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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast cells are a significant component of the mucosa in the gastrointestinal tract. There is increasing evidence that these cells are involved in the pathophysiology of various intestinal disorders ranging from food allergy to inflammatory bowel disease. When activated, mast cells release a host of potent mediators and cytokines which are capable of inducing pathophysiology. The bulk of the evidence has come from hypersensitivity studies in experimental animals sensitized either by parasitic infection or by active immunization to an antigen using adjuvants which stimulate IgE production. Subsequent antigen challenge of the gut results in mast cell activation associated with alterations in intestinal functions including ion transport and epithelial permeability. Intestinal secretory transport responses are inhibited by antagonists of mast cell mediators and neurotoxins, implicating mast cell-nerve interactions with the epithelium. In genetically mast cell-deficient mice, antigen-induced secretion is reduced approximately 70% and this component is not affected by neural or mast cell inhibitors; adoptive transfer of bone marrow containing mast cell precursors derived from congenic normal mice restores the complete antigen response. These results provide more direct proof that mast cell activation causes abnormal gut function. Recently, we have begun studies which indicate that activation of mast cells induces ion secretion in surgically resected human intestine. Reduced secretory responses in specimens from patients with IBD suggest that mast cells may play a role in the pathophysiology of inflammatory bowel disease.
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PMID:Functional abnormalities in the intestine associated with mucosal mast cell activation. 150 88

Food allergy, synonymous with food hypersensitivity (FHS), is defined as an immunologically-mediated adverse reaction to food. Initiation of FHS could result from a break in the immune mucosal barrier with abrogation of oral tolerance. Food hypersensitivity is mostly due to immediate-type reaction involving IgE-dependent mastocytes activation. Changes in intestinal function and structure have been mainly studies in an animal model of rat sensitized to egg albumin. Intraluminal antigen challenge resulted in abnormalities of gut absorption, secretion and motility in sensitized rats. In man, experimental data are scarce. Gastrointestinal manifestations of immediate FHS are varying and unspecific. A role for FHS in irritable bowel syndrome is debated. Participation of delayed-type FHS to digestive diseases is still questionable, but eosinophilic gastroenteritis might be an example. In clinical practice, diagnosis of FHS demands rigorous criteria. Double blind placebo-controlled food challenge has eventually proved to be the "gold standard" test for FHS diagnosis.
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PMID:[Digestive manifestations of food hypersensitivity in adults]. 175 69

The immunoglobulins level, were estimated in the sera of 51 patients with different colonic disorders and 12 controls. In 27 of them, tissue immunoglobulin level were estimated. In bilharzial patients there was significant increase in the serum level of IgG, IgM and IgE. IgA and IgD showed no change. IgA containing cells were (87.5%), IgG (50%) and IgM (16.7%). In patients with amoebic colitis, there was significant increase in serum IgG and IgE. IgA and IgD showed significant decrease while IgM was within normal limits. Tissue IgA and IgG were detected in all acses. IgM containing cells were detected in 2 cases. In patients with irritable bowel syndrome (I.B.S.), there was significant high levels of IgM and IgE. IgG showed significant low level, while IgG and IgA showed no change. Tissue IgA were detected in (70%), IgG in (10%) and IgM in (20%). In patients with ulcerative colitis (U.C.), there was significant high levels of IgM and IgE. IgD showed significant low level, while IgG and IgA showed no change. Tissue IgA, IgG and IgM were detected in all cases. In patients with Crohn's disease, the 3 immunoglobulins were detected.
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PMID:Estimation of serum and tissue immunoglobulins level in some colonic disorders. 190 1

We studied 14 patients with irritable bowel syndrome for the presence of increased intestinal permeability to food antigens and their responses to diet with and without disodium cromoglycate. After a standardized oral challenge with cow milk, serum beta-lactoglobulin was increased above control values in three patients. This finding did not correlate with response to hypoallergenic diet or treatment with disodium cromoglycate for 3 weeks. However over 50% of patients improved after diet with and without DSCG (2/5 on diet only and 5/7 with disodium cromoglycate of 12 evaluable cases). Since only two patients had elevated serum IgE levels, our results suggest that intolerance rather than hypersensitivity to foods may play a role in the disease. The tests we used to identify immunologic mechanisms could not predict which patients would do better on the diet and/or the drug.
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PMID:Intestinal permeability in irritable bowel syndrome. Effect of diet and sodium cromoglycate administration. 210 92

An intestinal permeability test analyzing the differential urinary elimination of lactulose and mannitol orally ingested at the same dosage was carried out first in fasting condition, then combined with specific food ingestion, in 17 children with clinical symptoms of irritable bowel syndrome (IBS). Foods were selected based on a suggestive clinical history or on a positive radioallergosorbent or prick test. Comparison of the results with those of a control population reported in a previous study showed that in nine IBS patients, specific food ingestion was associated with a modification of intestinal permeability. The nine children all had a personal and/or familial history of allergy and/or raised total IgE. The symptoms disappeared in the nine patients after food exclusion either alone (seven patients) or together with further treatment by cromolyn (two patients). We conclude that, at least in some children, symptoms of IBS may be related to food hypersensitivity.
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PMID:Modifications of intestinal permeability during food provocation procedures in pediatric irritable bowel syndrome. 211 53

Lymphoid cell subsets, including T cells as well as Ig-containing cells in the colonic mucosa and HLA-DR antigens on colonic epithelia, were examined in non-IBD colitis (colitis excluding ulcerative colitis (UC) and Crohn's disease) by the indirect immunoperoxidase staining method. Mouse anti-CD5, CD8, CD4, IgG, IgA1, IgA2, IgM, IgD, IgE, HLA-DR, and NuIa monoclonal antibodies were used as the first antibody. The results were compared to those of the normal controls and UC. T cell subsets in non-IBD colitis were almost similar to those of the controls and UC. The number of Ig-containing cells of all classes, except for IgA, tended to be increased in non-IBD colitis. In particular, both IgG- and IgE-containing cells were significantly increased compared to those in the controls. Compared to UC, IgG-containing cells were decreased in non-IBD colitis. Namely, in non-IBD colitis, as well as in UC, the change of Ig-containing cells (B cell lineage) was more pronounced than that of T cells. The frequency of the expression of HLA-DR antigens on colonic epithelia in non-IBD colitis was 70%, which was significantly higher than that in controls (0%), but significantly lower than that in UC (100%). Whether the differences in the number of IgG-containing cells, and the frequency of epithelial HLA-DR expression between non-IBD colitis and UC was due to the differences of the degree of local inflammation or due to the differences of the nature of the two diseases was not elucidated in this study.
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PMID:Lymphoid cell subsets in colonic mucosa and HLA-DR antigens on colonic epithelia in colitis excluding ulcerative colitis and Crohn's disease. 227 31

Ten patients with irritable bowel syndrome were evaluated for food hypersensitivity with skin testing (IgE) and IgG serum antibodies (RAST panel) to common food antigens. Patients also underwent an open elimination diet for 2 weeks followed by a 48-hour challenge of each food that was considered to be suspicious from patients diary, positive skin prick test, and/or positive IgG antibodies. Six patients had positive skin scratch test results and only one patient had RAST IgG food antibodies greater than 3,000 cpm which is a marked increase above normal. None of the patients however had an exacerbation of their irritable bowel symptoms with a food challenge. We conclude therefore that positive skin testing and IgG serum antibodies are not reliable indicators of food hypersensitivity in irritable bowel syndrome and that food hypersensitivity does not seem to play a role in the symptoms related to the irritable bowel syndrome.
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PMID:The irritable bowel syndrome and food hypersensitivity. 338 71

Food hypersensitivity as a cause of irritable bowel syndrome was investigated by means of exclusion diet and blind provocation. Twelve atopic and twelve non-atopic individuals entered into the study. Skin prick testing with 20 foods and food additives and RAST specific for food only, were done in all cases. Serum IgE level was also measured. In 14 patients one or several food or additives were shown to induce the typical symptoms of IBS. In at least nine cases of atopy, an IgE-mediated mechanism could be incriminated. Among other potential pathogenetic mechanisms, the presence in the intestinal tract of yeast (Candida albicans, Geotrichum candidum) seems to be of major importance. Yeast apparently favor the development of allergic as well as pseudo-allergic reactions, at least in some patients. Finally, at least in atopic patients complaining of IBS, it is of importance to search for a food component. Dramatic clinical improvements can result from the introduction of an adequate exclusion diet.
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PMID:Irritable bowel syndrome and hypersensitivity to food. 401 82

Adverse reactions to foods can be due to many causes, but only those involving an immunological mechanism can be defined as food allergic disease. An increasing number of gastrointestinal and other diseases are being shown to involve food intolerances. Immediate reactions with symptoms within hours of eating a particular food are most readily shown to be due to food allergy and are often associated with the presence of food-specific IgE as shown by skin prick tests and RASTs. When reactions are delayed for 24 to 48 hours or more, underlying food intolerance is harder to recognize and much less often shown to be due to allergy. At present, diagnosis and management depends on dietary manipulation, showing that symptoms improve on food avoidance and are reproduced by food challenge (preferably double-blind). Further understanding of the mechanisms involved in food allergy, in Crohn's disease and irritable bowel syndrome may allow the development of simple tests to identify the foods concerned and perhaps, in the case of allergic disease, cure by the induction of tolerance.
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PMID:Symptoms of food allergy. 406 57

Reaginic hypersensitivity in ulcerative colitis has been investigated in respect of a hypersensitivity to the cow's milk proteins and the frequency of atopic asthma, hay fever, and eczema. Intradermal tests were frequently positive, especially to casein, but the results did not differ from those found in healthy individuals and in groups of patients with Crohn's disease, hypolactasia, and the irritable colon syndrome. No circulating IgE-specific antibodies to the milk proteins were found. An increased frequency of atopic diseases was found in patients suffering from ulcerative colitis (15.7%) and Crohn's disease (13.3%) compared with the findings in a control group (1.2%). It is concluded that, if an allergy to milk proteins is a factor in the pathogenesis of ulcerative colitis, it is not mediated by reaginic antibodies. It is possible, however, that the frequent occurrence of atopy indicates a susceptibility to develop reaginic responses even though this mechanism does not apply to the milk proteins.
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PMID:Reaginic hypersensitivity in ulcerative colitis. 464 93


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