The contribution of inherited and acquired thrombophilic defects, alone or combined with antiphospholipid antibodies, to venous and arterial thromboembolism in patients with systemic lupus erythematosus
The contribution of inherited and acquired thrombophilic defects, alone or combined with antiphospholipid antibodies, to venous and arterial thromboembolism in patients with systemic lupus erythematosus
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DOI：
10.1182/blood-2003-11-4085
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发表时间：
2004-07-01
期刊：
影响因子：
20.3
通讯作者：
van der Meer, J
中科院分区：
文献类型：
--
作者：
Brouwer, JLR;Bijl, M;van der Meer, J
系统性红斑狼疮(SLE)与静脉血栓(VTE)和动脉血栓栓塞症(ATE)的风险增加有关。狼疮抗凝剂(LA)和抗心磷脂抗体(ACAs)是确定的危险因素。我们评估了抗凝血酶、蛋白C、总蛋白S、凝血因子V莱顿、凝血酶原G20210A突变和APC抵抗的缺乏，无论是单独缺乏还是与LA和/或ACAs的不同组合，对系统性红斑狼疮患者血栓形成风险的贡献。中位随访期为12.7年。10%的患者发生VTE，11%的患者发生ATE。LA、ACAs、F V Leiden和凝血酶原突变是VTE的危险因素。其中一种疾病患者的VTE年发病率为2.01(0.74-4.37)，两种疾病患者的VTE年发病率为3.05(0.63-8.93)。与正常人群相比，VTE的风险分别高出20倍和30倍。与LA和ACAS相比，血栓形成障碍并不影响ATE的风险。总之，凝血因子V Leiden和凝血酶原突变增加了SLE患者发生VTE的风险，当其中一种亲血栓缺陷与LA和/或ACAs合并时，会加剧这种风险。
Systemic lupus erythematosus (SLE) is associated with an increased risk of venous (VTE) and arterial thromboembolism (ATE). Lupus anticoagulant (LA) and anticardiolipin antibodies (ACAs) are established risk factors. We assessed the contribution of deficiencies of antithrombin, protein C, total protein S, factor V Leiden, the prothrombin G20210A mutation and APC resistance, either alone or in various combinations with LA and/or ACAs, to the thrombotic risk in a cohort of 144 consecutive patients with SLE. Median follow-up was 12.7 years. VTE had occurred in 10% and ATE in 11% of patients. LA, ACAs, factor V Leiden, and the prothrombin mutation were identified as risk factors for VTE. Annual incidences of VTE were 2.01 (0.74-4.37) in patients with one of these disorders and 3.05 (0.63-8.93) in patients with 2 disorders. The risk of VTE was 20-and 30-fold higher, respectively, compared with the normal population. In contrast with LA and ACAs, thrombophilic disorders did not influence the risk of ATE. In conclusion, factor V Leiden and the prothrombin mutation contribute to the risk of VTE in patients with SLE, and potentiate this risk when one of these thrombophilic defects are combined with LA and/or ACAs.