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Immunol Allergy Clin North Am. 2016 Nov;36(4):681-691. doi: 10.1016/j.iac.2016.06.005. Epub 2016 Sep 13.

Pathogenesis of Aspirin-Induced Reactions in Aspirin-Exacerbated Respiratory Disease.

Author information

1
Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, 1 Jimmy Fund Way, Smith Building, Room 638, Boston, MA 02115, USA.
2
Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, 1 Jimmy Fund Way, Smith Building, Room 638, Boston, MA 02115, USA. Electronic address: tlaidlaw@partners.org.

Abstract

The acute clinical symptoms that develop following the oral ingestion of aspirin, or any other inhibitor of cyclooxygenase-1, are well established in aspirin-exacerbated respiratory disease: nasal congestion, rhinorrhea, and bronchospasm. Less commonly, gastrointestinal distress, rash, angioedema, or urticaria also develops. However, the pathobiology that drives these clinical reactions is poorly understood. Use of an intranasal aspirin challenge protocol or administration of premedications inhibiting the leukotriene pathway decreases the severity of clinical reaction, which suggests the involvement of both local effector cells and cysteinyl leukotrienes in the pathogenesis of aspirin-induced reactions.

KEYWORDS:

Aspirin-exacerbated respiratory disease; Cysteinyl leukotrienes; Mast cell; Pathogenesis; Platelet-leukocyte aggregates; Prostaglandins

PMID:
27712763
DOI:
10.1016/j.iac.2016.06.005
[Indexed for MEDLINE]

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