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抗磷脂综合征中动脉血栓形成的发病机制及治疗新见解。

New insights into the pathogenic mechanisms and treatment of arterial thrombosis in antiphospholipid syndrome.

作者信息

Fujieda Yuichiro, Amengual Olga

机构信息

Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.

出版信息

Eur J Rheumatol. 2021 Apr;8(2):93-99. doi: 10.5152/eurjrheum.2020.20058.

Abstract

Antiphospholipid syndrome (APS) is a systemic disorder clinically characterized by widespread thrombosis and obstetric complications associated with the persistent presence of antiphospholipid antibodies (aPLs). The persistent presence of aPLs represents a thrombotic risk in APS, which can be stratified according to the aPL profile. Thrombosis occurs in both arteries and veins. Notably, arterial thromboses have a higher recurrence compared with venous thromboses and a tendency for recurrence in the same vascular (arterial) site. Secondary prevention of arterial thrombosis requires more intensive treatment than prevention of venous thrombosis. Data from randomized clinical trials indicated that factor Xa inhibitors should not be recommended for APS. Recurrent thromboses in patients with APS treated with factor Xa inhibitors were mainly arterial, with a high rate of stroke. Dual antiplatelet therapy may have some benefit for preventing the recurrence of arterial thrombosis in patients with APS. This review article describes pathogenic mechanisms, clinical features, risk assessment, and management of arterial thrombosis in patients with APS. Particularly, we discuss how secondary prophylaxis may be a useful approach to reduce the occurrence of arterial thrombosis.

摘要

抗磷脂综合征(APS)是一种全身性疾病,临床特征为广泛血栓形成以及与抗磷脂抗体(aPLs)持续存在相关的产科并发症。aPLs的持续存在是APS中的一种血栓形成风险,可根据aPL谱进行分层。动脉和静脉均可发生血栓形成。值得注意的是,与静脉血栓形成相比,动脉血栓形成的复发率更高,且有在同一血管(动脉)部位复发的倾向。动脉血栓形成的二级预防比静脉血栓形成的预防需要更强化的治疗。随机临床试验的数据表明,不应推荐因子Xa抑制剂用于APS。接受因子Xa抑制剂治疗的APS患者复发性血栓形成主要为动脉性,卒中发生率高。双重抗血小板治疗可能对预防APS患者动脉血栓形成的复发有一定益处。这篇综述文章描述了APS患者动脉血栓形成的发病机制、临床特征、风险评估和管理。特别是,我们讨论了二级预防如何可能是减少动脉血栓形成发生的一种有用方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8720/8133879/8c499c49eb52/EJR-8-2-93-g01.jpg

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