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[慢性荨麻疹中的自身免疫。历史与当前视角]

[Autoimmunity in chronic urticaria. A historical and current perspective].

作者信息

Hurtado-Avilés Hurtado-Avilés María Guadalupe, Martínez-Reculez María Guadalupe Carmen, Vargas-Camaño María Eugenia, Castrejón-Vázquez María Isabel

机构信息

Instituto de Seguridad y Servicios Sociales de los Trabajadores del Estado, Centro Médico Nacional 20 de Noviembre, Servicio de Inmunología Clínica y Alergia, Ciudad de México, México,

出版信息

Rev Alerg Mex. 2022;69 Suppl 1:s69-s80. doi: 10.29262/ram.v69iSupl1.1037.

Abstract

Chronic spontaneous urticaria is a condition that persists for more than six weeks, it occurs in the absence of an identifiable triggering factor and from the pathogenic activation of mast cells and basophils. The possibility of autoimmune etiology in up to 40 % of patients is presented, followed by subclinical infections and psychological factors. Two main mechanisms of the pathogenesis of chronic urticaria have been proposed: the former is the dysregulation of intracellular signaling pathways within mast cells and basophils, which leads to defects in the traffic or function of these cells. The latter is the development of autoantibodies against FcεRIα or IgE, in both mast cells and basophils. Numerous autoimmune diseases such as systemic lupus erythematosus, polymyositis, dermatomyositis, and rheumatoid arthritis have been associated with chronic urticaria; however, autoimmune thyroid disease deserves a special mention. A higher prevalence of antithyroid antibodies has been found, regardless of thyroid function (euthyroidism, hypo and hyperthyroidism) in patients with chronic spontaneous urticaria. Several infections have been linked to chronic urticaria. The best evidence is for Helicobacter pylori infection. Finally, stress is associated with the onset of the disease through the activation of the sympathetic and adrenomedullary system and the hypothalamic-pituitary- adrenal axis. Diagnosis may vary in different regions of the world, but the common feature is the completion of a thorough medical history.

摘要

慢性自发性荨麻疹是一种持续超过六周的病症,它在没有可识别触发因素的情况下发生,源于肥大细胞和嗜碱性粒细胞的致病性激活。高达40%的患者存在自身免疫病因的可能性,其次是亚临床感染和心理因素。慢性荨麻疹发病机制主要有两种:前者是肥大细胞和嗜碱性粒细胞内细胞内信号通路失调,导致这些细胞的运输或功能缺陷。后者是在肥大细胞和嗜碱性粒细胞中产生针对FcεRIα或IgE的自身抗体。许多自身免疫性疾病如系统性红斑狼疮、多发性肌炎、皮肌炎和类风湿性关节炎都与慢性荨麻疹有关;然而,自身免疫性甲状腺疾病值得特别提及。在慢性自发性荨麻疹患者中,无论甲状腺功能(甲状腺功能正常、减退和亢进)如何,抗甲状腺抗体的患病率都较高。几种感染与慢性荨麻疹有关。最有力的证据是幽门螺杆菌感染。最后,压力通过激活交感神经和肾上腺髓质系统以及下丘脑 - 垂体 - 肾上腺轴与疾病的发作有关。世界各地不同地区的诊断可能有所不同,但共同特点是要完成详尽的病史采集。

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