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[Acetylsalicylic acid: hypersensitivity, intolerance, or allergy?]
1Unité d'immuno-allergologie, Laboratoire Pasteur-Cerba, 95066 Cergy-Pontoise.
Summary
Acetyl salicylic acid (ASA) and NSAID sensitivity mechanisms remain unclear despite a century of use. Research suggests multiple pathways, including immune responses and cellular activation, contribute to adverse reactions.
Area of Science:
- Pharmacology
- Immunology
- Toxicology
Background:
- Acetyl salicylic acid (ASA) has been used therapeutically for a century.
- The precise mechanisms underlying ASA's therapeutic effects and adverse reactions in sensitive individuals are not fully understood.
- Non-steroidal anti-inflammatory drugs (NSAIDs) share similar reaction pathways.
Purpose of the Study:
- To review and consolidate the proposed mechanisms of acetyl salicylic acid (ASA) and NSAID hypersensitivity.
- To highlight the complexity and multifactorial nature of these reactions.
- To emphasize the need for accurate diagnosis in managing ASA/NSAID sensitivity.
Main Methods:
- Literature review of scientific results published over the last century.
- Analysis of proposed mechanisms including humoral, cellular, enzymatic, and protein-binding pathways.
- Comparison of ASA/NSAID reaction components with those of anaphylactic reactions.
Main Results:
- Multiple mechanisms are implicated in ASA/NSAID hypersensitivity.
- These include humoral immune reactions (IgE, IgG), cellular immune reactions (lymphocytes), cyclooxygenase inhibition, cellular activation (mast cells, basophils, eosinophils, platelets), serum albumin competition, and complement activation.
- Many components overlap with those found in anaphylactic reactions.
Conclusions:
- ASA and NSAID hypersensitivity reactions are complex and likely involve multiple interacting mechanisms.
- A single mechanism cannot explain all observed reactions.
- Accurate diagnosis is crucial for effective management of patients sensitive to ASA and other NSAIDs.