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Asthma-II: Pathophysiology and Classification01:26

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Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
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Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma
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Characterization of asthma endotypes: implications for therapy.

Jeffrey R Stokes1, Thomas B Casale2

  • 1Division of Allergy and Immunology, Creighton University, Omaha, Nebraska.

Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology
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Precision medicine for severe asthma utilizes biomarkers to target T-helper type 2 (TH2)-high and TH2-low endotypes. TH2-high therapies show promise, while TH2-low treatments are still developing.

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Area of Science:

  • Pulmonology
  • Immunology
  • Pharmacology

Background:

  • Severe asthma is characterized by distinct endotypes, primarily T-helper type 2 (TH2)-high and TH2-low.
  • TH2-high asthma typically involves elevated eosinophils, while TH2-low asthma is defined by neutrophils or a pauci-granulocytic profile.
  • Precision medicine aims to tailor treatments based on these identified asthma endotypes.

Purpose of the Study:

  • To outline the concept of precision medicine in severe asthma management.
  • To review the utility of biomarkers in differentiating and treating asthma endotypes.
  • To discuss the current landscape of targeted therapies for severe asthma.

Main Methods:

  • A literature search of PubMed was conducted for human clinical trials on biologics for TH2-high and TH2-low asthma.
  • Studies meeting criteria for double-masked, randomized, placebo-controlled trials in peer-reviewed journals were selected.
  • The review focused on therapies targeting specific inflammatory pathways and their biomarker associations.

Main Results:

  • Several immune response modifiers targeting pathways like IL-5, IL-13, and IgE are available or in development for TH2-high asthma.
  • Approved therapies for severe TH2-high asthma include anti-IgE and anti-IL-5 monoclonal antibodies.
  • Efficacy of TH2-high therapies often correlates with elevated biomarkers such as blood eosinophils.
  • TH2-low asthma lacks clear point-of-care biomarkers, leading to diagnosis by exclusion and lagging therapeutic development.
  • TH2-low asthma patients often exhibit increased steroid resistance.

Conclusions:

  • Biomarker-guided classification into TH2-high and TH2-low endotypes has facilitated the development of targeted therapeutics for severe asthma.
  • Current advancements in precision medicine have yielded significant progress in treating TH2-high asthma.
  • Further research is needed to develop effective therapies for the TH2-low asthma endotype due to biomarker limitations.