Purpose of review
In contrast to the phenotypic classification of chronic rhinosinusitis (CRS), endotyping categorizes disease variants based on their underlying pathophysiologic mechanisms. Defining CRS endotypes may provide information on the risk for disease progression, recurrence and comorbid conditions, as well as identify suitable therapeutic targets. With the emergence of biologics, endotyping may enable personalized pharmacotherapy for recalcitrant CRS. The purpose of this review is to briefly summarize the pathophysiology and endotypes of CRS, and highlight the biologics that target mediators of CRS.
CRS is due to dysregulated immunologic responses to external stimuli, which induces inflammatory mediators. The linkage between innate lymphoid cells, adaptive CD4+ T helper and CD8 + cytotoxic T cells has led to proposed endotypes that are based around immune response deviation into type 1, type 2 and type 3 responses. Cluster analysis has attempted to define endotypes, accounting for clinical characteristics, molecular and cellular biomarkers, and treatment response. Biologics targeting epithelial-derived cytokines and immunoglobulin E, as well as mediators of type 1, type 2 and type 3 inflammation, are being investigated in CRS.
Although there have been significant advances made in the understanding of the pathomechanisms of CRS, there currently remains a lack of full characterization of CRS endotypes.