Hemorheology and Haemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain.
Clin Hemorheol Microcirc. 2012;51(1):51-8. doi: 10.3233/CH-2011-1508.
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.
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。