The acute clinical symptoms that develop following the oral ingestion of aspirin, or any other inhibitor of cyclooxygenase-1, are well established in aspirin-exacerbated respiratory disease: nasal congestion, rhinorrhea, and bronchospasm. Less commonly, gastrointestinal distress, rash, angioedema, or urticaria also develops. However, the pathobiology that drives these clinical reactions is poorly understood. Use of an intranasal aspirin challenge protocol or administration of premedications inhibiting the leukotriene pathway decreases the severity of clinical reaction, which suggests the involvement of both local effector cells and cysteinyl leukotrienes in the pathogenesis of aspirin-induced reactions.
Keywords: Aspirin-exacerbated respiratory disease; Cysteinyl leukotrienes; Mast cell; Pathogenesis; Platelet-leukocyte aggregates; Prostaglandins.
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