Abstract
The pathomechanisms behind NSAID-exacerbated respiratory disease are complex and still largely unknown. They are presumed to involve genetic predisposition and environmental triggers that lead to dysregulation of fatty acid and lipid metabolism, altered cellular interactions involving transmetabolism, and continuous and chronic inflammation in the respiratory track. Here, we go through the recent advances on the topic and sum up the current understanding of the background of this illness that broadly effects the patients' lives.
Highlights
AERD or aspirin/non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease is an adult-onset triad characterized by asthma, eosinophilic chronic rhinosinusitis with nasal polyposis (CRSwNP), and respiratory reactions upon ingestion of COX-1 inhibitors such as NSAIDs or aspirin (ASA)
The acute inflammatory symptoms that occur within 30–180 min after ingestion of COX-1 inhibitors is a non-immunoglobulin (Ig)E-mediated hypersensitivity reaction that causes a release of multiple mast cell mediators, such as tryptase, cysteinyl leukotrienes (CysLTs), and prostaglandin D2 (PDG2) [1,2,3]
LT antagonists, such as montelukast, inhibit the actions of CysLTs by blocking their receptor CysLT1R, and have been shown to improve AERD-patients’ asthma [7] and in some patients inhibit the lower airway symptoms induced by NSAID ingestion [8]
Summary
AERD or aspirin/non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease is an adult-onset triad characterized by asthma, eosinophilic chronic rhinosinusitis with nasal polyposis (CRSwNP), and respiratory reactions upon ingestion of COX-1 inhibitors such as NSAIDs or aspirin (ASA). Both the upper and lower respiratory symptoms are typically difficultto-treat, and many patients suffer from frequent asthma exacerbations and require multiple endoscopic sinus surgeries despite good medical treatment including local and oral corticosteroids. The acute inflammatory symptoms that occur within 30–180 min after ingestion of COX-1 inhibitors is a non-immunoglobulin (Ig)E-mediated hypersensitivity reaction that causes a release of multiple mast cell mediators, such as tryptase, cysteinyl leukotrienes (CysLTs), and prostaglandin D2 (PDG2) [1,2,3]. The typical symptoms of reaction can include nasal congestion, rhinorrhea, sneezing, coughing, wheezing, and drop in lung function, though pruritic rash and gastrointestinal discomfort have been noted
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