There have frequently been doubts as to the relevance of food allergy, in particular as far as the involvement of the intestinal tract is concerned. Several studies, however, have confirmed the existence of allergic reactions in the gut, with an estimated prevalence of about 1–2% in adults. Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. In addition to classical IgE-dependent degranulation, further agonists have been demonstrated for mast cell activation, for example IL-4. The methods used to confirm the diagnosis of instestinal allergy are still insufficient. Until now, blinded oral challenge procedures with food antigens have been accepted as the ‘gold standard’ in diagnosing food allergy, although these tests have practical problems. Therefore, new test systems have been developed, such as endoscopic provocation tests, that may improve diagnostic procedures. Elimination diet still presents the main basis of therapy. Aspects to be focused on in the future are the role fo IgE-independent allergic mechanisms in intestinal allergy, the impact of cross-reactivity with other allergens and the relationship to other inflammatory bowel diseases such as Crohn’s disease, ulcerative colitis, celiac disease and irritable bowel syndrome.
Our data strongly suggest that the EG1 to EG2 ratio may be a marker of tissue eosinophil activation. Low ratios (<1) indicate eosinophil activation, whereas ratios > or =1 are found in healthy controls. Furthermore, we show that EOG is characterized by a pronounced intestinal eosinophil accumulation and activation, whereas in CD and UC, eosinophils seem to be activated but their number is not or only slightly elevated compared to controls.
Background: To improve the diagnosis of intestinal allergy, we developed a colonoscopic allergen provocation (COLAP) test. Methods: The cecal mucosa was challenged with three food antigen extracts, a buffer control and a positive control (histamine). The mucosal wheal and flare reaction was registered semi-quantitatively 20 min after challenge, and selected tissue biopsies were examined for mast cell and eosinophil activation by immunohistochemistry and electron microscopy. The COLAP test was performed on 70 adult patients with abdominal symptoms suspected to be related to food allergy and in 5 healthy volunteers. In parallel, skin prick tests were performed and IgE was measured in serum. Results: 97 out of 210 antigen challenges performed in the patient group induced a significant wheal and flare reaction of the mucosa (46%), whereas no reaction in response to antigen was observed in healthy volunteers. Antigen-induced wheal and flare reactions were dependent on patients’ histories of adverse reactions to food, but not on serum levels of specific IgE or skin test results. Degranulation of mast cells was observed in almost all tissues in which food antigens caused a wheal and flare reaction. Eosinophil activation was also highly correlated with the extent of the wheal and flare reaction (rs = 0.86). Conclusions: The data suggest that the COLAP test may be a useful diagnostic means in patients with suspected intestinal food allergy and a new tool for the study of underlying mechanisms.
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