Abstract

BackgroundEndotyping chronic rhinitis has proven hardest for the subgroup of non-allergic rhinitis (NAR) patients. While IgE-related inflammation is typical for allergic rhinitis (AR), no markers have been found that can be seen to positively identify NAR. A further complication is that AR and NAR might co-exist in patients with mixed rhinitis. As previous studies have considered only a limited number of inflammatory mediators, we wanted to explore whether a wider panel of mediators could help us refine the endotyping in chronic rhinitis patients.ObjectiveTo endotype chronic rhinitis, and non-allergic rhinitis in particular, with help of molecular or cellular markers.MethodIn this study we included 23 NAR patients without allergen sensitizations and with persistent rhinitis symptoms, 22 pollen sensitized rhinitis patients with seasonal symptoms, 21 mixed rhinitis patients with pollen-related symptoms and persistent symptoms outside of the pollen season, and 23 healthy controls without any symptoms. Nasal secretions were collected outside of pollen season and differences between the endotypes were assessed for a broad range of inflammatory mediators and growths factors using a multiplex ELISA.ResultsAlthough we were able to identify two new nasal secretion makers (IL-12 and HGF) that were low in mixed and AR patients versus NAR and healthy controls, the most intriguing outcome is that despite investigating 29 general inflammatory mediators and growth factors no clear profile of non-allergic or mixed rhinitis could be found.ConclusionClassical inflammatory markers are not able to differentiate between non-allergic or mixed rhinitis patients and healthy controls.

Highlights

  • BackgroundEndotyping chronic rhinitis has proven hardest for the subgroup of non-allergic rhinitis (NAR) patients

  • Rhinitis can be subdivided into a number of discrete pheno- and endotypes [1]

  • NAR can be subdivided into the following phenotypes: environmental, hormones, medicationinduced (rhinitis medicamentosa, NSAIDS, aspirin etc.), gustatory, age and/or inflammation (non-allergic rhinitis with eosinophilia syndrome (NARES) or local allergic rhinitis (LAR))

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Summary

Background

Endotyping chronic rhinitis has proven hardest for the subgroup of non-allergic rhinitis (NAR) patients. While IgE-related inflammation is typical for allergic rhinitis (AR), no markers have been found that can be seen to positively identify NAR. A further complication is that AR and NAR might co-exist in patients with mixed rhinitis. As previous studies have considered only a limited number of inflammatory mediators, we wanted to explore whether a wider panel of mediators could help us refine the endotyping in chronic rhinitis patients

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