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Presentation

Advances in Chronic Urticaria Treatment: Guidelines, Phenotyping, and New Therapies

Description

The talk reviews chronic spontaneous urticaria (CSU), emphasizing that it is a common, often long-lasting and highly burdensome disease that significantly affects physical comfort, work, social life, and mental health. The speaker explains that CSU involves mast-cell driven inflammation with at least two broad phenotypes: a classic autoallergic/IgE-mediated form and a type 2b autoimmune form, and notes that triggers such as NSAIDs or viral infections can worsen disease without causing it. Treatment should start by maximizing second-generation non-sedating antihistamines, including dose escalation up to fourfold, since many patients respond and these medications are inexpensive and safe. For antihistamine-refractory disease, historical options included omalizumab and cyclosporine; omalizumab is effective for many patients but can take months to work, may be less effective in some endotypes, and can sometimes be tapered or stopped after sustained control, while cyclosporine works quickly but requires monitoring and has safety concerns. Newer therapies have expanded options, including dupilumab, which improves itch and quality of life, works regardless of IgE level, and is especially attractive in patients with atopic comorbidities, and remibrutinib, an oral BTK inhibitor with rapid and sustained symptom improvement, though mild transient mucocutaneous bleeding is a notable safety signal. The speaker also discusses using select labs to phenotype patients and guide therapy: elevated inflammatory markers suggest need for advanced treatment, low basophils/eosinophils and low IgE point toward type 2b autoimmune disease, high IgE supports omalizumab use, and low IgE may favor dupilumab or remibrutinib. Overall, the message is that CSU should be actively treated, phenotyped when useful, and managed with a stepwise but increasingly personalized approach.

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Conclusions

Chronic urticaria is common, burdensome, and often long-lasting, so it warrants active treatment rather than dismissal as a minor condition.
Most patients should first receive maximized second-generation antihistamines, often up to four times the standard dose, because this controls a substantial proportion of cases at low cost.
Omalizumab remains a highly effective and cost-effective standard option for refractory chronic spontaneous urticaria, but response may take 12 to 16 weeks and not all patients respond.
Patients who do well on omalizumab can sometimes stop or space treatment after sustained control, which may preserve remission and reduce costs.
Cyclosporine is still a useful option for difficult cases, especially when other therapies fail, though monitoring and safety concerns limit its use.
Dupilumab is an effective newer option, particularly when IgE is low or when atopic comorbidities are present, and its benefit appears independent of baseline IgE.
BTK inhibition with remibrutinib appears to provide rapid and durable symptom improvement and may be especially useful in both IgE-mediated and autoimmune phenotypes.
Bleeding with BTK inhibitors is usually mild mucocutaneous bruising or petechiae rather than major hemorrhage, and appears to diminish over time.
Phenotyping chronic spontaneous urticaria using features such as IgE level, basophils/eosinophils, inflammatory markers, and autoimmune history can help guide more rational therapy selection.
Routine diagnostic lab testing is not needed to diagnose chronic urticaria, but select biomarkers may be useful for predicting treatment response and choosing the right next therapy.
A practical treatment strategy is to escalate from optimized antihistamines to targeted biologic or oral therapy based on phenotype, reserving cyclosporine and clinical trial options for the most refractory patients.

Lang DM. NEJM. 2022;387(9):824-31.
Zuberbier T, et al. Allergy. 2018; 73(7):1393-1414.
Zuberbier, Bernstein, and Maurer, from J Allergy Clin Immunol, December 2022.