Sok John C, Ferguson Berrylin J
Curr Allergy Asthma Rep. 2006 May;6(3):203-14. doi: 10.1007/s11882-006-0036-1.
Eosinophilic chronic rhinosinusitis (ECRS) encompasses a wide variety of etiologies. To date, a unifying pathophysiologic mechanism remains elusive. Eosinophilia is frequently, but not exclusively, caused by immunoglobulin (Ig)E-mediated hypersensitivity and is dominated by the associated cytokine milieu of Th2 inflammation. The provisional subcategories of ECRS include superantigen-induced eosinophilic chronic rhinosinusitis, allergic fungal sinusitis, nonallergic fungal eosinophilic chronic rhinosinusitis, and aspirin-exacerbated eosinophilic chronic rhinosinusitis. Within each subcategory, recent findings supporting distinct mechanisms that promote eosinophilic infiltration are presented, and, therefore, targeted therapeutic interventions with specific antibacterial, antifungal, or immune modulation may be indicated.
嗜酸性粒细胞性慢性鼻-鼻窦炎(ECRS)病因多样。迄今为止,尚未明确统一的病理生理机制。嗜酸性粒细胞增多常由免疫球蛋白(Ig)E介导的超敏反应引起,但并非唯一原因,且以Th2炎症相关的细胞因子环境为主导。ECRS的暂定子类别包括超抗原诱导的嗜酸性粒细胞性慢性鼻-鼻窦炎、变应性真菌性鼻窦炎、非变应性真菌性嗜酸性粒细胞性慢性鼻-鼻窦炎以及阿司匹林加重的嗜酸性粒细胞性慢性鼻-鼻窦炎。在每个子类别中,均介绍了支持促进嗜酸性粒细胞浸润的不同机制的最新研究结果,因此,可能需要针对性地采取特定的抗菌、抗真菌或免疫调节治疗干预措施。