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Immunol Allergy Clin North Am. 2013 May;33(2):195-210. doi: 10.1016/j.iac.2012.11.006. Epub 2012 Dec 23.

Pathogenesis of aspirin-exacerbated respiratory disease and reactions.

Author information

1
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.

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).

PMID:
23639708
PMCID:
PMC3781366
DOI:
10.1016/j.iac.2012.11.006
[Indexed for MEDLINE]
Free PMC Article

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