Internal Medicine

Aspirin exacerbated respiratory disease (AERD)

Characterized by asthma, chronic rhinosinusitis with nasal polyposis, and pathognomonic respiratory reactions to aspirin (Samter’s triad).

Characterized by asthma, chronic rhinosinusitis with nasal polyposis, and pathognomonic respiratory reactions to aspirin (Samter’s triad).


Hypersensitivity reactions to aspirin were described as early as 1902 but it was not until 1922 that Widal et al. first described the correlation between aspirin sensitivity, asthma, and nasal polyposis. 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. Samter’s Triad is defined as chronic rhinosinusitis with nasal polyposis (CRSwNP), bronchial asthma, and reactions to aspirin or cyclooxygenase-1 (COX-1) inhibitors. Since its first description by Widal, there has been considerable literature published on the epidemiology, pathophysiology, and treatment of what is now termed aspirin-exacerbated respiratory disease (AERD).

Originally from Berlin, Max Samter immigrated to the United States before World War II and soon became a leader of American allergology. He was president of the American Academy of Allergy, Asthma, and Immunology 1958-59 and was honored in 1982 as Allergist of the Year by the Asthma and Allergy Foundation of America. He helped establish the International Association of Allergology in the 1950s.


Non-IgE hypersensitivity reaction to ASA/COX-1 inhibitors that is commonly comorbid with but not due to underlying allergic disease.

Metabolism of arachidonic acid. Pathways of arachidonic acid metabolism involved in the pathogenesis of AERD. Enzymes are in italics, relevant receptors are in dashed boxes, and consequences of signaling through each receptor are in bulleted lists. Thick gray arrows show whether expression and function of each enzyme or product are increased or decreased in patients with AERD. | Laidlaw, T. M., & Boyce, J. A. (2013). Pathogenesis of aspirin-exacerbated respiratory disease and reactions. Immunology and allergy clinics of North America, 33(2), 195–210. doi:10.1016/j.iac.2012.11.006

Characterized by marked eosinophilic inflammation and ongoing mast-cell activation in the respiratory mucosa.

Schematic diagram depicting the role of Cys-LT1 activation and mast cell activation in pathogenesis of aspirin exacerbated respiratory disease (AERD) symptoms. INF-γ—interferon-gamma; IL-4—interleukin-4; Cys-LT—cysteinyl-leukotriene; Cys-LT1—cysteinyl-leukotriene 1; LTC4—leukotriene C4; LTD4—leukotriene D4; LTE4—leukotriene E4; IL-33—interleukin-33; PGD2—prostaglandin D2. | Li, K. L., Lee, A. Y., & Abuzeid, W. M. (2019). Aspirin Exacerbated Respiratory Disease: Epidemiology, Pathophysiology, and Management. Medical sciences (Basel, Switzerland), 7(3), 45. doi:10.3390/medsci7030045

Clinical features

Samter’s triad:

  • Chronic rhinosinusitis with nasal polyposis (CRSwNP)
  • Bronchial asthma
  • Reactions to aspirin/cyclooxygenase-1 (COX-1) inhibitors

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