Aspirin exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis (CRS) with nasal polyposis, and acute upper and lower respiratory tract reactions to ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 (COX-1) inhibiting nonsteroidal antiinflammatory drugs (NSAIDs).
The first case of aspirin sensitivity in a patient with asthma was described in 1902, a few years after the introduction of aspirin into clinical use. In 1968, Samter and Beers described a triad consisting of asthma, aspirin sensitivity, and nasal polyps , which came to be known as Samter's triad.
An overview of AERD with emphasis on pathophysiology and the management of asthma will be presented here. Other types of hypersensitivity reactions to NSAIDs and the treatment of patients with asthma, CRS, and nasal polyposis are discussed separately. (See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions" and "Diagnostic challenge and desensitization protocols for NSAID reactions" and "An overview of asthma management" and "Management of chronic rhinosinusitis".)
NSAIDs — The primary effect of nonsteroidal antiinflammatory drugs (NSAIDs) is to inhibit cyclooxygenase (also called prostaglandin synthase), thereby impairing the ultimate transformation of arachidonic acid (AA) to prostaglandins, prostacyclin, and thromboxanes and enhancing production of leukotrienes. Two related isoforms of the cyclooxygenase (COX) enzyme have been described, COX-1 and COX-2. Some NSAIDs have a greater inhibitory effect on COX-1 and others on COX-2. COX-1 inhibition is the stimulus for acute reactions to aspirin (ASA)/NSAIDs in AERD.
In this topic review, the term NSAID includes aspirin (ASA). However, in some clearly marked sections, aspirin is discussed exclusive of other NSAIDs.