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Pathogenesis of aspirin-exacerbated respiratory disease and reactions
Tanya M Laidlaw1, Joshua A Boyce
1Brigham 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.
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).
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