Updates in biologic therapy for chronic rhinosinusitis with nasal polyps and NSAID‐exacerbated respiratory disease

Abstract

Chronic rhinosinusitis with nasal polyps (CRSwNP) associated with type 2 inflammation and non‐steroidal anti‐inflammatory drug (NSAID)‐exacerbated respiratory disease (N‐ERD) can be difficult to control with standard medical therapy and sinus surgery. In this group, biologicals are potentially promising treatment options. The phase III clinical trials for omalizumab, dupilumab, mepolizumab and benralizumab in CRSwNP have demonstrated favourable outcomes. Moving forward, direct comparisons among biologicals, refining patient selection criteria for specific biologicals, determining optimal treatment duration and monitoring long‐term outcomes are areas of emerging interest. This review summarizes the clinical evidence from the recent 2 years on the role of biologicals in severe CRSwNP and N‐ERD, and proposes an approach towards decision‐making in their use.

Biologics for Nasal Polyps: Synthesizing Current Recommendations into a Practical Clinical Algorithm

“…Additional complexity is brought about by the availability of other treatments (surgery or aspirin desensitization for example), patient and disease heterogeneity, comorbid conditions, drug availability, patient preferences, and provider training and comfort with prescribing. 13 It is worth noting that the FDA approval for biologics has been granted in all cases for "add-on maintenance therapy for adults with chronic rhinosinusitis with nasal polyps." Indications for omalizumab further specify "for patients with inadequate response to nasal corticosteroids."…”

“…Additional complexity is brought about by the availability of other treatments (surgery or aspirin desensitization for example), patient and disease heterogeneity, comorbid conditions, drug availability, patient preferences, and provider training and comfort with prescribing. 13…”

Two‐year results of tapered dupilumab for CRSwNP demonstrates enduring efficacy established in the first 6 months

“…14,15 Despite optimal care, a subpopulation of patients with severe CRSwNP-especially those with T2-predominant CRSwNP and associated co-morbidity-remains poorly controlled, or not at all. [16][17][18][19][20][21] This group of patients is often subject to cumulative high-dose OCS therapy and/or repeated and extensive revision surgery imposing risks of iatrogenic damage with potentially long-term sequelae. 19,[22][23][24] The last decades gave rise to biologicals targeting T2inflammatory pathway components, which have been registered for and implemented in the treatment strategies of atopic dermatitis, asthma, eosinophilic esophagitis, and, as of late 2019, CRSwNP, and is of interest for allergic rhinitis.…”

S2k-Leitlinie zur fachärztlichen Diagnostik und Therapie von Asthma 2023

“…Die Identifizierung dieses Asthmasubtyps ist von klinisch-praktischer Bedeutung, da einerseits eine COX-1-Hemmer-Einnahme vermieden werden muss (empfohlene Alternative: Paracetamol) und andererseits eine Dauertherapie mit ASS ("adaptive Desaktivierung") sowohl die CRSwNP als auch das Asthma deutlich bessern kann [71]. Patienten mit Widal-Trias (Samter-Trias) werden jedoch immer häufiger mit Biologika statt mit einer adaptiven Desaktivierung behandelt, v. a. aufgrund der besseren Verträglichkeit und Praktikabilität der Biologika-Therapie, aber auch aufgrund der guten Wirksamkeit der Biologika in dieser Konstellation [73,74]. Nur bei einem Teil der Patienten mit schwerem Asthma und N-ERD werden unter einer Biologika-Therapie COX-1-Hemmer wieder vertragen [75,76]: Dies spricht dafür, dass sowohl die Pathogenese der N-ERD als auch die Wirkung der adaptiven Desaktivierung komplex ist und nicht auf einen singulären Mechanismus zurückzuführen ist [77].…”