Chronic spontaneous urticaria (CSU) is a chronic, disabling disease characterized by the occurrence of wheals (hives), angioedema or both for greater than six weeks1,2. CSU has been shown to have a significant impact on patients’ quality of life, including sleep, daily activity, work productivity, and emotional well-being, leading to a significant humanistic and economic burden2. The diagnostic algorithm of CSU is completed via a thorough patient history1. However, the delay from symptom onset to diagnosis is approximately two years2.
The signs and symptoms of CSU are due to activation of skin mast cells1. At least two possible causes of CSU are recognized – type I autoimmune (autoallergic) and type IIb autoimmune3. Type I autoimmune CSU is characterized by the production IgE antibodies to self-antigens (autoallergens), whereas type IIb autoimmune CSU is characterized by the production IgG to IgE or FcεRI3. Central to both endotypes is Bruton’s tyrosine kinase (BTK), a cytoplasmic enzyme which is the positive regulator of FcεRI-mediated mast cell activation and cytokine production4. Despite significant advances in the understanding of CSU etiology and pathogenesis, further research is warranted4.
The first-line therapy for CSU is second-generation H1-antihistamines1. However, up to 60% of patients remain symptomatic despite treatment with second-generation H1-antihistamines2. Moreover, few patients are escalated to more advanced care, which may contribute to the significant impact on patients’ quality of life2.
Innovative strategies to better understanding underlying pathophysiologic mechanisms and optimal management pathways are needed to improve the care of CSU patients, which may in turn lead to improvements in quality of life and better health outcomes for these patients.