Upper airways in aspirin-exacerbated respiratory disease

Purpose of review 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. Recent findings Recent studies have shown that prostaglandin E-2 (PGE(2)) deficiency induces an AERD phenotype in PGE2 synthase-1 knock-out mice and also PGE(2) 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-gamma 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(+) T cell-derived cytokines, including INF-gamma and IL-10, in line with the newly defined role of INF-gamma in AERD. Summary Recent findings further support the notion that arachidonic acid metabolism is dysregulated in AERD patients. This is reflected by resistance to PGE(2), overproduction of CysLTs by enhanced numbers of platelet-adherent leukocytes, and cellular stimulation by INF-gamma released from eosinophils. Aspirin desensitization may be a useful treatment option in AERD patients exhibiting recalcitrant CRSwNP.