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Type-2 inflammation: a key treatable trait associated with lung function decline in chronic airways disease
Thorax ( IF 10 ) Pub Date : 2024-04-01 , DOI: 10.1136/thorax-2023-221329
Nayia Petousi , Ian D Pavord , Brian Daniel Kent

The chronic airways diseases, asthma and Chronic Obstructive Pulmonary Disease (COPD), are highly prevalent conditions causing significant morbidity and mortality worldwide. Both are acknowledged to be heterogeneous with respect to clinical presentation, prognosis and driving mechanisms.1 Type-2 airway inflammation is arguably the most important and treatable underlying mechanism to identify,1 as it can be successfully targeted by inhaled and systemic corticosteroids,2 3 or by biological therapies (anti-IL5/IL5R, anti-IL4/IL4R/IL13 and anti-TSLP) in patients with refractory disease.4 Type-2 airway inflammation is not only a key driver of morbidity and mortality but can be identifiable with two easily accessible biomarkers: the peripheral blood eosinophil count (BEC) and fractional exhaled nitric oxide (FeNO).5 There is consistent and compelling evidence linking raised type-2 biomarkers to exacerbation frequency6 7 and increased risk of exposure to oral corticosteroids with their associated toxicity leading to ‘people remodelling’8 ; and that treatments which reduce type-2 inflammation have a significant positive impact on exacerbation risk1 4 9 and mortality.10 However, there has been less focus on the role of type-2 inflammation in the airway remodelling associated with lung function decline and progressive airflow limitation. In this issue of Thorax , Çolak et al 11 have used a large and well-characterised Danish population-based cohort followed for 10 years, to investigate the relationship between BEC (measured before and after the observation period in 15 605 individuals), FeNO (measured in a subset of 2853 patients after the observation period) and …

中文翻译:

2 型炎症:与慢性气道疾病肺功能下降相关的关键可治疗特征

慢性气道疾病、哮喘和慢性阻塞性肺病(COPD)是非常普遍的疾病,在全世界范围内造成显着的发病率和死亡率。众所周知,两者在临床表现、预后和驱动机制方面存在异质性。1 2 型气道炎症可以说是最重要且可治疗的潜在机制,1 因为它可以通过吸入和全身性皮质类固醇成功靶向,2 3或通过生物疗法(抗 IL5/IL5R、抗 IL4/IL4R/IL13 和抗 TSLP)治疗难治性疾病患者。4 2 型气道炎症不仅是发病率和死亡率的关键驱动因素,而且可以通过两种易于获取的生物标志物:外周血嗜酸性粒细胞计数 (BEC) 和呼出一氧化氮分数 (FeNO)。5 有一致且令人信服的证据表明 2 型生物标志物升高与急性加重频率 6 7 以及口服皮质类固醇暴露风险增加及其相关毒性导致“人重塑”8;减少 2 型炎症的治疗对恶化风险 1 4 9 和死亡率具有显着的积极影响。 10 然而,人们很少关注 2 型炎症在与肺功能下降和进行性气流相关的气道重塑中的作用。局限性。在本期 Thorax 中,Çolak 等人 11 使用了一个大型且特征良好的丹麦人群队列,跟踪了 10 年,以调查 BEC(在 15 605 名个体的观察期前后测量)、FeNO(在观察期后对 2853 名患者的子集进行测量)和……
更新日期:2024-03-15
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