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抗磷脂综合征(APS)是指血清中出现抗磷脂抗体(APLs),同时伴有循环中血栓(包括动脉和静脉)、复发的妊娠丢失(RPL)和与APS在有关的血小板减少症等症状之一的自身免疫性疾病。现将近几年的研究进展综述如下。1 APS病因及病理生理变化 APS病因不明,其主要病理改变为血栓形成。近年研究表明,PL—结合蛋白,如β_2—糖蛋白Ⅰ(β_2—GPI)在APS血栓形成中起了重要的作用。APLs是一组对机体带磷脂负电荷的蛋白复合物产生的特异抗体,而β_2—GPI分子上带有抗心磷脂抗体(ACLs)的抗原决定簇,ACLs与β_2—GPI结合后能识别带负电荷的磷脂复合物,并使β_2—GPI的表面结构发生变化,出现被ACLs识别的表位,β_2—GPI具有抑制凝血酶原、二磷酸腺苷(ADP)等引起的血小板聚集及其表面生成凝血酶,并阻滞磷
Antiphospholipid syndrome (APS) refers to the presence of antiphospholipid antibodies (APLs) in the serum in association with circulating thrombi (including arteries and veins), recurrent pregnancy loss (RPL), and symptoms associated with APS such as thrombocytopenia One of the autoimmune diseases. The recent research progress in recent years are summarized as follows. 1 APS causes and pathophysiological changes APS etiology is unknown, the main pathological changes for thrombosis. Recent studies have shown that PL-binding proteins, such as β_2-GPI, play an important role in APS thrombosis. APLs is a group of specific antibodies to the negatively charged protein complexes of the body with phospholipid, and β_2-GPI molecules with antigenic determinants of anticardiolipin antibodies (ACLs), ACLs and β_2-GPI can recognize negative The phospholipid complex, and changes the surface structure of β_2-GPI. The epitopes recognized by ACLs appear. Β_2-GPI can inhibit platelet aggregation and surface formation caused by prothrombin, adenosine diphosphate (ADP) Thrombin, and block phosphorus