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系统性红斑狼疮患者的流变学改变和血栓事件。

Rheological alterations and thrombotic events in patients with systemic lupus erythematosus.

机构信息

Hemorheology and Haemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain.

出版信息

Clin Hemorheol Microcirc. 2012;51(1):51-8. doi: 10.3233/CH-2011-1508.

Abstract

Systemic lupus erythematosus (SLE) is characterised by increased venous and arterial thrombotic risk. Nevertheless, how hemorheological alterations contribute to thrombotic risk remains a question of debate. We aimed to determine the rheological profile in 105 patients with SLE (24 with a thrombotic event) and 105 healthy controls. We determined blood viscosity and erythrocyte aggregation along with plasma lipids and fibrinogen. Although SLE patients showed lower blood viscosity at 230 s(-1) at a native hematocrit when compared with controls (p < 0.001), differences disappeared after adjusting the hematocrit to 45% (p = 0.095). When comparing SLE patients with and without thrombotic events, no differences in any rheological parameter were found (p > 0.05), except in fibrinogen which was higher in patients with thrombosis (p = 0.013). No differences in the rheological parameters were observed when venous and arterial thrombotic events were compared, although a tendency for higher fibrinogen was observed in patients with venous thrombosis (p = 0.053). Only hematocrit, fibrinogen and triglycerides were independent predictors of native blood viscosity in the multivariate regression analysis, even after adjusting for continuous variables and for tobacco and hypertension: beta coefficient: 0.727 p < 0.001; beta coefficient: 0.152 p = 0.003 and beta coefficient: 0.133 p = 0.015, respectively. The logistic regression analysis revealed that neither increased native blood viscosity (BVn > 4.33) nor increased erythrocyte aggregation (EA1 > 7.85) increased thrombotic risk: OR 0.636, CI 0.313-3.12, p = 0.578 and OR 2.01, CI 0.77-5.20, p = 0.152, respectively. However, hyperfibrinogenemia (Fbg > 342 mg/dL) increased thrombotic risk by around three times: OR 3.44 CI 1.32-8.96, p = 0.011. Our results suggest that the role of blood viscosity and erythrocyte aggregation in thrombotic risk in SLE patients fails to demonstrate any association.

摘要

系统性红斑狼疮(SLE)的特点是静脉和动脉血栓形成风险增加。然而,血液流变学改变如何导致血栓形成风险仍然存在争议。我们旨在确定 105 例 SLE 患者(24 例有血栓形成事件)和 105 例健康对照者的流变学特征。我们测定了血液粘度和红细胞聚集以及血浆脂质和纤维蛋白原。尽管与对照组相比,SLE 患者在原生红细胞比容为 230s(-1) 时的血液粘度较低(p<0.001),但在将红细胞比容调整至 45%(p=0.095)后差异消失。比较有血栓形成事件和无血栓形成事件的 SLE 患者,在任何流变学参数方面均无差异(p>0.05),除了血栓形成患者的纤维蛋白原较高(p=0.013)外。比较静脉和动脉血栓形成事件时,在任何流变学参数方面均无差异,尽管静脉血栓形成患者的纤维蛋白原水平呈升高趋势(p=0.053)。多元回归分析显示,仅红细胞比容、纤维蛋白原和三酰甘油是原生血液粘度的独立预测因子,即使在调整连续变量和烟草和高血压后也是如此:β系数:0.727,p<0.001;β系数:0.152,p=0.003;β系数:0.133,p=0.015。Logistic 回归分析显示,原生血液粘度升高(BVn>4.33)和红细胞聚集升高(EA1>7.85)均未增加血栓形成风险:OR 0.636,CI 0.313-3.12,p=0.578 和 OR 2.01,CI 0.77-5.20,p=0.152。然而,高纤维蛋白原血症(Fbg>342mg/dL)使血栓形成风险增加近三倍:OR 3.44,CI 1.32-8.96,p=0.011。我们的结果表明,血液粘度和红细胞聚集在 SLE 患者血栓形成风险中的作用未能证明存在任何关联。

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