xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

fungal hyphae. 1693,1709 Eosinophilic mucin is not present in all forms of CRSwNP. 1709 Dematiaceous fungi and Aspergillus are commonly identified in mucin from AFRS, but fungi are diverse and vary based on geographical region. 622,1692,1696,1709,1710 In 1 Australian study, correlation between fungal species in mucin and systemic fungal allergy was weak. 633 However, mucin collected specifically from the sinuses found a strong correlation between the fungal species and Type 2 T cell memory to the specific fungi in AFRS patients. 622 Certain biomarkers can distinguish AFRS from other CRSwNP patients. AFRS patients often have extremely ele vated serum total and fungal-specific IgE and relatively normal serum eosinophil levels compared to CRSwNP patients. 1692,1693,1695 Serum specific IgE levels (to both fun gal and non-fungal allergens) have been shown to correlate with clinical severity and recurrence. 1443,1692,1696,1705 How ever, controversy exists over the importance of type I hyper sensitivity in AFRS pathophysiology, driving additional investigation. Humoral immunity and Ig-independent pathways may contribute. Fungal-specific IgG is typi cally elevated in AFRS. 1692,1696,1711 Elevated IgG3 levels specific to Alternaria alternata and Aspergillus fumiga tus distinguished eosinophilic RS, including AFRS, from control groups. 633 S. aureus is a common organism in CRSwNP and may modify these disease processes as a direct pathogen or via superantigen production. 1697,1712–1714 S. aureus colonization is more prevalent in AFRS vs other CRSwNP subtypes. 1697 Recent microarray data analysis comparing AFRS and CRSwNP highlighted unique activated genes and molec ular pathways. 625 AFRS is characterized by upregulated pathways critical in T cell activation and the adaptive immune response, correlating with the elevated serum IgE levels commonly found in AFRS. 625,1715 In terms of specific genes, the most significantly downregulated gene in AFRS as compared to CRSwNP was histatin 1 (HTN1), an anti fungal peptide. HTN1 is produced by respiratory epithelial cells, and its limited expression in AFRS may contribute to the accumulation of fungal hyphae within inflamed sinus cavities. 625 AFRS is a distinct, often more severe, subclass of CRSwNP. Although the precise AFRS pathophysiology remains unclear, limited antifungal activity may allow ger mination of inhaled fungal spores. In the presence of a breakdown in the epithelial cell barrier, fungal hyphae either alone or synergistically with S. aureus upregulate Type 2 immune responses leading to the characteristic type I hypersensitivity, eosinophilic inflammation, and Type 2 cytokine profiles associated with AFRS. Environ ment, socioeconomic factors, and genetic predisposition also likely contribute.

asthma showed clinical improvement after desensitization

desensitization up to 3years Long term effectiveness Significant improvement for CRS symptoms, asthma, olfaction, number of surgical revisions, and

corticosteroid use

Poor adherence in patients with GI problems

Study Year LOE Study Design Study Groups Clinical Endpoint Conclusions

77% of patients without

Improvement after aspirin

desensitization

Adherence to low dose ASA in Patients with GI problems

incomplete AERD

Stevenson 1673 1996 4 Large cohort study 65 AERD patients undergoing

Moberg 1683 2011 5 Online questionnaire Primary cardiovascular (CV) prevention Secondary CV prevention

Lumry 1668 1983 4 Cohort study Patients with

TABLE X-29 (Continued)