Aspirin-exacerbated respiratory disease: An easy-to-overlook diagnosis

Patients who have aspirin-exacerbated respiratory disease (AERD) usually experience upper and lower respiratory tract symptoms about 1Z|x to 2 hours after taking aspirin or another NSAID that inhibits the enzyme cyclooxygenase-1. In addition to symptoms such as nasal congestion, rhinorrhea, paroxysmal sneezing, periorbital edema, laryngospasm, and intense flushing, patients may have severe--often life-threatening--exacerbations of asthma. AERD occurs in about 10% to 20% of patients with asthma and in about 30% of asthmatic patients with nasal polyposis. However, AERD also occurs in patients who do not have any of these predisposing conditions. In patients with AERD, aspirin desensitization can improve asthma control, reduce the need for corticosteroids, and reduce the need for sinus surgery. (J Respir Dis. 2006;27(7):282-290) Asthma is a chronic inflammatory disease of the lung that affects millions of Americans and tens of millions of persons worldwide. The prevalence of asthma has increased dramatically over the past 50 years. It is estimated that 10% to 20% of all persons with asthma experience an exacerbation of respiratory symptoms on ingestion of aspirin or other NSAIDs. The incidence of adverse reactions increases to 30% in persons with asthma and radiographic evidence of sinusitis and nasal polyps. Given the prevalence of asthma, it is imperative that pulmonologists, allergists, emergency department physicians, and primary care physicians be aware of aspirinexacerbated respiratory disease (AERD). In this article, we will discuss the epidemiology, pathogenesis, and management of AERD.Aspirin: A brief history Over the centuries, the use of aspirin has extended from the treatment of pain and fever to the prevention and management of a multitude of diseases and chronic conditions, including coronary artery disease, stroke, colon cancer, and mastocytosis. The first documented use of aspirin-related compounds was in 200 bce when the Greek physician Hippocrates prescribed the bark and leaves of the willow tree (rich in salicin) as a treatment for pain and fever. The use of willow leaves is also mentioned in the works of Dioscorides in 100 ce and Galen in 200 ce. It was not until 1838 that the Italian chemist Raffaele Piria synthesized salicylic acid from salicin. In 1897, Felix Hoffman, a chemist working at Bayer (a then little-known company in Germany), started experimenting with different techniques to decrease the irritating gastric effects of salicylic acid for his father who had rheumatism. He succeeded with the creation of acetylsalicylic acid, which has been the most frequently used medication worldwide since 1899. Aspirin has been available over the counter (OTC) in the United States since 1915. Although it has proved to be a miracle drug for millions, it is a source of considerable morbidity for others. In 1922, Widal and associates1 described the first case of aspirin sensitivity, asthma, and nasal polyps along with the first successful attempt at aspirin desensitization. The constellation of aspirin sensitivity, asthma, and nasal polyposis was described by Max Samter in the 1960s and is still often referred to as Samter's triad. It is increasingly recognized that many patients with AERD do not have asthma and experience respiratory symptoms only after ingestion of aspirin. Since not all patients who react adversely to aspirin meet all criteria for Samter's triad, the term "aspirin-exacerbated respiratory disease" was adopted to more accurately describe this syndrome. The term "AERD" is used to describe a condition in patients who experience upper or lower respiratory tract symptoms after ingestion of aspirin or other NSAIDs that inhibit the enzyme cyclooxygenase (COX)-1. This term is preferable to "aspirin-intolerant asthma" because some of these patients do not have asthma, and ingestion of aspirin elicits only upper airway symptoms.Epidemiology and presentation More than 26 million Americans have asthma.2 Of these persons, it is estimated that 10% to 20% experience an idiosyncratic reaction after ingestion of aspirin or other NSAIDs that inhibit COX-1.3-5 It is estimated that 20% to 30% of patients with chronic hyperplastic eosinophilic sinusitis (CHES) have an exacerbation of upper and lower airway symptoms on exposure to aspirin and other