Department of Internal Medicine, University of Milan, Via Pace 9, 20122 Milano, Italy.
Curr Vasc Pharmacol. 2012 Sep;10(5):653-8. doi: 10.2174/157016112801784558.
Urticaria is a skin disease characterised by short-lived surface swellings of the dermis (wheals) frequently accompanied by itching. It is classified as acute or chronic depending on whether the wheal recurrence occurs for less or more than six weeks. Acute urticaria is often due to a hypersensitivity reaction, whereas about 50% of the cases of chronic urticaria are regarded as autoimmune. Urticaria may occur alone or in association with a deeper swelling (angioedema) involving the subcutaneous and/or submucosal tissues, and last from hours to a few days. Angioedema can also develop alone, and may be idiopathic or be caused by allergies, inherited or acquired deficiencies of C1-inhibitor protein, or adverse drug reactions. An interplay between inflammation and coagulation has been proposed as a pathomechanism in urticaria and urticaria-associated angioedema (in which histamine and thrombin are involved), as well as in angioedema due to C1-inhibitor deficiency, which involves various biological systems. An increase in the plasma markers of thrombin generation, fibrinolysis and inflammation has been documented during exacerbations of urticaria and angioedema, with the marker levels decreasing to normal during remission. However, the hypercoagulable state in chronic urticaria and angioedema has not been reported to be associated with any increased risk of thrombosis, although there have been a number of reports of cardiovascular events occurring during episodes of acute urticaria. These observations have provided the rationale for the clinical evaluation of anticoagulant and antifibrinolytic drugs, the efficacy of which has sometimes been demonstrated.
荨麻疹是一种皮肤疾病，其特征为真皮表面短暂肿胀（风团），常伴有瘙痒。根据风团复发是否少于或多于 6 周，可将其分为急性或慢性。急性荨麻疹通常是由于过敏反应引起的，而大约 50%的慢性荨麻疹被认为是自身免疫性的。荨麻疹可单独发生，也可与深部肿胀（血管性水肿）相关联，涉及皮下和/或黏膜下组织，持续数小时至数天。血管性水肿也可单独发生，可能是特发性的，也可能是由过敏、C1 抑制剂蛋白的遗传性或获得性缺乏、或药物不良反应引起的。炎症和凝血之间的相互作用被提出是荨麻疹和荨麻疹相关血管性水肿（其中涉及组胺和凝血酶）以及 C1 抑制剂缺乏引起的血管性水肿的发病机制，涉及各种生物系统。在荨麻疹和血管性水肿的加重期间，已记录到血浆凝血酶生成、纤维蛋白溶解和炎症的标志物增加，在缓解期间标志物水平降至正常。然而，慢性荨麻疹和血管性水肿的高凝状态尚未被报道与任何增加的血栓形成风险相关，尽管有许多报道称急性荨麻疹发作期间发生了心血管事件。这些观察结果为抗凝和抗纤维蛋白溶解药物的临床评估提供了依据，这些药物的疗效有时已得到证实。
