Anfuso Antony, Ramadan Hassan, Terrell Andrew, Demirdag Yesim, Walton Cheryl, Skoner David P, Piedimonte Giovanni
Department of Otolaryngology, West Virginia University, Morgantown, West Virginia.
Department of Pediatrics, West Virginia University, Morgantown, West Virginia.
Ann Allergy Asthma Immunol. 2015 Feb;114(2):103-10. doi: 10.1016/j.anai.2014.10.024.
Chronic rhinosinusitis (CRS) and asthma frequently coexist in children and adults. However, the precise pathophysiologic mechanism of this interaction is still poorly understood, especially in children, owing to the lack of direct measurements of mucosal inflammation in the upper airways.
To determine the pathophysiologic mechanism by analyzing the expression of a large array of inflammatory cytokines and chemokines in the sinus and adenoid tissues surgically removed from pediatric patients with CRS refractory to medical management.
Twenty-eight children 2 to 12 years old diagnosed with CRS with or without asthma and 10 controls were included in this prospective, nonrandomized study. Mucosal expression of 40 inflammatory cytokines was measured with a multiplex assay and was normalized to total tissue protein.
Compared with children with CRS and without asthma, children with CRS and asthma had significantly higher sinus levels of tumor necrosis factor-α and adenoid levels of epidermal growth factor, eotaxin, fibroblast growth factor-2, growth-related oncogene, and platelet-derived growth factor-AA.
The inflammatory response in the upper airway mucosa of children with asthma and CRS was similar, but more severe, compared with children with CRS without asthma. This observation is consistent with the hypothesis that asthma in these patients is caused or exacerbated by severe upper airway disease and supports the concept that treating sinus disease is paramount in the management of chronic asthma in children using, for the first time, direct measurements of airway inflammation in children.
慢性鼻-鼻窦炎（CRS）和哮喘在儿童及成人中常同时存在。然而，这种相互作用的确切病理生理机制仍知之甚少，尤其是在儿童中，因为缺乏对上呼吸道黏膜炎症的直接测量。
通过分析从药物治疗无效的小儿CRS患者手术切除的鼻窦和腺样体组织中大量炎性细胞因子和趋化因子的表达来确定病理生理机制。
本前瞻性、非随机研究纳入了28例2至12岁诊断为CRS伴或不伴哮喘的儿童及10例对照。采用多重分析法测量40种炎性细胞因子的黏膜表达，并将其标准化为总组织蛋白。
与不伴哮喘的CRS患儿相比，伴哮喘的CRS患儿鼻窦中肿瘤坏死因子-α水平及腺样体中表皮生长因子、嗜酸性粒细胞趋化因子、成纤维细胞生长因子-2、生长相关癌基因和血小板衍生生长因子-AA水平显著更高。
与不伴哮喘的CRS患儿相比，伴哮喘的CRS患儿上呼吸道黏膜的炎症反应相似，但更严重。这一观察结果与这些患者的哮喘由严重上呼吸道疾病引起或加重的假说一致，并首次通过对儿童气道炎症的直接测量支持了治疗鼻窦疾病在儿童慢性哮喘管理中至关重要的概念。
