Giselle Mosnaim, MD, MS 

Current CSU Treatment Approach and the Role of Bruton Tyrosine Kinase (BTK)

Video content above is prompted by the following:

What mechanisms and targets are currently being utilized or studied for the treatment of CSU?

Why are so many patients (more than half) with CSU unable to achieve adequate control with antihistamines alone?

What role does BTK play in the pathogenesis of CSU?

BTK signaling is involved in pathways that lead to the degranulation of skin mast cells, which are key pathogenic drivers of CSU.

BTK also presents in B cells and basophils, the latter of which activate and degranulate similarly to mast cells.

Videos

Panelists discuss how chronic spontaneous urticaria (CSU) treatment targets multiple pathways through antihistamines, anti-IgE therapy, and BTK inhibitors, with BTK emerging as a key target.

Current CSU Treatment Approach and the Role of Bruton Tyrosine Kinase 

Pathophysiology of Chronic Spontaneous Urticaria

Describe the pathogenesis of chronic spontaneous urticaria (CSU), including the IgE (autoallergic; type I) and IgG (autoimmune; type IIb) CSU subtypes.

Panelists discuss how chronic spontaneous urticaria develops through 2 distinct pathways: autoallergic CSU involving IgE-mediated mast cell activation (type I hypersensitivity) and autoimmune CSU where IgG autoantibodies target FcεRI receptors or IgE itself (type IIb hypersensitivity), both ultimately leading to mast cell degranulation and wheal formation.

Giselle Mosnaim, MD, MS

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