68 search results for: asthma
ADVENT On Air | Breathing Easy: Navigating Lung Function in Pediatric Severe Asthma With Spirometry and Beyond
Join Drs. Wanda Phipatanakul and Theresa Guilbert as they discuss the importance of routine lung function assessment in pediatric asthma patients.
Why Is It Important to Assess Lung Function in Pediatric Asthma?
Learn about FEV1pp and the downstream effects of lung function decline in children with severe asthma.
How Type 2 Inflammation Drives Eosinophils in Asthma
Explore how type 2 inflammation drives the production of eosinophils in severe asthma.
Pathways Driving Chronic Airway Remodeling in Asthma
See how type 2 inflammation underlies remodeling processes in asthma.
Eosinophils as a Biomarker for Type 2 Asthma
Dr. Elliot Israel presents the utility of eosinophils as a biomarker of type 2 inflammation and their role in the disease burden of asthma.
FeNO as a Biomarker for Type 2 Asthma
Dr. Eugene Bleecker presents the utility of FeNO as a biomarker of type 2 inflammation, and its role in the disease burden of asthma.
The Cycle of Inflammation in Adult Asthma
Explore the role of chronic type 2 inflammation in the cycle of exacerbations and worsening lung function in patients with asthma.
Multifaceted Role of IL-13 in Airway Remodeling
Join Dr. Celeste Porsbjerg as she discusses on how IL-13 contributes to mucus plugging in asthma.
IgE as a Biomarker for Type 2 Asthma
Dr. Jonathan Corren describes the diagnostic, predictive, and prognostic role of IgE as a biomarker of type 2 inflammation in asthma.
FeNO Is a Noninvasive Biomarker That Can Support Diagnosis and Management for Asthma Patients
Learn how FeNO, a noninvasive biomarker for type 2 inflammation, can be used to optimize care for asthma patients.
Airway Remodeling in Type 2 Asthma is Driven by IL-4 and IL-13
Dr. Reynold Panettieri discusses how IL-4 and IL-13 drive airway remodeling in type 2 asthma.
Type 2 Inflammation Mediates Severe Asthma in Pediatric Patients
Dr. Leonard Bacharier discusses how type 2 inflammation underlies the pathophysiology of pediatric severe asthma and contributes to burden.
