An Often-Overlooked Cause of Asthma

Nicholas Gross, MD, PhD


June 14, 2012

Aspirin-Exacerbated Respiratory Disease: Burden of Disease

Chang JE, White A, Simon RA, Stevenson DD
Allergy Asthma Proc. 2012;33:117-121


Aspirin-exacerbated respiratory disease (AERD) is a syndrome consisting of asthma and 3 other components, each of which contributes to a significant burden of morbidity, cost, and impaired quality of life. The attacks of bronchospasm are typically precipitated by the use of aspirin or another cyclooxygenase (COX)-1 inhibitor, a nonsteroidal anti-inflammatory drug (NSAID). The other 2 components of this disease are nasal polyposis and chronic rhinosinusitis. The syndrome usually commences in early adulthood, sometimes after a viral infection, and tends to become worse and more difficult to control as it progresses.

Frequent exacerbations, sometimes requiring repeated hospitalizations and tracheal intubation, may occur. Attacks often seem to come "out of the blue," but the use of an NSAID may precipitate an acute attack. Allergies are not a feature of this syndrome. High doses of inhaled corticosteroids or even maintenance oral corticosteroids are often required. Lung function and quality of life tend to be worse in asthmatic patients with AERD than in asthmatic patients without AERD.

Patients with AERD often have severe chronic rhinosinusitis and nasal polyposis. They also tend to have nasal congestion and loss of smell; facial pain; and nasal discharge, which can be mucopurulent. Mucosal swelling and lack of ciliary clearance contribute to the sinusitis. High doses of intranasal corticosteroids are needed but may not completely relieve obstruction, and sleep may be disturbed.

Most patients have undergone nasal polypectomy, sometimes repeatedly, because the polyps are likely to recur. In fact, the need for repeated nasal polypectomy has called into question the value of this procedure.


Also called intrinsic adult-onset asthma or the Samter triad, AERD is estimated to constitute 9% of all asthma diagnoses. However, the syndrome is not widely recognized in clinical practice, which means that the condition goes undiagnosed in many patients and is inadequately treated.

The mechanism of AERD is not entirely understood but is believed to be caused in part by a defect in eicosanoid metabolism.[1] In AERD, the products of arachidonic acid breakdown are directed toward leukotriene production and away from prostaglandin production, resulting in an increase in proinflammatory cysteinyl leukotrienes and a reduction in the anti-inflammatory prostaglandin E2.

COX inhibitors, unless selective for COX-2, intensify the shunt toward leukotriene production, resulting in airway inflammation, bronchoconstriction, and the inflammation of upper respiratory mucosae. Thus, it is essential that patients with this condition be instructed to avoid NSAIDs and NSAID-containing medications.

Patients who require antiplatelet therapy for cardiovascular conditions should use an aspirin alternative, such as clopidogrel. Physicians should also recognize the limited utility of sinus surgery, because polyps and obstruction are likely to recur rapidly.[2,3] Aspirin desensitization may be a beneficial treatment modality but should be performed by experienced personnel only.[4]There is no specific cure for AERD.



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