Chronic rhinosinusitis (CRS) is one of the most common chronic diseases worldwide. It is a heterogeneous disease, and geographical or ethnic differences in inflammatory pattern in nasal mucosa are major issues. Tissue eosinophilia in CRS is highly associated with extensive sinus disease, recalcitrance, and a higher nasal polyp (NP) recurrence rate after surgery. The prevalence of eosinophilic CRS (ECRS) is increasing in Asian countries within the last 2 decades, and this trend appears to be occurring across the world. International consensus criteria for ECRS are required for the accurate understanding of disease pathology and precision medicine. In a multicenter large-scale epidemiological survey, the “Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis study,” ECRS was definitively defined when the eosinophil count in nasal mucosa is greater than or equal to 70 eosinophils/hpf (magnification, ×400), and this study proposed an algorithm that classifies CRS into 4 groups according to disease severity. The main therapeutic goal with ECRS is to eliminate or diminish the bulk of NP tissue. NPs are unique abnormal lesions that grow from the lining of the nasal and paranasal sinuses, and type 2 inflammation plays a critical role in NP development in patients with ECRS. An imbalance between protease and endogenous protease inhibitors might play a pivotal role in the initiation and exacerbation of type 2 inflammation in ECRS. Intraepithelial mast cells in NPs, showing a tryptase+, chymase− phenotype, may also enhance type 2 inflammation. Intense edema and reduced fibrosis are important histological features of eosinophilic NPs. Mucosal edema mainly consists of exuded plasma protein, and excessive fibrin deposition would be expected to contribute to the retention of proteins from capillaries and thereby perpetuate mucosal edema that may play an etiological role in NPs. Upregulation of the coagulation cascade and downregulation of fibrinolysis strongly induce abnormal fibrin deposition in nasal mucosa, and type 2 inflammation plays a central role in the imbalance of coagulation and fibrinolysis.

慢性鼻-鼻窦炎（CRS）是全球最常见的慢性疾病之一。它是一种异质性疾病，鼻粘膜炎症模式的地理或种族差异是主要问题。CRS中的组织嗜酸性粒细胞增多与广泛的鼻窦疾病，顽固性以及术后鼻息肉（NP）复发率较高相关。在过去的20年中，嗜酸性CRS（ECRS）在亚洲国家的患病率呈上升趋势，并且这种趋势似乎在世界范围内正在发生。为了准确理解疾病病理学和精密医学，需要有ECRS的国际共识标准。在一项多中心的大规模流行病学调查中，“日本难治性嗜酸性慢性鼻鼻窦炎的流行病学调查，当鼻粘膜中嗜酸性粒细胞计数大于或等于70嗜酸性粒细胞/ hpf（放大倍数×400）时，就明确定义了ECRS（这项研究提出了一种根据疾病严重程度将CRS分为4组的算法）。ECRS的主要治疗目标是消除或减少大部分NP组织。NP是从鼻和鼻旁窦内膜生长的独特异常病变，而2型炎症在ECRS患者的NP形成中起关键作用。蛋白酶和内源性蛋白酶抑制剂之间的失衡可能在ECRS中2型炎症的发生和加剧中起关键作用。NP中的上皮内肥大细胞表现出类胰蛋白酶+，糜酶-表型，也可能会增强2型炎症。强烈的水肿和纤维化减少是嗜酸性NP的重要组织学特征。粘膜水肿主要由渗出的血浆蛋白组成，过度的血纤蛋白沉积将有助于保留毛细管中的蛋白质，从而使粘膜水肿永久化，这可能在NP中起病因作用。凝血级联反应的上调和纤维蛋白溶解的下调强烈地诱导了鼻粘膜中异常的纤维蛋白沉积，而2型炎症在凝血和纤维蛋白溶解的失衡中起着核心作用。