Role of Interleukin 5 Inhibition in the Treatment of Eosinophilic Otitis Media

白细胞介素 5 抑制剂在嗜酸性中耳炎治疗中的作用

阅读:1

Abstract

OBJECTIVE: Eosinophilic otitis media (EOM) is a rare form of middle ear disease characterized by a viscous effusion rich in eosinophils, a resistance to conventional treatments, and an association with bronchial asthma. The relationship between asthma and EOM suggests similarities in pathogenesis and treatment possibilities. Recent biologic therapies, specifically those that target interleukin 5 (IL-5), have demonstrated efficacy in controlling eosinophil-driven asthma, yet their impact on the treatment of pathologically similar diseases remains unmeasured. This study identifies patients who have EOM, reviews their otologic clinical course, and investigates the impact of anti-IL-5 drugs on chronic ear disease. STUDY DESIGN: Retrospective chart review. SETTING: University of Florida Health, an academic medical center. METHODS: A review of 120 patients treated with benralizumab or mepolizumab was performed. Imaging evidence of otomastoiditis was used to identify 9 patients with possible EOM. Two patients were treated with benralizumab, and the remaining 7 received mepolizumab injections. RESULTS: After starting treatment, 5 patients had complete resolution of middle ear effusions (3 with mepolizumab and 2 with benralizumab); 1 had stable middle ear effusion; and 1 patient's disease status could not be determined due to a lack of follow-up. The remaining 2 patients did not have effusions at the time when anti-IL-5 therapy was initiated, and they have not relapsed since starting treatment. CONCLUSION: EOM is a rare disease that otolaryngologists should include in their differential diagnosis, especially in refractory cases. Anti-IL-5 agents show efficacy in treating EOM, and prospective multicenter clinical trials are needed to further characterize the effect of anti-IL-5 therapies.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。