title: Pathogenesis of aspirin-exacerbated respiratory disease and reactions.
abstract: Physiologic and pharmacologic studies support the hypothesis that aspirin-exacerbated respiratory disease (AERD) involves fundamental dysregulation in the production of and end-organ responsiveness to both antiinflammatory eicosanoids (prostaglandin E2) and proinflammatory effectors (cysteinyl leukotrienes). The acquired nature of AERD implies a disturbance in a potential epigenetic control mechanism of the relevant mediator systems, which may be a result of incompletely clarified environmental factors (eg, viral or bacterial infections, inhaled pollutants).
authors: Brigham and Women's Hospital, Department of Medicine, Division of Rheumatology, Immunology and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Boston, MA 02115, USA.
authors: Tanya M
authors: TM
authors: Laidlaw
authors: Joshua A
authors: JA
authors: Boyce
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D004342:Drug Hypersensitivity / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D050356:Lipid Metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D012140:Respiratory Tract Diseases / Q000209:etiology*; D015398:Signal Transduction
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin
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