Abstract
The correlation between aspirin sensitivity, asthma, and nasal polyposis was recognized in the early 20th century. Today, this classic triad of symptoms, eponymously named Samter’s Triad, is known as aspirin exacerbated respiratory disease (AERD). Aspirin exacerbated respiratory disease affects approximately 0.3–0.9% of the general population in the USA and approximately 7% of asthmatic patients. The management of AERD is challenging as no single modality has proven to have high rates of symptom control. Consequently, disease management typically involves a multimodality approach across both medical and surgical disciplines. This review describes the epidemiology of AERD and the current state-of-the-art as it relates to the underlying pathophysiologic mechanisms of this disease process. A significant proportion of the review is focused on the appropriate diagnostic workup for AERD patients including the utility of aspirin provocation testing. The spectrum of medical treatments, including aspirin desensitization and recently introduced immunotherapies, are discussed in detail. Furthermore, surgical approaches to disease control, including advanced endoscopic techniques, are reviewed and treatment outcomes presented.
Highlights
Hypersensitivity reactions to aspirin were described as early as 1902 but it was not until 1922 thatWidal et al first described the correlation between aspirin sensitivity, asthma, and nasal polyposis [1].Subsequently, in 1968, Samter and Beer described the full clinical characteristics of aspirin sensitivity and elucidated the classic triad of symptoms, eponymously named Samter’s Triad [1,2]
The authors found that fluticasone propionate completely prevented ASA-precipitated nasal reactions in 8 of 13 participants as measured by negative ASA provocation tests in previously positive individuals compared to 2 of 12 in the placebo arm. These results suggest that fluticasone propionate and other topical glucocorticoids are effective in treating rhinosinusitis in aspirin exacerbated respiratory disease (AERD) [54]
Mepolizumab targets IL-5 and was originally designed to treat eosinophilic asthma, but Gevaert et al found in a randomized, double-blind placebo-controlled study in chronic rhinosinusitis with nasal polyposis (CRSwNP) patients that injection of two 750 mg doses significantly reduced the total polyp score (−1.30, p = 0.028) and showed improved computed tomography (CT) scan results in 12 of 20 patients when reviewed by three separate raters (Fleiss κ = 0.679) [71,72,73]
Summary
Widal et al first described the correlation between aspirin sensitivity, asthma, and nasal polyposis [1]. In 1968, Samter and Beer described the full clinical characteristics of aspirin sensitivity and elucidated the classic triad of symptoms, eponymously named Samter’s Triad [1,2]. Samter’s Triad is defined as chronic rhinosinusitis with nasal polyposis (CRSwNP), bronchial asthma, and reactions to aspirin or cyclooxygenase-1 (COX-1) inhibitors [3,4,5,6]. Since its first description by Widal, there has been considerable literature published on the epidemiology, pathophysiology, and treatment of what is termed aspirin exacerbated respiratory disease (AERD)
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