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

Abstract and Introduction


Aspirin is not only one of the best-documented medicines in the world, but also one of the most frequently used drugs of all times. In addition to its role as an analgesic, aspirin is being increasingly used in the prophylaxis of ischemic heart disease and strokes. The prevalence of aspirin intolerance is around 5 to 6%. Up to 20% of the asthmatic population is sensitive to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) and present with a triad of rhinitis, sinusitis, and asthma when exposed to the offending drugs. This syndrome is referred to as aspirin-induced asthma (AIA). The pathogenesis of AIA has implicated both the lipoxygenase (LO) and the cyclooxygenase (COX) pathways. By inhibiting the COX pathway, aspirin diverts arachidonic acid metabolites to the LO pathway. This also leads to a decrease in the levels of prostaglandin (PG) E2, the anti-inflammatory PG, along with an increase in the synthesis of cysteinyl leukotrienes (LTs). Evidence suggests that patients with AIA have increased activity of LTC4 synthase, the rate-limiting enzyme in the cysteinyl LT synthesis, in their bronchial biopsy specimens, thereby tilting the balance in favor of inflammation. LT-modifying drugs are effective in blocking the bronchoconstriction provoked by aspirin and are used in the treatment of this condition. Aspirin desensitization has a role in the management of AIA, especially in patients who need prophylaxis from thromboembolic diseases, myocardial infarction, and stroke. This review covers the latest understanding of pathogenesis, clinical features, and management of AIA.


A hundred years have passed since Felix Hoffmann, a German chemist, developed aspirin as a treatment for his father's arthritis. Since then, aspirin, or acetylsalicylic acid (ASA), has remained one of the world's safest, least expensive, and most consumed analgesics. In the United States, the annual consumption of aspirin is approximately 80 billion tablets, while in the United Kingdom it is approximately 100 tons. Apart from its analgesic and antipyretic properties, aspirin also possesses antiplatelet activity and is, therefore, used in the prophylaxis of thromboembolism, the prevention of transient ischemic attacks, and the reduction of the risk of morbidity and mortality in patients with unstable angina and myocardial infarction.

The association of aspirin sensitivity, asthma, and nasal polyposis was first described by Widal et al [1] in 1922. Aspirin-induced asthma (AIA) refers to the development of bronchoconstriction in asthmatic individuals following the ingestion of aspirin. This syndrome encompasses classic symptoms of chronic rhinoconjunctivitis, nasal polyps, and asthma akin to a protracted viral respiratory infection. In patients with AIA, acute symptoms are superimposed on a background of chronic severe asthma. The attacks may be precipitated following the ingestion of small amounts of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). The prevalence of AIA in the community is not certain, but patients with AIA constitute about 10 to 20% of the asthmatic population, [2,3] and AIA is more common in women. A Finnish study [4] showed an overall aspirin intolerance of 5.7% and the prevalence of AIA to be 1.2%. Over the last few years, there has been an increased under-standing of the pathogenesis and management of AIA. This review discusses the clinical features, the pathogenic mechanisms, and the management of AIA.


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