Abstract
Aspirin-exacerbated respiratory disease (AERD) is characterized by overproduction of the pro-inflammatory eicosanoids. Although immunoglobulin E-mediated sensitization to aeroallergens is common among AERD patients, it does not belong to the defining disease characteristics. In this study of 133 AERD patients, we sought to find a relationship between sensitization to aeroallergens and local (leukotriene E4, prostaglandin E2 and prostaglandin D2) and/or systemic (leukotriene E4) production of arachidonic acid metabolites. Interestingly, a negative association between pro-inflammatory eicosanoid levels in induced sputum supernatant or urine and sensitization to aeroallergens was observed. This inverse relationship might suggest the presence of a protective effect of atopic sensitization to aeroallergens against stronger local airway inflammation and higher systemic AERD-related inflammatory activity.
Highlights
Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, difficult to treat chronic rhinosinusitis with nasal polyps, and acute respiratory reactions precipitated by aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) [1–6]
Atopy is not a defining feature of the disease, atopic sensitization to aeroallergens and/or related characteristics, such as elevated total serum immunoglobulin E (IgE) levels, is common in subjects with AERD, as it is with classic asthmatics [12–15]
Elevated levels of total serum IgE have been observed in AERD patients even in the absence of atopy [11]
Summary
Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, difficult to treat chronic rhinosinusitis with nasal polyps, and acute respiratory reactions precipitated by aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) [1–6]. Dysregulation of arachidonic acid metabolism leading to the overproduction of the pro-inflammatory eicosanoids, such as leukotriene E4 (LTE4), by eosinophils, platelet-leukocyte aggregates and mast cells (MCs) is a biochemical hallmark of AERD [7–10]. Because specific immunoglobulin E (IgE) antibodies to aspirin have not been identified and all the structurally different cyclooxygenase-1 inhibitors cause respiratory reactions in these patients, AERD is not an IgE-mediated allergy, despite the allergic-like reactions to aspirin and NSAIDs that define the disease. Beneficial clinical and biochemical (reduced LTE4 production) effects of omalizumab have been observed in AERD subjects [16,17]. Omalizumab is a humanized recombinant monoclonal antibody interfering with IgE-dependent MC activation [18,19]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
