Chronic rhinosinusitis (CRS) has now been discovered as a frequent disease affecting about 11 % of the European population. In clinical terms, CRS may be differentiated in two phenotypes, CRS with and without nasal polyps. This differentiation is also confirmed by immunohistochemical studies on the remodeling pattern of those diseases, identifying TGF-6 as the key regulator. Further differentiation may be based on the inflammatory patterns, differentiating endotypes based on prominent T helper cell cytokines such as interleukin-5 and the presence of IgE antibodies against Staphylococcus aureus enterotoxins. The importance of those endotypes has been confirmed by innovative studies using humanized antibodies applied to nasal polyp disease, and by their predictive value for asthma comorbidity. Biomarkers may thus be needed to fully appreciate the CRS disease spectrum and its link to asthma.
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