Upper airways in aspirin-exacerbated respiratory disease. Issue 1 (February 2015)

• Record Type: Journal Article
• Authors: Choi, Jeong-Hee; Kim, Ji-Hye; Park, Hae-Sim
• Is Part Of: Current opinion in allergy and clinical immunology. Volume 15:Issue 1(2015:Feb.)
• Publication Date: 2015-02
• Subjects: Allergy -- Periodicals; Clinical immunology -- Periodicals; Hypersensitivity; Immunity; Immune System Diseases; Allergy and Immunology; 616.079
• DOI: 10.1097/ACI.0000000000000122
• Languages: English
• ISSNs: 1528-4050

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <title>Purpose of review</title> <p>This review updates the status of chronic rhinosinusitis with nasal polyps (CRSwNP) in aspirin-exacerbated respiratory disease (AERD) in the contexts of epidemiology, diagnosis, pathogenesis, and treatment.</p> </sec> <sec> <title>Recent findings</title> <p>Recent studies have shown that prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) deficiency induces an AERD phenotype in PGE<sub>2</sub> synthase-1 knock-out mice and also PGE<sub>2</sub> resistance in granulocytes of AERD patients. The numbers of platelet-adherent leukocytes increase in AERD patients, enhancing production of cysteinyl leukotrienes (CysLTs) via transcellular metabolism of arachidonate. INF-γ released from eosinophils of the sinus tissue of AERD patients promotes eosinophil maturation, increases leukotriene-associated gene expression, and releases CysLTs. The serum periostin level has been suggested to be a useful biomarker predicting the AERD/CRSwNP phenotype. Aspirin desensitization was reported to decrease the levels of CD4<sup>+</sup> T cell-derived cytokines, including INF-γ and IL-10, in line with the newly defined role of INF-γ in AERD.</p> </sec> <sec> <title>Summary</title> <p>Recent findings further support the notion that arachidonic acid metabolism is dysregulated in AERD patients. This is reflected by resistance to PGE<sub>2</sub>, overproduction of CysLTs by enhanced numbers of platelet-adherent leukocytes, and cellular stimulation by INF-γ released from eosinophils. Aspirin desensitization may be a useful treatment option in AERD patients exhibiting recalcitrant CRSwNP.</p> </sec> </abstract>