PATHOPHYSIOLOGY AND MANAGEMENT FOR EOSINOPHILIC CHRONIC RHINOSINUSITIS

Abstract

　The major pathophysiology of eosinophilic chronic rhinosinusitis (ECRS) is thought to be type 2 inflammation by the innate and acquired immune responses of the sinonasal mucosae to external stimuli, centered on type 2 cytokines (IL-4, 5, and 13). Formation of albumin-based edema due to vascular hyperpermeability and excessive fibrin deposition due to hypercoagulation and fibrinolytic system suppression are thought to play the important roles on the causes of nasal polyps in the remodeling of the sinonasal mucosae. A definitive diagnosis of ECRS based on diagnostic criteria corresponds to the intractable disease designated by the Ministry of Health, Labor and Welfare. The accompanying eosinophilic otitis media, bronchial asthma, and systemic overlap type 2 inflammatory diseases should be also considered. The goal of ECRS treatment is to improve and stably maintain respiratory and olfactory function. For cost-effectiveness, management with an appropriate combination of pharmacotherapy that suppress type 2 cytokines, such as corticosteroids and biotics, and surgical therapy (full house of endoscopic sinus surgery) is critical.