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Related Concept Videos

Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

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.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...
Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
Antiasthma Drugs: Leukotriene Modifiers01:19

Antiasthma Drugs: Leukotriene Modifiers

Leukotriene modifiers, or cysteinyl leukotriene receptor antagonists, are medications used to manage chronic asthma. These agents target specific inflammatory mediators produced during arachidonic acid metabolism, an essential process in generating inflammation in the body.
Leukotriene modifiers work through two distinct mechanisms:
Allergic Reactions02:06

Allergic Reactions

Overview

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Related Experiment Video

Updated: May 31, 2026

Identification and Characterization of Immunogenic RNA Species in HDM Allergens that Modulate Eosinophilic Lung Inflammation
08:44

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Published on: May 30, 2020

Steroid responsiveness and wheezing phenotypes.

Francine M Ducharme1, Maja Krajinovic

  • 1Departments of Pediatrics and of Social Preventive Medicine, University of Montreal, Montreal, Quebec, Canada. francine.m.ducharme@umontreal.ca

Paediatric Respiratory Reviews
|July 5, 2011
PubMed
Summary

Corticosteroid resistance in childhood asthma, particularly in preschool viral-induced cases, necessitates higher doses. Identifying factors like age, triggers, and genetics is crucial for effective asthma management.

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Published on: April 13, 2010

Area of Science:

  • Pediatric Pulmonology
  • Clinical Immunology
  • Pharmacogenetics

Background:

  • Corticosteroids are essential for managing childhood asthma, with oral forms for acute exacerbations and inhaled forms for prevention.
  • Variability in patient response to corticosteroids is a recognized clinical challenge.
  • Emerging evidence suggests corticosteroid resistance in preschool children with viral-induced asthma.

Purpose of the Study:

  • To explore the determinants of corticosteroid responsiveness in children with asthma.
  • To investigate potential factors contributing to corticosteroid resistance in specific pediatric asthma phenotypes.
  • To inform phenotype-specific therapeutic strategies for childhood asthma.

Main Methods:

  • Review of published trials examining corticosteroid response in pediatric asthma populations.
  • Analysis of potential influencing factors including age, asthma triggers, phenotype, environmental exposures (e.g., tobacco smoke), and genetic variations.
  • Exploration of mechanistic pathways, including gene-environment interactions and inflammatory profiles.

Main Results:

  • Heterogeneity in study populations and asthma phenotypes complicates the identification of response determinants.
  • Key potential determinants identified include patient age, specific asthma triggers, underlying asthma phenotype, exposure to tobacco smoke, and genetic factors.
  • A proposed mechanism for corticosteroid resistance involves gene-environment interactions leading to non-eosinophilic airway inflammation.

Conclusions:

  • Accurate asthma diagnosis and precise phenotyping are critical for selecting optimal, phenotype-specific therapies.
  • Understanding determinants of corticosteroid resistance can guide personalized treatment approaches in pediatric asthma.
  • Further research is needed to elucidate the complex interplay of factors influencing corticosteroid response in children.