Allergy, Asthma and Immunology: Pathogenesis of aspirin-exacerbated respiratory disease and reactions.

November 20, 2013

Pathogenesis of aspirin-exacerbated respiratory disease and reactions.

NIHPA Author Manuscripts
PMC3781366

Immunol Allergy Clin North Am. Author manuscript; available in PMC 2013 September 24.

Published in final edited form as:

Immunol Allergy Clin North Am. 2013 May; 33(2): 195–210.

Published online 2012 December 23. doi: 10.1016/j.iac.2012.11.006

PMCID: PMC3781366

NIHMSID: NIHMS508776

Tanya M. Laidlaw, MD and Joshua A. Boyce, MD*

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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).