Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, recurrent nasal polyposis, and respiratory reactions on ingestion of COX-1 inhibitors.
Administration of a COX-1-selective antagonist to mice completely prevented the generation of both PGD<sub>2</sub> and LTC<sub>4</sub> in a model of AERD in which MC activation is IL-33 driven.
Aspirin-exacerbated respiratory disease (AERD) is a recalcitrant inflammatory disorder defined by asthma, nasal polyposis, and sensitivity to cyclooxygenase-1 inhibitors.
Samter's Triad is a disorder characterized by chronic rhinosinusitis (CRS) with nasal polyps (NPs), asthma, and intolerance to cyclooxygenase-1 inhibitors.
Aspirin-exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme.
Aspirin-exacerbated respiratory disease (AERD) is defined as asthma, chronic rhinosinusitis with nasal polyposis, and hypersensitivity to cyclooxygenase-1 inhibitors.
ILC2 numbers significantly increased in nasal mucosal samples and decreased in blood at the time of COX-1 inhibitor reactions in 12 patients with AERD.
Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs.
Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors.
Aspirin-exacerbated respiratory disease (AERD) is characterized by respiratory reactions on ingestion of COX-1 inhibitors and cysteinyl leukotriene overproduction.
Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by severe persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and an intolerance to aspirin and other NSAIDs that preferentially inhibit COX-1.
In clinical tests, FEV-1, FVC, and asthma severity in the AIA group were higher than control and additionally IgE levels were lower in this group(p<0>T and HSPA1B1267A>G are related with AERD in the Kurdistan population.
Despite the need for further functional evaluations and replications, we conclude that DDR1 polymorphisms are not likely to contribute to predispositions of AERD, but may be potentially associated with FEV(1) decline by aspirin provocation in asthmatics.
After testing for multiple comparisons, only the association signal from rs2517449 was retained (P(corr) = .04), while other polymorphisms showed no associations with the risk of AERD and FEV(1) decline.
To investigate whether GTF2H4 genetic variants could be a causative factor for AERD development and FEV(1) decline by aspirin provocation, five common single-nucleotide polymorphisms (SNPs) were genotyped in 93 patients with AERD and 96 aspirin-tolerant asthma (ATA) controls.
Results showed that none of the analyzed CD58 single-nucleotide polymorphisms and haplotypes was significantly associated with AERD development and fall rate of FEV(1) by aspirin provocation, an important diagnostic marker of aspirin hypersensitivity.
Administration of a COX-1-selective antagonist to mice completely prevented the generation of both PGD<sub>2</sub> and LTC<sub>4</sub> in a model of AERD in which MC activation is IL-33 driven.
Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, recurrent nasal polyposis, and respiratory reactions on ingestion of COX-1 inhibitors.
We hypothesized that the peculiar mixed interleukin-4 (IL-4/Th2) and interferon gamma INF-γ (INF-γ/Th1) inflammatory milieu found in the airways of patients with aspirin-exacerbated respiratory disease (AERD) is responsible for the altered regulation of the IL-1β/IL-1RI-/EP<sub>2</sub>/COX-2 autocrine loop also found in these patients.