120 search results for: Pathophysiology
The Benefits of Early Intervention in Reducing the Burden of Disease in Children With Atopic Dermatitis
This page presents educational material, infographics, and video highlights from our recent ADVENT symposia, including the 2025 World Congress of Pediatric Dermatology (WCPD) in Buenos Aires, Argentina, exploring the pathophysiology of type 2 inflammation and atopic dermatitis, the burden of disease leading to cumulative life course impairment (CLCI), and the risk of the atopic march in pediatric patients with atopic dermatitis.
The Role of IL-4 and IL-13 in CSU Pathogenesis
Dive into the complex pathophysiology of chronic spontaneous urticaria (CSU), where mast cell degranulation drives the hallmark signs and symptoms. This interactive infographic elucidates how key type 2 cytokines, specifically IL-4 and IL-13, contribute to mast cell activation, immune cell trafficking into the skin, and neuronal sensitization in CSU, which ultimately leads to the release of mediators like histamine that cause wheals, angioedema, and itch.
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
The March 2025 ADVENT symposium in Orlando, Florida brought together 4 dermatology experts to explore the evolving science of type 2 inflammation. Type 2 inflammation plays a central role in the pathophysiology of multiple dermatological diseases, driving chronic immune dysregulation that affects patients with atopic dermatitis (AD) prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP). Understanding the mechanisms behind type 2 inflammation is key to advancing care and improving patient quality of life.
ADVENT in Orlando, 2025
Type 2 inflammation contributes to many dermatologic diseases, which may lead to potentially life-changing burdens and challenges to patients and caregivers. By uncovering the role of type 2 inflammation in the pathophysiology of AD, PN, CSU, and BP, we can move forward in our understanding of each disease. Join global experts for an educational symposium on March 8th that will uncover the role of type 2 inflammation in the pathophysiology of AD, PN, CSU, and BP and explore questions driving current research in each disease.
Loss of Smell is a Key Symptom of CRSwNP
Learn how loss of smell in CRSwNP is a key symptom for both patients and providers.
Pathways to Disease: Inflammation in Chronic Obstructive Pulmonary Disease Video
Learn about the significant burden that patients with COPD experience and the role of inflammatory mechanisms in this chronic, often progressive disease.
Gastro Forum 2025 | EoE: How Far We've Come
Prof. Salvatore Oliva and Dr. Milli Gupta discuss the evolution in understanding EoE and the impact of chronic, underlying type 2 inflammation.
World Anosmia Day 2026
Join the effort to improve CRSwNP care. World Anosmia Day serves as an opportunity to raise awareness about the loss of the sense of smell. Access some of countless educational resources with ADVENT below.
CRSwNP at Center Stage: Impact of Biologics in Patients with Co-existing Type 2 Asthma
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.
How Biologic Therapy May Lead to Disease Modification in Infants and Children with Atopic Dermatitis
The underlying pathophysiology of atopic dermatitis (AD) is driven by dysregulation of type 2 immunity that contributes to skin barrier dysfunction. AD typically develops very early in life and children with AD often develop other atopic conditions such as food allergy, asthma, and allergic rhinitis in a progression called the atopic march. Early treatment may help reduce the atopic march and other comorbidities to lessen the lifetime burden created by these diseases. There may even be a window of opportunity for disease modification.
