Perspectives in Therapy of Chronic Rhinosinusitis

Abstract

The recent classification of chronic rhinosinusitis (CRS) focusses on investigating underlying immunopathophysiological mechanisms. Primary CRS is subdivided based on endotype dominance into type 2 (that relates mostly to the Th2 immune response with high levels of IL-5, IL-13, and IgE), or non-type 2 (that corresponds to the mix of type 1 and type 3). The treatment selection of CRS is dependent on endotype dominance. Currently, the majority of patients receive standardized care-traditional pharmacological methods including local or systemic corticosteroids, nasal irrigations or antibiotics (for a selected group of patients). If well-conducted drug therapy fails, endoscopic sinus surgery is conducted. Aspirin treatment after aspirin desensitization (ATAD) with oral aspirin is an option for the treatment in nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) patients. However, in this review the focus is on the role of biological treatment-monoclonal antibodies directed through the specific type 2 immune response targets. In addition, potential targets to immunotherapy in CRS are presented. Hopefully, effective diagnostic and therapeutic solutions, tailored to the individual patient, will be widely available very soon.

Keywords: biologics; chronic rhinosinusitis; sinusitis; treatment.

Figure 1

Classification of CRS created by Grayson et al. with general information about appropriate treatment for particular endotypes ([2,18], modified). AFRS, allergic fungal rhinosinusitis; OMC, ostiomeatal complex; CCAD, central compartment atopic disease; eCRS, eosinophilic CRS; PCD, primary ciliary dyskinesia; CF, cystic fibrosis; GPA, granulomatosis with polyangiitis; EGPA, eosinophilic granulomatosis with polyangiitis; CVID, common variable immunodeficiency; OCS, oral corticosteroid; ESS, endoscopic sinus surgery; ATAD, aspirin treatment after desensitization; N-ERD, non-steroidal anti-inflammatory drugs-exacerbated respiratory disease.

Figure 2

Selected immune activity mechanisms involved in type 2 and non-type 2 immune response in case of chronic rhinosinusitis described by Grayson et al. ([18], modified).

Figure 3

General immune mechanism involved in the pathogenesis of CRS and targets for selected biologics. Immune response combines the airway epithelium response as a first line of defence in sinuses that meet environmental factors with innate immune activity which leads to adaptive immune activation ([2,13], modified).