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

Clinical Presentation

A classic triad, first described by Samter and Beers [25] in 1968, consists of rhinitis with nasal polyps, sinusitis, asthma, and aspirin sensitivity. Typically, the disease often begins after a viral infection. The symptoms usually start after the age of 10 years and peak around the third decade of life. After the ingestion of ASA or NSAIDs, an acute asthma exacerbation occurs within 3 h accompanied by profuse rhinorrhea, conjunctival injection, periorbital edema, and, sometimes, a scarlet flushing of the face and neck. Fifty percent of the patients with AIA have chronic, severe, corticosteroid-dependent asthma, 30% have moderate asthma that can be controlled with inhaled steroids, and the remaining 20% of patients have mild and intermittent asthma. [26] Bronchoconstriction may be severe and life-threatening, requiring hospital admission, and, at times, requiring mechanical ventilation. Up to 25% of hospital admissions for acute asthma requiring mechanical ventilation may be due to NSAID ingestion. [27] Based on the clinical features, intolerance to aspirin and other NSAIDs was divided into the following three major groups: type A (asthmatic and/or rhinitic); type B (urticaria/angioedema); and type C (a combination of type A and type B).[28,29]


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