Vayá Amparo, Santaolaria Marisa, Micó Luisa, Calvo Javier, Oropesa Roberto, Villa Piedad, Todoli Jose, Simó María, Corella Dolores, Ricart Jose M
Hemorheology and Thrombosis Unit, Department of Clinical Pathology, La Fe University Hospital, and Department of Preventive Medicine, School of Medicine, University of Valencia, Valencia, Spain.
Clin Hemorheol Microcirc. 2008;40(2):79-87.
Systemic lupus erythematosus (SLE) is characterised by increased venous and arterial thrombotic risk. Although antiphospholipid antibodies (APAs) have been shown to be related with thrombotic tendency in these patients, in more than 40% of them, thrombosis occurs without the presence of such antibodies. We analysed the association of venous and arterial thrombotic events with acquired (anticardiolipin antibodies (ACAs) and lupus anticoagulant (LA)) and inherited (antithrombin (AT), protein C (PC), protein S (PS) deficiencies, factor V Leiden and the prothrombin G20210A mutation), thrombophilic risk factors in 86 SLE patients and 89 healthy controls. Patients showed a higher significant percentage of ACAs titres IgG>41 GPL u/ml and LA than controls (P=0.009; P<0.001, respectively), although no differences in AT, PC, PS deficiencies, factor V Leiden and prothrombin G20210A mutation was observed (P>0.05). When patients with and without thrombosis were compared, those with thrombosis showed a statistically higher percentage of ACAs IgG>41 GPL u/ml and LA (P=0.048; P=0.001, respectively), OR 4.33; 95% CI 1.01-18.50 and OR 11.57; 95% CI 3.28-40.75, respectively. When venous and arterial thrombotic events were considered separately, the presence of LA constituted a risk factor for arterial thrombosis (P=0.010), OR 11.33; 95% CI 1.86-68.89, as well as for venous thrombosis (P=0.005), OR 10.15; 95% CI 2.12-48.64, while ACAs IgG>41 GPL u/ml on their own, were not associated with arterial or venous thrombosis (P=0.142, P=0.233, respectively). In addition inherited thrombophilic risk factors AT, PC, PS deficiencies, factor V Leiden and PT G20210A mutation do not seem to increase thrombotic risk in SLE patients.
系统性红斑狼疮（SLE）的特征是静脉和动脉血栓形成风险增加。尽管抗磷脂抗体（APAs）已被证明与这些患者的血栓形成倾向有关，但在超过40%的患者中，血栓形成发生在不存在此类抗体的情况下。我们分析了86例SLE患者和89例健康对照者中静脉和动脉血栓形成事件与获得性（抗心磷脂抗体（ACAs）和狼疮抗凝物（LA））和遗传性（抗凝血酶（AT）、蛋白C（PC）、蛋白S（PS）缺乏、因子V莱顿突变和凝血酶原G20210A突变）血栓形成风险因素之间的关联。患者中ACAs滴度IgG>41 GPL u/ml和LA的百分比显著高于对照组（分别为P=0.009；P<0.001），尽管在AT、PC、PS缺乏、因子V莱顿突变和凝血酶原G20210A突变方面未观察到差异（P>0.05）。比较有血栓形成和无血栓形成的患者时，有血栓形成的患者中ACAs IgG>41 GPL u/ml和LA的百分比在统计学上更高（分别为P=0.048；P=0.001），OR分别为4.33；95%CI为1.01 - 18.50和OR为11.57；95%CI为3.28 - 40.75。当分别考虑静脉和动脉血栓形成事件时，LA的存在是动脉血栓形成的危险因素（P=0.010），OR为11.33；95%CI为1.86 - 68.89，也是静脉血栓形成的危险因素（P=0.005），OR为10.15；95%CI为2.12 - 48.64，而单独的ACAs IgG>41 GPL u/ml与动脉或静脉血栓形成无关（分别为P=0.142，P=0.233）。此外，遗传性血栓形成风险因素AT、PC、PS缺乏、因子V莱顿突变和凝血酶原G20210A突变似乎并未增加SLE患者的血栓形成风险。
