Atopy in chronic urticaria: an important yet overlooked issue

Abstract

Chronic urticaria (CU) is one of the most common dermatological diseases and has a significant impact on the quality of life of patients. However, the pathogenesis of this disease remains unclear. Autoimmunity in chronic spontaneous urticaria (CSU) has received considerable attention and has been studied previously. Atopy is an important characteristic of CU; however, it has not been fully recognized. Atopy predisposes individuals to immune responses to allergens, leading to type 2 inflammation and immunoglobulin E (IgE) overproduction. Compared with healthy individuals, patients with CU have a higher proportion of atopy, and an atopic background is correlated with the clinical characteristics of CU. The total IgE levels in patients with CU is significantly higher than those in healthy individuals. Although its level is not higher than that in classic allergic diseases, it is closely related to CU. Exogenous allergens, auto-allergens, and specific IgEs, which are closely related to atopy, have been reported, and their roles in CU pathogenesis are also being studied. Local and systemic atopic inflammation is present in patients with CU. This review summarizes the current knowledge regarding atopy and CU, speculating that there are CU subtypes, such as atopic CSU or atopic chronic inducible urticaria (CIndU) and that atopy may be involved in the pathogenesis of CU. These findings provide a new perspective for a comprehensive understanding of the clinical features of CU and further research regarding its pathogenesis.

Changes in Serum IL-12 Levels following the Administration of H1-Antihistamines in Patients with Chronic Spontaneous Urticaria

“…It is known that urticarial lesions are induced by vasoactive mediators, with the histamine released by mast cells remaining the main representative process. The genetic polymorphism of mast-cell-derived interleukins and the predisposition to develop CSU are also areas that require study and exploration [ 12 , 13 , 14 , 15 , 16 , 17 ].…”

“…Numerous inflammatory cells (mast cells, macrophages, basophils, eosinophils) have been detected in the skin lesions of patients with CSU in association with an excessive production of inflammatory mediators (IL-4, IL-13, IL-5, IL-9, IL-10, IL-17, TNFα, IL-31, and IL-33). Systemic inflammation in CSU is supported by significantly elevated serum/plasma levels (compared to healthy individuals) of pathogenic cytokines involved in Th2 inflammation [ 5 , 14 , 16 , 17 ]. Many studies have examined the role of T cells and related cytokines in the development of CSU, but there has been limited research focusing on changes in cytokine levels during treatment.…”