Aspirin and Asthma

K. Suresh Babu, MD, DNB; and Sundeep S. Salvi, MD, DNB, PhD, From the Department of Respiratory Cell and Molecular Biology, University of Southampton, Southampton General Hospital, Southampton, UK.


CHEST. 2000;118(5) 

In This Article

Pathogenesis of AIA

Asthma is an inflammatory condition of the airways characterized by the shedding of airway epithelium, sub-basement membrane fibrosis, airway smooth muscle hypertrophy, excessive secretion of mucus, and multicellular inflammation involving activated mast cells, eosinophils, neutrophils, macrophages, basophils, and lymphocytes. In this state of continuous inflammation, exposure to aspirin in a subset of asthmatic patients appears to temporarily accentuate the inflammatory process, leading to asthma exacerbations.

The precipitation of an acute attack by aspirin is similar to the immediate hypersensitivity reaction and suggests an antigen antibody reaction. However, the skin test responses with ASA lysine are negative, and repeated attempts to demonstrate an antibody against ASA or its derivatives have been futile. [5] Hypersensitivity reactions to aspirin and other NSAIDs are, therefore, unlikely to be mediated by IgE-dependent mechanisms. Consistent and reliable identification of IgE antibodies against either aspirin or NSAIDs has not been accomplished in patients receiving AIA, hence, the reactions could be termed as anaphylactoid. In recent years, it has become increasingly clear that aspirin hypersensitivity is likely to be mediated by a deviation of the arachidonic acid metabolic pathway toward excessive leukotriene (LT) production, which then produces all the clinical features of AIA.


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