• Journal of Life Science
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• v.20 no.1
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• pp.147-152
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• 2010

Exercise-induced anaphylaxis (EIA) is a physical allergy, sometimes severe, triggered by exertion following specific food intake. It was defined for the first time in 1980. EIA is associated with different kinds of exercise. The clinical manifestations progress from itching, erythema and urticaria to some combination of cutaneous angioedema and vascular collapse. Mast cell participation in the pathogenesis of this syndrome has been proved by the findings of an elevated serum histamine level during exhaustive exercise. As predisposing factors of EIA, a specific or even nonspecific sensitivity to food has been reported. Food-dependent exercise-induced anaphylaxis (FDEIA) is a distinct form of food allergy induced by physical exercise. It is typified by the onset of anaphylaxis during exercise which was preceded by the ingestion of the causal food allergens. The diagnosis of FDEIA is heavily dependent on clinical history. Allergy tests may need to be performed using a broad panel of food and food additives. As with food allergies, FDEIA diagnosis is based on interview, biological test and skin test. Prophylaxis aims to prevent a recurrence; the patient should be given an emergency kit to deal with any recurrent episodes. After the food allergen has been identified, it should be avoided for at least 4 to 5 hours before any exercise. Two cases of EIA are presented (EIA to circumstances; FDEIA) in this paper, The diagnosis, pathophysiology and therapy of FDEIA are also reviewed.

• Journal of Life Science
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• v.20 no.4
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• pp.511-518
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• 2010

Exercise-induced anaphylaxis (EIA) is defined as the onset of allergic symptoms during, or immediately after, exercise, the clinical signs being various degrees of urticaria, angioedema, respiratory and gastrointestinal signs, and even anaphylactic shock. Food-dependent exercise-induced anaphylaxis (FDEIA) is a specific variant of exercise-induced anaphylaxis that requires both vigorous physical activity and the ingestion of specific foods within the preceding several hours. To describe the physiopathologic mechanism, etiologic factors, and clinical manifestations, we evaluated the supplementation of vitamin C and catalase on spleen index, proliferation assay, ROS, and ASAS in sensitized and exercise trained mice. The results were as follows: Spleen index showed the highest level in the ST12 group compared to other groups; this level increased in a time dependent manner and in significant amounts. In proliferation assay of Med and OVA, the ST12 group showed the highest level compared to other groups; this level also increased in a time dependent manner. On the other hand, spleen ROS did not show a statistically significant difference, and peritoneal ROS showed the highest level in the ST12 group. ASAS showed the highest level in the ST12 compared to the S; this was also in a time dependent manner and in significant amounts. From the results, we chose the ST9 and ST12 groups to evaluate allergy anaphylaxis with supplementation of Vitamin C and catalase. In both the ST9 and ST12 groups, peritoneal ROS and ASAS were lower in vitamin C treatment group than in the catalase treatment group. This was a statistically significant difference. From the results, allergy anaphylaxis showed a higher level in the long trained group than in the short trained group. Also, treatment with vitamin C was more effective in lowering allergy anaphylaxis than catalase treatment.

• Nutrition Research and Practice
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• v.7 no.5
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• pp.347-351
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• 2013

Food-dependent exercise-induced anaphylaxis (FDEIAn) is induced by different types and various intensities of physical activity, and is distinct from food allergies. It has been shown that consumption of allergenic food followed by exercise causes FDEIAn symptoms. Intake of allergenic food or medication before exercise is a major predisposing factor for FDEIAn. Urticaria and severe allergic reactions are general symptoms of FDEIAn. Dermatological tests and serum IgE assays are the typical prescreening methods, and have been used for several decades. However, these screening tests are not sufficient for detecting or preventing FDEIAn. It has been found that exercise may stimulate the release of mediators from IgE-dependent mast cells that can result in FDEIAn when a certain threshold level has been exceeded. Mast cell degradation might be a major factor to induce FDEIAn but this has not been determined. A number of foods have been reported to be involved in the onset of FDEIAn including wheat, eggs, chicken, shrimp, shellfish, nuts, fruits, and vegetables. It is also known that aspirin increases the occurrence of type I allergy symptoms when combined with specific foods. Moreover, high intensity and frequent exercise are more likely to provoke an attack than low intensity and less frequent exercise. In this paper, we present the current views of the pathophysiological mechanisms underlying FDEIAn within the context of exercise immunology. We also present a detailed FDEIAn definition along with etiologic factors and medical treatment for cholinergic urticaria (UC) and exercise-induced anaphylaxis (EIA).