Chronic spontaneous #urticaria (CSU) is associated with a substantial disease burden due to its prolonged course and significant impairment of quality of life. The diagnostic process for #CSU involves confirming the diagnosis itself and identifying disease phenotypes or endotypes, cofactors, and comorbid conditions, which may affect disease activity and severity. Immunoglobulin E (IgE) and non-IgE-mediated mast cell degranulation are the major pathogenic mechanisms of CSU, where FcεRIα, a high-affinity IgE receptor, is the critical therapeutic target. Although the first-line treatment for CSU is typically second-generation H1-antihistamines, anti-IgE antibodies are recommended for patients who are refractory to up-dosed antihistamines. However, some patients with autoimmune phenotypes show incomplete responses. Recently, dupilumab, an anti-interleukin (IL)-4/IL-13 receptor antibody that inhibits type 2 inflammation, was approved by the US Food and Drug Administration. Patients with autoimmune phenotypes treated with Bruton’s tyrosine kinase inhibitors have shown promising efficacy. Additionally, emerging biological agents, such as anti-KIT antibodies targeting mast cell activation and survival, and novel anti-IgE therapies (e.g., YH35324), are currently under investigation and are anticipated to become potential therapeutic options. This review provides an update on the pathogenic mechanisms of CSU, including IgE- and non-IgE-mediated mechanisms, and suggests potential therapeutic targets for improving clinical remission rates.
2 Medical News 