Key result
Hyperfibrinogenemia (>342 mg/dL) increased thrombotic risk in patients with systemic lupus erythematosus (OR 3.44; 95% CI 1.32-8.96; p=0.011), whereas blood viscosity showed no association.
Why the study?
Do rheological alterations such as increased blood viscosity and erythrocyte aggregation contribute to thrombotic risk in patients with systemic lupus erythematosus?
Observational (n=210)
Do rheological alterations such as increased blood viscosity and erythrocyte aggregation contribute to thrombotic risk in patients with systemic lupus erythematosus?
Odds Ratio: 3.44 (95% CI 1.32–8.96)
p-value: p=0.011
In patients with systemic lupus erythematosus, hyperfibrinogenemia is associated with increased thrombotic risk, while blood viscosity and erythrocyte aggregation do not appear to play a significant role.
Hyperfibrinogenemia may aid thrombotic risk stratification in SLE; case-control data leave open causal and therapeutic implications.
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.
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Vayá et al. (2012) conducted an observational in Systemic lupus erythematosus (n=210). Hyperfibrinogenemia vs. Normal fibrinogen levels was evaluated on Thrombotic risk (OR 3.44, 95% CI 1.32-8.96, p=0.011). Hyperfibrinogenemia (>342 mg/dL) increased thrombotic risk in patients with systemic lupus erythematosus (OR 3.44; 95% CI 1.32-8.96; p=0.011), whereas blood viscosity showed no association.
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