Abstract
Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory disease with an as-yet-undefined etiology. The management of CRS has historically been phenotypically driven, and the presence or absence of nasal polyps has frequently guided diagnosis, prognosis, and treatment algorithms. Research over the last decade has begun to question the role of this distinction in disease management, and renewed attention has been placed on molecular and cellular endotyping and a more personalized approach to care. Current research exploring immunologic mechanisms, inflammatory endotypes, and molecular biomarkers has the potential to more effectively delineate distinct and clinically relevant subgroups of CRS. The focus of this review will be to discuss and summarize the endotypic characterization of CRS and the potential diagnostic and therapeutic implications of this approach to disease management.
Highlights
Chronic rhinosinusitis (CRS) affects more than 4% of the US population and results in substantial economic burden to the health-care system[1,2,3,4]
These analyses have moved beyond simple phenotypic classifications of CRS and instead have set out to differentiate CRS on the basis of cytokines and other inflammatory mediators that may be more relevant to disease mechanisms
The identification of multiple putative inflammatory endotypes, with relative consistency between studies, suggests that this may be a valid approach for characterizing CRS inflammation, predicting treatment outcomes, and identifying patients who may benefit from targeted therapeutics
Summary
Chronic rhinosinusitis (CRS) affects more than 4% of the US population and results in substantial economic burden to the health-care system[1,2,3,4]. The identification of multiple putative inflammatory endotypes, with relative consistency between studies, suggests that this may be a valid approach for characterizing CRS inflammation, predicting treatment outcomes, and identifying patients who may benefit from targeted therapeutics. Identified putative inflammatory endotypes using mucus alone[33] This minimally invasive approach could be more efficiently incorporated into clinical practice and has the potential to assign patients to disease clusters without attaining tissue and prior to any surgical intervention. Pro-inflammatory neutrophilic inflammation identified in a large subset of patients may represent a recalcitrant CRS subpopulation that could benefit from targeted therapies[32,33,44] Based on this characteristic inflammatory signature, these patients would be expected to be less responsive to topical or systemic corticosteroids, further highlighting the need for novel interventions in this group. It is further likely that the identification of uncharacterized CRS endotypes or unique immune signatures will lead to the recognition of novel mechanisms of disease and additional targeted therapies going forward
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