Watch this CSU pathomechanism video, which describes the definition, features (specifically wheals), angioedema and erythema that may or may not accompany CSU. It then goes on to outline the three main mechanisms of the pathophysiology, which are divided into 2 major mechanisms:

  1. Autoallergy – affects more than half of patients and involves elevated levels of immunoglobulin (IgE) autoantibodies against thyroid peroxidase (TPO).1 IgE molecules that are bound to the high affinity receptor (FCεR1) on mast cells and basophils are cross linked by TPO. This activates degranulation and histamine is released.1,2
  2. Autoimmunity, which is further separated into two primary mechanisms:
    1. IgG autoantibodies against IgE – IgG anti IgE autoantibodies cross link high affinity receptor bound IgE and trigger mast cells and basophils degranulation, releasing histamine.2
    2. IgG autoantibodies are directed against high affinity receptor (FCεR1) the latter cross link (x2 high affinity receptors). This activates degranulation and histamine is released.2


This video highlights that the current primary treatment is to eliminate triggers such as drugs that can cause non-allergic hypersensitivity reactions and to prevent mast cell activation and degranulation.2


CSU, chronic spontaneous urticaria; IgE, immunoglobulin E; IgG, immunoglobulin G; TPO, thyroid peroxidase.


  1. Metz M & Maurer M. Curr Opin Allergy Clin Immunol 2012;12(4):406–411.
  2. Bracken SJ, et al. Front Immunol 2019;10:627.
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UK | March 2022 | 181754

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