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Pharmacotherapy

Treatment of severe, uncontrolled eosinophilic asthma: Where we are heading

, MD & , MD
Pages 459-472 | Received 21 Feb 2018, Accepted 28 Apr 2018, Published online: 16 Oct 2018
 

Abstract

Objective: We sought to highlight how our understanding of the pathophysiology of severe asthma has evolved over time and discuss the role of biomarkers in treatment advances and emerging new therapies. Data Sources: Nonsystematic PubMed literature search. Study Selection: Articles were selected based on areas of relevance to the classification of asthma by endotype, with an emphasis on the evolution of current treatment guidelines for severe asthma. Results: Unlike older guidelines for the treatment of severe asthma, recent updates now distinguish between asthma severity and control. Moreover, asthma classification is shifting from phenotype to endotype with the development of biomarkers used to determine the mechanism driving a patient's disease. Many cases of severe asthma are associated with type-2 inflammation with elevated eosinophil counts in the airways. In recent studies, patients with severe, uncontrolled asthma and high eosinophil counts respond to biologic therapies targeting the type-2 signaling pathway and eosinophils themselves (eg, anti-IL-5 therapy). New treatments that address the pathophysiology of asthma offer a promising alternative to control severe asthma for patients who do not respond to traditional therapies. Conclusion: Understanding and using new treatment guidelines that separate the concepts of asthma severity and control may help clinicians to identify patients with severe, uncontrolled asthma who may benefit from new treatment options, such as anti-IL-5 therapies.

Acknowledgements

Medical writing support was provided by Courtney St. Amour, PhD, of MedErgy (Yardley, PA, USA), which was in accordance with Good Publication Practice (GPP3) guidelines and funded by AstraZeneca (Wilmington, DE, USA).

Additional information

Funding

This work was supported by the AstraZeneca (P01-HL114471-01A1, NIH P01-HL114471-03).

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