38 search results for: mechanism of disease

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Cracking the Code: Diagnosing and Managing Skin Diseases With Type 2 Inflammation

This symposium delves into the pivotal role of type 2 inflammation in diverse skin conditions, including atopic dermatitis, prurigo nodularis, chronic spontaneous urticaria, and bullous pemphigoid. It highlights both shared and distinct disease mechanisms and patient burdens, providing crucial insights for optimizing clinical management strategies through a series of engaging panel discussions with Drs Eichenfield, Elmariah, Culton, and Hawkes.

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ADVENT Forum 2025 On Demand page

Watch on-demand expert soundbites recorded at the April 2025 ADVENT Forum in Lisbon, Portugal, featuring dermatology and immunology perspectives on mechanisms and clinical practice. Topics range from disease mechanism to patient care and quality of life, spanning atopic dermatitis (AD), prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP).

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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.

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Emerging Perspectives on the Disease Burden and Management of Children with Atopic Dermatitis

Join Christine Bangert, Mark Boguniewicz and Perla Lansang for an educational symposium on atopic dermatitis (AD) in children, exploring the diagnosis and pathophysiology of AD in children, the life-long effects of uncontrolled disease beyond the skin, and current and emerging therapies.

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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.

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Which Biomarkers of AD Might Be Robust Enough to Be Evaluated as a Measure of Disease Modification?

In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Prof. Oscar Palomares reviews the cellular and molecular pathways underlying atopic dermatitis and considers which biomarkers may one day serve as robust measures of disease modification, despite no validated options currently being available.

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Shared and Distinct: The Role of Type 2 Inflammation in Skin Diseases

Dr Donna Culton walks through the pathophysiology of type 2 inflammation in inflammatory skin diseases, using bullous pemphigoid as an example. Drs Eichenfield, Elmariah, and Hawkes join to discuss the role of type 2 inflammation across atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria, respectively. 

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Digging Deeper: Reducing Non-Atopic Comorbidities and Multidimensional Disease Burden

In this video from the April 2025 WCPD symposium, Dr Paula Luna discusses the multidimensional disease burden in pediatric patients with AD and the data regarding how early intervention may lead to long-term disease control and a reduced risk of developing non-atopic comorbidities.

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How Biologic Therapy May Lead to Disease Modification in Infants and Children With Atopic Dermatitis

This full video presentation of the April 2025 WCPD symposium features Dr Amy Paller, Dr Paula Luna, and Dr Eulàlia Baselga. The faculty present the latest data on the possibility of achieving disease modification in infants and children with atopic dermatitis.