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ABSTRACT
Introduction
In recent years, endotypes of chronic rhinosinusitis (CRS) based on the underlying immune mechanisms provided a better understanding of this heterogeneous disease and are frequently applied in diagnosis and treatment.
Areas covered
In this manuscript, we aim to review novel treatment approaches for this often uncontrolled disease and highlight endotype-driven medical algorithms that could be beneficial in daily clinical practice.
Expert opinion
With the development of endotyping and the mucosal inflammatory concept, several type 2–targeted biologics and surgical options are nowadays available for treating CRS. However, a better understanding based on clinical trials and real-life experience in daily practice is needed to optimize patient selection, biological drug selection, treatment duration, prediction, and long-term follow-up strategies. Indirect comparison analysis suggested that dupilumab might be the most effective biologic for treating CRS with nasal polyps, but the role and timing of surgery remain unclear. More real-life studies and comparative trials are needed for the optimal integration of biologics into clinical pathways in combination with established treatment approaches such as nasal and oral glucocorticosteroids and adequate surgery to provide long-term perspectives.
Article highlights
Type 2 inflammation plays an important role in the pathogenesis of CRSwNP.
Type 2–targeted biologics and surgical options are available for treating severe uncontrolled CRSwNP.
Provide long-term perspectives for disease control with the optimal integration of biologics into clinical pathways in combination with established treatment approaches such as nasal and oral glucocorticosteroids and adequate surgery.
Still, more rigorous studies and trials are needed in the future.
Abbreviations
| AERD | = | Aspirin-exacerbated respiratory disease |
| BAFF | = | B cell-activating factor |
| CLC | = | Charcot-Leyden crystal |
| CRSsNP | = | Chronic rhinosinusitis without nasal polyps |
| CRSwNP | = | Chronic rhinosinusitis with nasal polyps |
| CSF | = | Colony stimulating factor |
| ECP | = | Eosinophil cationic protein |
| ILC2 | = | type2 innate lymphoid cells |
| MBP | = | Major basic protein |
| MMP | = | matrix metallopeptidase |
| NERD | = | Nonsteroidal anti-inflammatory drug-exacerbated respiratory disease |
| NETosis | = | Neutrophilic extracellular trap cell death |
| PAF | = | Platelet-activating factor |
| RANTES | = | regulated upon activation, normal T cell expressed and presumably secreted |
| SA | = | Staphylococcus aureus |
| TIMPs | = | tissue inhibition of metalloproteinases |
Declaration of interest
C Bachert: Advisory Board member and speaker for Novartis, GSK, Astra-Zeneca, Sanofi, ALK, and Mylan. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Author contributions
C. Bachert and N. Zhang contributed to the scientific concept of the review. Y. Huang conceived the article structure, wrote the article, and searched the literature. C. Bachert and N. Zhang critically revised the manuscript. All these authors read and approved the final manuscript for publication.