The current state of chronic rhinosinusitis with nasal polyps (CRSwNP) in aspirin-exacerbated respiratory disease (AERD) in terms of epidemiology, diagnosis, aetiology, and therapy is discussed in this study. PGE2 shortage produces an AERD phenotype in PGE2 synthase-1 knock-out mice, as well as PGE2 resistance in AERD patients’ granulocytes, according to recent research. AERD patients have an increase in platelet-adherent leukocytes, which increases the synthesis of cysteinyl leukotrienes (CysLTs) via transcellular arachidonate metabolism. INF-, which is produced by eosinophils in AERD patients’ sinus tissue, stimulates eosinophil maturation, boosts leukotriene-associated gene expression, and releases CysLTs. The serum periostin level has been proposed as a biomarker for predicting the AERD/CRSwNP phenotype. Aspirin desensitisation has been shown to lower levels of CD4+ T cell-derived cytokines such as INF- and IL-10, which is consistent with INF-‘s recently recognised function in AERD.
Recent research lends credence to the hypothesis that arachidonic acid metabolism is dysregulated in AERD patients. Resistance to PGE2, increased synthesis of CysLTs by platelet-adherent leukocytes, and cellular activation by INF- produced by eosinophils all reflect this. In AERD patients with persistent CRSwNP, aspirin desensitisation may be a helpful therapeutic choice.
