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

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.

SUMMARY

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.