First AD

Second AD

Pathophysiology of CSU and Role of BTK

Video content above is prompted by the following:

What have we learned about the possible mechanisms involved with CSU pathogenesis?

How has the identification and characterization of novel mechanisms of mast cell activation helped us to better understand CSU?

Can you describe the role of BTK as a mediator in mast cell degranulation and histamine release?

Peer Exchange: Evolving Perspectives and Treatment Strategies in Chronic Spontaneous Urticaria 

HCPLive® Peer Exchange panel discussions feature authoritative insights, opinions, and perspectives on important issues facing today's care professionals.

Peer Exchange

Chronic spontaneous urticaria (CSU) pathogenesis involves complex mechanisms, including mast cell activation and degranulation. Recent insights into novel mechanisms of mast cell activation have enhanced understanding of CSU, revealing potential therapeutic targets. Bruton's tyrosine kinase (BTK) plays a crucial role as a mediator in mast cell degranulation and histamine release, offering a promising target for intervention. The identification of these pathways has provided a deeper understanding of CSU's underlying biology, paving the way for more effective treatments and improved patient outcomes.

Panelists discuss recent insights into the mechanisms involved in chronic spontaneous urticaria (CSU) pathogenesis, emphasizing how the identification of novel mast cell activation pathways enhances our understanding of the condition, particularly highlighting the role of Burton tyrosine kinase (BTK) as a key mediator in mast cell degranulation and histamine release.