Aspirin-induced asthma (AIA) is a distinct clinical entity and appears to be a specific subtype of asthma. It is characterised by asthma triggered within one to three hours of ingestion of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). The asthma attack is often accompanied by or even preceded by symptoms of rhinitis (nasal obstruction, rhinorrhoea and sneezing) and facial flushing. The asthma attack triggered by aspirin and NSAIDs may be very severe and life threatening. The common feature of medications that trigger this reaction is their inhibition of the cyclo-oxygenase 1 (COX-1) enzyme.^{2 <LE IV>}

The clinical picture of this asthma syndrome differs from that of the majority of patients with childhood onset or allergic asthma. The initial onset of symptoms appears at an average age of 30 years, with rhinitis characterised by persistent watery rhinorrhoea, nasal obstruction and sneezing. Loss of a sense of smell, with development of troublesome nasal polyps (often requiring repeated nasal polypectomies), occurs in up to two thirds of patients. On average, asthma develops two years after the onset of rhinitis, with intolerance to aspirin and other NSAIDs occurring about four years later.^{3 <LE III-3>} Other names for this syndrome include Francis’ Triad, Samter’s Triad and the Aspirin Triad.⁴ As previously mentioned, it may co-exist with other patterns and subtypes of asthma.

Patients with AIA may often be unaware of their intolerance to aspirin. They may have taken aspirin or NSAIDS in the past, before onset of this syndrome, without any adverse reactions. However, in contrast to other types of allergies, the development of AIA does not depend on having had previous exposure to aspirin or NSAIDs. Although avoidance of all NSAIDS is important to prevent acute attacks, the condition tends to be progressive, despite avoidance of these medications. Avoidance of dietary salicylates has not been shown to improve the condition.

How common is aspirin-induced asthma?

Reports of the prevalence of this condition in adults with asthma have varied between 3-22%,^{5 <LE I>} depending on the diagnostic methods used. Recent Australian data based on questionnaires alone show that about 10-11% of adults with asthma report asthma triggered by aspirin or NSAIDs.^{6 <LEIII-2>} However, prevalence by oral provocation testing was estimated at 22% in adults, 10% in children, according to a recent evidence-based review. ^{5 <LE I>} The condition appears to be more common in patients with moderate to severe persistent asthma, particularly those with a history of nasal polyposis. Many of these patients are not atopic, and have increased baseline production of leukotrienes.

What is the mechanism of aspirin-induced asthma?

The central characteristic of these patients is their sensitivity to medications that inhibit the COX-1 enzyme. The COX enzymes produce a range of mediators that are responsible for regulating normal body functions (mainly COX-1) as well as inflammation, fever and pain (mainly COX-2). One of the mediators produced by COX-1 that regulates normal body function is prostaglandin E2. Evidence suggests that reduction of prostaglandin E2 levels by medications that inhibit COX allows activation of an enzyme pathway to produce increased amounts of inflammatory mediators called leukotrienes.
These leukotrienes are responsible for many of the manifestations of an asthma attack, triggered in these patients by aspirin and NSAIDs.

Figure 1 The mechanism of aspirin-induced asthma

Content Updated March 2005