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Review
. 2025 Jul;156(1):17-23.
doi: 10.1016/j.jaci.2025.04.004. Epub 2025 Apr 10.

Endotypes of chronic spontaneous urticaria and angioedema

Dennis Wong  1 , Susan Waserman  2 , Gordon L Sussman  3
Affiliations
Free article
Review

Endotypes of chronic spontaneous urticaria and angioedema

Dennis Wong et al. J Allergy Clin Immunol. 2025 Jul.
Free article

Abstract

The current understanding of chronic spontaneous urticaria (CSU) suggests that a complex network of inflammatory pathways is involved in its pathogenesis. Recent development highlighted autoimmunity as one of the key pathogenic mechanisms of CSU. Two endotypes, type I autoallergic (associated with IgE antibodies against autoantigens) and type IIb autoimmune (mediated by IgG autoantibodies against IgE or its high-affinity receptor [FcεRI]), have been characterized. A subpopulation of the patients has an overlap of the 2 endotypes. About 10% of patients with CSU present with only angioedema. Patients with isolated mast cell-mediated angioedema have distinct clinical and demographic features and should be distinguished from bradykinin-mediated angioedema. Multiple potential biomarkers such as total IgE level and IgG anti-thyroid peroxidase have been identified and, together with the corresponding endotypes, have been linked to disease severity, duration, and response to treatments. Currently, the use of these biomarkers is limited in clinical settings given the few options of therapy. However, with the advent of novel treatments, endotyping CSU might help with tailoring treatment approaches.

Keywords: Angioedema; autoallergy; biomarkers; chronic spontaneous urticaria; endotypes; phenotypes; type IIb autoimmunity; urticaria.

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Conflict of interest statement

Disclosure statement Disclosure of potential conflict of interest: S. Waserman received grants/research support from the Canadian Allergy, Asthma and Immunology Foundation (CAAIF), ALK-Abelló, Pfizer Canada, Aimmune, Schroeder Foundation, and Sean Delaney Foundation; received speaker fees/honoraria and consulting fees from GlaxoSmithKline, Novartis, CSL Behring, Pfizer Canada, Sanofi Canada, AstraZeneca, Takeda, Medexus, Mylan, AbbVie, Sanofi, Miravohealth, Bausch & Lomb, Avir Pharma, ALK-Abelló, and Valeo; was an employee at McMaster University, Hamilton Health Sciences, St Joseph’s Healthcare Hamilton, University Health Network Toronto Western Hospital (UHN-TWH), BOD Asthma Canada, and CHAEN; and is the president of CAAIF. G. L. Sussman received research support from Aimmune, Amgen, AstraZeneca, DBV Technologies, Genentech, Leo Pharma Novartis, Sanofi-Regeneron, and ALK-Abelló; and is a medical advisor for Novartis, CSL Behring, Pfizer, AbbVie, AstraZeneca, Nuvo Pharmaceuticals, and the Allergy Asthma and Immunology Society of Ontario. The rest of the authors declare that they have no relevant conflicts of interest.

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