RESUMO
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. For more than 30 years, aspirin desensitization has proven to be of significant long-term benefit in carefully selected patients with AERD. Despite this, the exact mechanisms behind the therapeutic effects of aspirin desensitization remain poorly understood. In this article, we review the current understanding of the mechanisms of aspirin desensitization and discuss future areas of investigation.
Assuntos
Anti-Inflamatórios não Esteroides/administração & dosagem , Anti-Inflamatórios não Esteroides/efeitos adversos , Aspirina/administração & dosagem , Aspirina/efeitos adversos , Dessensibilização Imunológica , Doenças Respiratórias/etiologia , Doenças Respiratórias/terapia , Citocinas/metabolismo , Dessensibilização Imunológica/métodos , Humanos , Leucotrienos/genética , Leucotrienos/metabolismo , Receptores de Leucotrienos/genética , Receptores de Leucotrienos/metabolismo , Doenças Respiratórias/metabolismoRESUMO
Aspirin-exacerbated respiratory disease is a clinical syndrome characterized by severe, persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and reactions to aspirin and other nonsteroidal antiinflammatory drugs that preferentially inhibit cyclooxygenase 1. The mechanisms behind the therapeutic effects of aspirin desensitization remain poorly understood. Recent studies suggest that the clinical benefits may occur through direct inhibition of tyrosine kinases and the signal transducer and activator of transcription 6 signaling pathway, which results in inhibition of interleukin 4 production. In this article, the current understanding of the mechanisms of aspirin desensitization is reviewed and future areas of investigation are discussed.