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The broken balance in aspirin hypersensitivity
Andrzej Szczeklik1, Marek Sanak
1Department of Medicine, Jagiellonian University School of Medicine, Skawinska 8, 31-066 Krakow, Poland. mmszczek@cyf-kr.edu.pl
European Journal of Pharmacology
|February 7, 2006
Summary
Aspirin hypersensitivity, causing asthma and urticaria, is linked to leukotriene overproduction and cyclooxygenase inhibition. Genetic and environmental factors may trigger these underdiagnosed reactions in susceptible individuals.
Area of Science:
- Immunology
- Pharmacology
- Clinical Medicine
Background:
- Aspirin, a widely used drug, can trigger hypersensitivity reactions.
- Recent insights link these reactions to cysteinyl leukotriene overproduction and arachidonic acid metabolism.
- Aspirin hypersensitivity encompasses conditions like aspirin-induced asthma, rhinosinusitis, and urticaria.
Purpose of the Study:
- To describe common clinical presentations of aspirin hypersensitivity.
- To elucidate the biochemical background of these reactions.
- To highlight the underdiagnosis of aspirin hypersensitivity worldwide.
Main Methods:
- Review of clinical presentations and biochemical pathways.
- Analysis of cyclooxygenase (COX) inhibition mechanisms.
- Discussion of mast cell activation and prostaglandin E2 (PGE2) roles.
Main Results:
- Acute reactions are triggered by non-steroid anti-inflammatory drugs (NSAIDs) via COX inhibition.
- Selective COX-2 inhibitors (Coxibs) do not typically induce symptoms.
- Aspirin-induced asthma and urticaria involve mast cell mediator release, potentially influenced by PGE2 levels.
Conclusions:
- Aspirin hypersensitivity, particularly aspirin-induced asthma and urticaria, is driven by inflammatory mediator release.
- While COX inhibition is implicated, the precise origins remain unclear.
- Genetic predisposition combined with environmental factors, such as viral infections, may trigger the condition in susceptible individuals.