Chronic Spontaneous Urticaria and Bruton Tyrosine Kinase: A Multispecialty Expert Discussion - Episode 7
Differentiating BTK Inhibition From Genetic BTK Deficiency
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Panelists discuss how pharmacological Bruton tyrosine kinase (BTK) inhibition with agents like remibrutinib appears safer than genetic BTK deficiency (X-linked agammaglobulinemia [XLA]), as clinical studies show the drug doesn't significantly impact immunoglobulin levels or infection rates in patients with chronic spontaneous urticaria (CSU), unlike the severe immunodeficiency seen in XLA.
Video content above is prompted by the following:
- How does inhibition of the BTK mechanism differ from manifestations of genetic BTK deficiency (XLA)?
- BTK signaling plays a role in B-cell development, and BTK mutation linked to XLA has been shown to affect immunoglobulin levels, making patients with XLA more susceptible to serious infections; remibrutinib did not affect total serum Ig levels or infection rates in CSU patients in phase 2b core and extension studies or in phase 3 studies
