Interaction between foods and nonsteroidal anti-inflammatory drugs and exercise in the induction of anaphylaxis

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Purpose of review

To assess the studies that focus on the study of food-dependent exercise-induced anaphylaxis (FDEIA) and food-dependent NSAID-induced anaphylaxis (FDNIA).

Recent findings

Cofactors, as exercise and nonsteroidal anti-inflammatory drugs (NSAIDs), are relevant in up to 30% of episodes of anaphylaxis. Gliadin and lipid transfer proteins are the main allergens involved. The attempts to reproduce FDEIA and FDNIA in a controlled setting have an important failure rate. The cyclooxigenase (COX) pathway could play an important role in the underlying mechanisms: NSAIDs and exercise increase the permeability of the intestinal barrier. This effect is stronger with NSAID that inhibit both isoforms than with preferential COX-2 inhibitor. Basophils obtained from FDNIA patients, showed an increase of its activation with the food allergen with lysine–aspirin compared with the food allergen alone. This potentiating effect was not observed when basophils were stimulated with the food allergen with selective COX-2 inhibitor. Other mechanisms including transient receptor potential superamily, reactive oxygen species, altered B-cell pathway and increased neutrophil activation markers have been speculated.


The frequent implication of cofactors, as exercise and NSAID, in food-induced anaphylaxis highlights the importance of recognizing and including them into diagnostic workup. The understanding of the underlying mechanisms would help in the development of diagnostic and therapeutic strategies.

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