Dupilumab efficacy and safety in patients with asthma and blood eosinophils ≥500 cells·µL−1

K. Rabe, I. Pavord, M. Castro, M. Wechsler, N. Daizadeh, U. Kapoor, B. Ortiz, A. Radwan, Robert R. Johnson, P. Rowe, Y. Deniz, J. Jacob-Nara
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引用次数: 1

Abstract

Uncontrolled, moderate-to-severe asthma in patients with high baseline blood eosinophils (≥500 cells·µL−1) can be difficult to treat [1]. Global Initiative for Asthma guidelines recommend biologics as add-on therapy for patients with severe type 2 inflammatory asthma that remains uncontrolled despite treatment with high-dose inhaled corticosteroids [2]. Surrogate markers of type 2 inflammation, such as elevated levels of blood or sputum eosinophils and fractional exhaled nitric oxide (FeNO) can be used to identify patients with a type 2 signature who might be eligible for such treatment [1–3]. Several biologics are now available that target different molecules in type 2 inflammatory pathways, notably IgE and type 2 cytokines [1–3]. One of these, dupilumab, is a fully human VelocImmune-derived [4, 5] monoclonal antibody that blocks the shared receptor component for interleukin-4 and -13, cytokines that are key and central drivers of type 2 inflammation in multiple diseases, thus inhibiting their signalling [6, 7]. Dupilumab is well tolerated and improves clinical outcomes in patients with asthma and high eosinophils (≥500 cells·µL−1). Improvements in clinical outcomes correlate with eosinophil counts, demonstrating dupilumab efficacy in those with high eosinophils. https://bit.ly/3Jxvicb
Dupilumab在哮喘和血嗜酸性粒细胞≥500 cells·µL−1患者中的疗效和安全性
基线血嗜酸性粒细胞高(≥500细胞·µL−1)的中度至重度哮喘患者难以治疗[1]。全球哮喘倡议指南推荐生物制剂作为严重2型炎症性哮喘患者的附加治疗,尽管使用大剂量吸入皮质类固醇治疗,但仍无法控制。2型炎症的替代标志物,如血液或痰中嗜酸性粒细胞和分数呼气一氧化氮(FeNO)水平升高,可用于识别具有2型特征的患者,这些患者可能有资格接受此类治疗[1-3]。目前已有几种针对2型炎症通路中不同分子的生物制剂,特别是IgE和2型细胞因子[1-3]。其中之一,dupilumab,是一种完全由人类velocimmune衍生的单克隆抗体[4,5],可阻断白细胞介素-4和-13的共享受体成分,白细胞介素-4和-13是多种疾病中2型炎症的关键和核心驱动因子,从而抑制其信号传导[6,7]。Dupilumab耐受性良好,可改善哮喘和高嗜酸性粒细胞(≥500细胞·µL−1)患者的临床结果。临床结果的改善与嗜酸性粒细胞计数相关,证明dupilumab对嗜酸性粒细胞高的患者有效。https://bit.ly/3Jxvicb
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