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慢性荨麻疹与凝血:病理生理学与临床方面。

Chronic urticaria and coagulation: pathophysiological and clinical aspects.

机构信息

U.O. Allergologia e Immunologia Clinica, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milano, Italy.

出版信息

Allergy. 2014 Jun;69(6):683-91. doi: 10.1111/all.12389. Epub 2014 Mar 27.

DOI:10.1111/all.12389
PMID:24673528
Abstract

Chronic urticaria (CU) is a widespread skin disease, characterized by the recurrence of transient wheals and itch for more than 6 weeks. Besides autoimmune mechanisms, coagulation factors, in particular tissue factor and thrombin, might also participate in the disease pathophysiology. Tissue factor expressed by eosinophils can induce activation of blood coagulation generating thrombin which in turn can increase vascular permeability both directly, acting on endothelial cells, and indirectly, inducing degranulation of mast cells with release of histamine, as demonstrated in experimental models. D-dimer, a fibrin degradation product, generated following activation of the coagulation cascade and fibrinolysis, has been found to be increased during urticaria exacerbations; moreover, it has been proposed as a biomarker of severity and resistance to H1-antihistamines in CU patients. The possible role of coagulation in CU is also supported by case reports, case series and a small controlled study showing the efficacy of anticoagulant therapy in this disease. The purpose of this review was to summarize the available data on the possible contribution of coagulation to the pathophysiology of CU focusing on clinical aspects and possible future therapeutic developments.

摘要

慢性荨麻疹(CU)是一种广泛存在的皮肤疾病,其特征为反复发作的短暂风团和瘙痒超过 6 周。除了自身免疫机制外,凝血因子,特别是组织因子和凝血酶,也可能参与疾病的病理生理学过程。嗜酸性粒细胞表达的组织因子可诱导血液凝固的激活,生成凝血酶,后者可直接作用于内皮细胞,或间接通过诱导肥大细胞脱颗粒释放组胺,从而增加血管通透性,这在实验模型中得到了证实。纤维蛋白降解产物 D-二聚体在凝血级联和纤维蛋白溶解激活后产生,在荨麻疹恶化期间被发现增加;此外,它被提出作为 CU 患者严重程度和对 H1 抗组胺药耐药性的生物标志物。凝血在 CU 中的可能作用也得到了病例报告、病例系列和一项小型对照研究的支持,这些研究表明抗凝治疗在该疾病中的疗效。本综述的目的是总结关于凝血可能对 CU 病理生理学的贡献的现有数据,重点关注临床方面和可能的未来治疗发展。

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