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Review
. 2016 Sep;117(3):234-40.
doi: 10.1016/j.anai.2016.06.006.

Chronic rhinosinusitis phenotypes

Affiliations
Review

Chronic rhinosinusitis phenotypes

John W Steinke et al. Ann Allergy Asthma Immunol. 2016 Sep.

Abstract

Objective: To review the current knowledge surrounding different chronic rhinosinusitis (CRS) presentations and the relative roles of nasal polyps, eosinophilia, and allergies in discerning phenotypes.

Data sources: PubMed literature review.

Study selections: Articles discussing the various phenotypes of CRS with emphasis on pathologic and immune mechanistic studies that distinguish disease.

Results: Current guidelines primarily separate CRS based on the presence or absence of nasal polyps. This is largely driven by the tendency of eosinophilic disease to present with nasal polyps (NPs) in contrast to noneosinophilic presentations, which less often lead to the development NPs. Further separations have been proposed based on expression of aeroallergen sensitization.

Conclusion: The presence of NPs may only poorly predict the presence of an underlying eosinophilic process and as such may have poor utility in forming the basis for recommending eosinophil-target therapies. Similarly, there is little evidence to support a significant role for aeroallergen exposure in contributing to the presence, severity, or natural history of CRS. Appropriate separation of CRS into specific phenotypes will allow therapeutic approaches to be individualized to each distinct presentation.

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Conflict of interest statement

All authors report no conflicts of interest

Figures

Figure 1
Figure 1
Model of interaction of frequent protracted acute bacterial sinusitis in the pathogenesis of non-eosinophilic chronic rhinosinusitis. See text for details.
Figure 2
Figure 2
Pathological similarity of E-CRS nasal polyps (figures 2a and 2b) to asthma (figures 2c and 2d). H&E-stained sections (2a and 2c) show epithelial denudation (black arrows) and both early (yellow arrows) and advanced (white arrows) basement membrane thickening. Major basic protein immunofluorescence-staining (figures 2b and 2d) demonstrates intensity of eosinophilic infiltration. Reproduced with permission from.
Figure 3
Figure 3
Cytokine signature in eosinophilic CRS and AERD. Tissue samples were homogenized following surgical removal, RNA isolated and quantitative polymerase chain reactions performed for IL-4, IL-5, IL-13 and IFN-γ. Data (mean±SEM) reflect relative expression of each gene in comparison to β-actin (2ΔCT). Control samples (n=9) are depicted in black bars, E-CRS (n=30) in grey bars, and AERD (n=15) in white bars. *p<0.05 as compared to control. Reproduced with permission from.
Figure 4
Figure 4
Seasonal patterns of CRS exacerbation visits (n-1217). Each bar represents 1 week. Reproduced with permission from.

References

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