Pathogenesis of Aspirin-exacerbated Respiratory Disease and Reactions

Overview

Journal Immunol Allergy Clin North Am

Specialty Allergy & Immunology

Date 2013 May 4

PMID 23639708

Citations 31

Authors

Tanya M Laidlaw

Joshua A Boyce

Affiliations

Soon will be listed here.

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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