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    Chronic spontaneous urticaria (CSU) is a frequent and often severely disabling disease. A large number of studies were performed during the last 2 decades to clarify its pathogenesis. These studies shed light on the underlying autoimmune mechanisms of CSU pathogenesis and have led us to understand that different mechanisms may exist and, sometimes, coexist behind the same clinical presentation. The present article reviews the meaning of the terms autoreactivity, autoimmunity, and autoallergy, which have been variably used over the years to define different endotypes of the disease.

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    Chronic urticaria and angioedema are recurrent conditions that significantly impact patients’ quality of life. Over the past 2 decades, extensive research has been conducted to elucidate the underlying mechanisms and improve the management of these conditions. Recent investigations of the pathophysiology of chronic spontaneous urticaria (CSU) have highlighted the role of autoimmune mechanisms, and 2 endotypes have been characterized: type I autoallergic CSU, associated with immunoglobulin E (IgE) antibodies against autoantigens, and type IIb autoimmune CSU, driven by autoantibodies that activate mast cells, including anti- FcεRI (high-affinity receptor for the Fc region of IgE) and anti-IgE.

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  • Mashup Score: 4

    Chronic urticaria is a common condition presenting with intensely pruritic wheals. Although individual lesions resolve within 24 hours, by definition, chronic urticaria lasts for a duration of at least 6 weeks. Both spontaneous and inducible forms exist. In the spontaneous variant, chronic urticaria occurs in the absence of clearly identifiable triggers. In chronic inducible urticaria, specific triggers may include dermatographism, cholinergic (heat), cold, exercise, delayed pressure, and solar.

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