome").The points of interest are capitalized.MNL_________________________________________Gastrointest Endosc 2000 Oct;52(4):511-516 Related Articles, Books, LinkOut MUCOSAL ABNORMALITIES OF THE COLON IN PATIENTS WITH PORTAL HYPERTENSION: AN ENDOSCOPIC STUDYBini EJ, Lascarides CE, Micale PL, Weinshel EHDivision of Gastroenterology, VA New York Harbor Healthcare System, Bellevue Hospital, and New York University School of Medicine, New York, New York.BACKGROUND: Controversy still exists regarding colonic mucosal abnormalities in patients with portal hypertension (portal colopathy). The aims of this study were to better define portal colopathy and to identify risk factors for these colonic mucosal abnormalities. METHODS: We reviewed the medical records of 437 patients with cirrhosis and portal hypertension and 224 WITH IRRITABLE BOWEL SYNDROME (CONTROL PATIENTS) who underwent colonoscopy over a 6-year period. RESULTS: Individuals with portal hypertension were significantly more likely than control patients to have colitis-like abnormalities (38% vs. 3%, p < 0.001) and vascular lesions (13% vs. 3%, p < 0.001). In the multivariate model, portal hypertensive gastropathy (odds ratio 5.64: 95% CI [3.39, 9.41]; p < 0.001), 2+ or larger esophageal varices (odds ratio 4.76: 95% CI [2.78, 8.15]; p < 0.001), and Child-Pugh class C cirrhosis (odds ratio 2.64: 95% CI [1.40, 4.97]; p = 0.003) were independently associated with an increased risk of having portal colopathy, whereas the use of beta-blockers independently decreased the risk of having these findings (odds ratio 0.23: 95% CI [0.13, 0.40]; p < 0.001). -----MUCOSAL BIOPSIES OF THE COLON IN PATIENTS WITH "COLITIS-LIKE ABNORMALITIES" REVEALED A MILD, NON-SPECIFIC, INFLAMMATORY INFILTRATE WITH EDEMA AND VASCULAR ECTASIAS IN THE MAJORITY OF CASES.-------------CONCLUSIONS: Mucosal abnormalities in portal colopathy include edema, erythema, granularity, friability, and vascular lesions, findings that may be confused with colitis. A standardized grading system to classify the endoscopic appearance and severity of portal colopathy should be adopted.__________________ www.leapallergy.com


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## wanderingstar (Dec 1, 1999)

Mike, do you know if there is any study on ESR rates in IBS and IBD? Or doesn't ESR get implicated in the same way? I'm wondering if an ESR rate which is unexpectedly high (i.e. higher than even the highest rate that would be expected in an inflammatory illness) can be down to IBS?susan


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## Mike NoLomotil (Jun 6, 2000)

HI WANDERINSUSAN...Sorreee so long....hectic hectic day...head may explode from the phone being in my ear without letup...whoa, there's an ugly mental picture...In general, patients with "inflammatory bowel disease" will have an elevated sed rate and patients with "reactive bowel disease" (IBS) will not. I think someone once found 2 or 3% of a group to have a somewhat elevated sed rate but it is not associated with functional bowel disorders (D or C or cyclic) that I know of.Oh yeah you asked in that other place if I had a good time in Miami last night. Actually I did because it was not busines!!Have a VFDMNL


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## wanderingstar (Dec 1, 1999)

Hi Mike, life sounds tres hectic for you! Thanks for your reply, it was helpful. I didn't think there could be a connection for most people with IBS and high ESR, seems to be different mechanisms. Just wondering!susan


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## Guest (Nov 7, 2000)

Mike,The 224 IBS subjects in the control group exhibited the following breakdown of results from a colonoscopy:Normal colonoscopy: 98 (44%)Hemorrhoids: 96 (42%)Vascular lesions: 7 (3%)Colitis-like abnormalities: 6 (3%)Rectal varices: 2 (1%)The # of IBS subjects with "colitis-like abnormalities" was extremely small compared to the group with portal hypertension. Of the latter, 167 (38%) exhibited such abnormalities. Biopsies of five of the six IBS controls with "colitis-like abnormalities" revealed a "mild, nonspecific inflammatory infiltrate; the remaining biopsy specimens did not reveal any abnormalities. Vascular dilatation and/or ectasia were not seen in any of the remaining mucosal biopsy specimens from patients in the control group."The authors go on to note that: "Studies, including our own, have shown that the endoscopic appearance of colonic mucosal edema and erythema is not associated with significant inflammatory infiltrates, but rather mucosal vessel changes." (thickening and increased branching of mucosal vessels.)


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## Mike NoLomotil (Jun 6, 2000)

GUY:First of all the functional phraseology is infiltrate and secondly site of insult. The residual tissue response in the colon will always be far lower in frequency of incidence as it is far from the site of insult (the point in the GI tract where the specific allergen is absorbed and exposed to circulating immune cells). As much as 20 feet away.Also the inflammatory reactions in IBS patients do not produce any eosinophilia, at least not in the colon, and this a cardinal sign of inflammtory infiltrate. No population "IBS symptom-set" patients have been subjected to mid-gut full thickness biopsy and in vivo examintaion of the microvasculature and surrounding tissue. But their circulating immune system has and, the finidngs have been such that this will be accelearted over the next 2-5 years. It is not a tissue response it is an intravascular response.To to the etiology and anatomy, the local effects in the colon are far less pronounced and in a smaller population of IBS patients, and when present generally reflect only the most pronounced reactivity (as this is far from the site of insult) and the involvement in THOSE patients of circulating vasoactive mediators. Keep in mind, "the allergen has already been presented" and the microvascular-specific reactions have already taken place elsewhere and long before any chyme reaches the colon. Effects seen, if any, in the colon tend to reflect any effects of mediators which are in the plasma of blood circulating within the systemic circulation, of which colonic microvasculature is a part. If the mast cells are activated (which is likely episodic and not a primary mechanism of IBS at all) only then would it be likely to see an infltrative inflammatory response as there is nothing occurring to elicit eosiniophilia in this particlualr type of reactivity. Its just never there. Any non-specific signs of intravascular or tissue response are the tip of an iceberg, and ususlly the this tip will not show except in the population of either the most reactive subjects and/or those significant amounts of vasocative mediators are circulating as a result of reaction which occurred up in the small gut.This is the problem with any investigation of IBS is focuses on the colonic tissue...this is not the site of insult, merely an organ which reacts to stimuli which are triggered by reactions taking place elsewhere (exception being those episodes where a mast cell reaction may be transiently invoked, as mast cell concentration in the cecum is increased so the reaction will be clinically more pronounced should one occur).This is why newer in vitro analysis methods seeking the end-points of the reactions were developed. Not for IBS specifically, but because it was discovered long ago that all the symptom-sets associated with these types of reactions are inscrutable from a tissue exam view, and even from a "molecular biology" view as the various mechanisms of immunologic response are not thotoughly understood. So certain immunologists realized This is where the actual investigation of the underlying causes of these symtpomologic-sets needs to start: find the evidence of the common end-point of all the reactions thast may be involved regardless of mechanism in the circulating immunologic structures, establish their correlation clinically, and then work down in that tedious fashion that must be followed to separate each and every mechanism by the various markers. Sort of a "top-down" approach. The mediator-specific approach could take eons, as we constantly are reminded by the inconsistency of the mainstream approach vis a vis looking at colonic tissue. In 1985 at the group working at U of M identified in the selected symptomatic subjects an entire array of indicators were found to be present, even immune complexes, suggesting immune responses outside-the-box of traditional classification (which is based upon incomplete knowledge in the first place). The reactivity seen in the granulocytic, lymphocytic and even platelet mechanisms bordered on bizarre, and still does, in the context of "Gell & Coombs Classification".MNL________________ www.leapallergy.com


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