To evaluate research focusing on the investigation of food-dependent exercise-induced anaphylaxis (FDEIA) and food-dependent NSAID-induced anaphylaxis (FDNIA). Exercise and nonsteroidal anti-inflammatory medications (NSAIDs) are cofactors in up to 30% of anaphylactic reactions. The primary allergens implicated are gliadin and lipid transfer proteins. Attempts to replicate FDEIA and FDNIA in a controlled setting fail frequently. The cyclooxygenase (COX) pathway may be essential in the following mechanisms: NSAIDs and exercise enhance gut barrier permeability. This impact is greater with NSAIDs that block both isoforms than with COX-2 inhibitors that target only one isoform. Basophils from FDNIA patients demonstrated increased activation with the food allergen when treated with lysine–aspirin compared to the food allergen alone. When basophils were stimulated with the food allergen while using a specific COX-2 inhibitor, this potentiating effect was not detected. Other hypotheses include transient receptor potential superamily, reactive oxygen species, a changed B-cell route, and enhanced neutrophil activation markers.
The frequent involvement of cofactors in food-induced anaphylaxis, such as exercise and NSAID, emphasises the significance of detecting and incorporating them in the diagnostic workup. Understanding the underlying mechanisms might aid in the development of diagnostic and treatment approaches.
