In this video soundbite from the EAACI 2025 symposium, Dr. Philippe Gevaert explains how biologic options for uncontrolled CRSwNP are increasing, and phase 3 studies of approved biologics show improved outcomes and decreased SCS use/surgery in patients with CRSwNP. Additionally, he explains how biologics targeting type 2 inflammatory pathophysiology potentially improve outcomes for eligible patients with co-existing CRSwNP and asthma.
Navigate through this interactive infographic to learn more about why lung function is important to monitor in pediatric patients with asthma and the noninvasive procedures that are available for implementation in clinical practice.
Learn about FEV1pp and the downstream effects of lung function decline in children with severe asthma.
Explore how type 2 inflammation drives the production of eosinophils in severe asthma.
See how type 2 inflammation underlies remodeling processes in asthma.
Join Dr. Celeste Porsbjerg as she discusses on how IL-13 contributes to mucus plugging in asthma.
Learn how FeNO, a noninvasive biomarker for type 2 inflammation, can be used to optimize care for asthma patients.
Learn about the multifaceted burden of uncontrolled pediatric asthma on patients and their caregivers.
Join pediatric respirologist Dr. Sharon Dell and adult respirologist Dr. Simon Couillard as they discuss the prognostic and diagnostic power of asthma biomarkers and their impact on optimizing patient management across all ages.
Explore 3 hypothetical patient cases using guideline-based checklists for assessment and diagnosis of type 2 inflammation in adult asthma
Review a patient case to learn more about identifying uncontrolled asthma and type 2 inflammation in pediatric patients
Professors Brian Lipworth, Zuzana Diamant, and Philippe Gevaert delve into the complexities of managing patients with both severe and/or uncontrolled CRSwNP and co-existing asthma through an evaluation of the diagnostic challenges, personalized treatment strategies, and the latest advancements in understanding the interconnected pathophysiology of these type 2 airway diseases.