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Role of Biologics in Asthma.
American Journal of Respiratory and Critical Care Medicine ( IF 24.7 ) Pub Date : 2019-02-15 , DOI: 10.1164/rccm.201810-1944ci
Mary Clare McGregor 1 , James G Krings 1 , Parameswaran Nair 2 , Mario Castro 1
Affiliation  

Patients with severe uncontrolled asthma have disproportionally high morbidity and healthcare utilization as compared with their peers with well-controlled disease. Although treatment options for these patients were previously limited, with unacceptable side effects, the emergence of biologic therapies for the treatment of asthma has provided promising targeted therapy for these patients. Biologic therapies target specific inflammatory pathways involved in the pathogenesis of asthma, particularly in patients with an endotype driven by type 2 (T2) inflammation. In addition to anti-IgE therapy that has improved outcomes in allergic asthma for more than a decade, three anti-IL-5 biologics and one anti-IL-4R biologic have recently emerged as promising treatments for T2 asthma. These targeted therapies have been shown to reduce asthma exacerbations, improve lung function, reduce oral corticosteroid use, and improve quality of life in appropriately selected patients. In addition to the currently approved biologic agents, several biologics targeting upstream inflammatory mediators are in clinical trials, with possible approval on the horizon. This article reviews the mechanism of action, indications, expected benefits, and side effects of each of the currently approved biologics for severe uncontrolled asthma and discusses promising therapeutic targets for the future.

中文翻译:

生物制剂在哮喘中的作用。

与疾病控制良好的同龄人相比,严重的不受控制的哮喘患者的发病率和医疗保健利用率高得多。尽管这些患者的治疗选择先前受到限制,且副作用不可接受,但是出现了用于治疗哮喘的生物疗法,为这些患者提供了有希望的靶向治疗。生物疗法的目标是哮喘发病机制中涉及的特定炎症途径,特别是在具有由2型(T2)炎症驱动的内型的患者中。除了可以在过敏性哮喘中改善疗效的抗IgE疗法十多年来,最近还出现了三种抗IL-5生物制剂和一种抗IL-4R生物制剂作为治疗T2哮喘的有希望的方法。这些靶向疗法已被证明可以减少哮喘发作,改善肺功能,减少口服皮质类固醇的使用,并改善在适当选择的患者的生活质量。除了当前批准的生物制剂外,针对上游炎症介质的多种生物制剂正在临床试验中,并且可能会获得批准。本文回顾了每种目前批准用于严重不受控制的哮喘的生物制剂的作用机理,适应症,预期收益和副作用,并讨论了未来有希望的治疗目标。
更新日期:2019-11-01
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