Abstract
BackgroundThe causes of increased cardiovascular risk in systemic lupus erythematosus (SLE) are not understood thoroughly, although presence of traditional cardiovascular risk factors and disease-specific agents were also proposed. In this study, we investigated the quantitative changes in the lipid profile, as well as qualitative characteristics of high-density lipoprotein (HDL) and markers of inflammation and disease activity in SLE patients.MethodsLipoprotein levels were determined in 51 SLE patients and 49 healthy controls, matched in age and gender. HDL antioxidant capacity was determined spectrophotometrically with a cell-free method of hemin-induced low-density lipoprotein (LDL) oxidation. Polyacrylamide gel-electrophoresis was used for HDL subfraction analysis. Human paraoxonase-1 (PON1) activity, apolipoprotein A1 (ApoA1) and oxidized LDL concentrations, as well as interleukin-6, high-sensitivity C-reactive protein, serum amyloid A and monocyte chemotactic protein-1 levels were determined.ResultsHDL-cholesterol and ApoA1 concentrations decreased significantly in SLE subjects. Also, PON1 arylesterase activity (125.65 ± 26.87 vs. 148.35 ± 39.34 U/L, p = 0.001) and total HDL antioxidant capacity (165.82 ± 58.28 % vs. 217.71 ± 54.36 %, p < 0.001) were significantly reduced in patients compared to controls. Additionally, all HDL subfraction concentrations were significantly decreased in patients, while the levels of the examined inflammatory markers were significantly elevated in SLE subjects. The latter correlated positively with disease activity, and negatively with HDL concentration and total HDL antioxidant capacity, respectively. PON1 arylesterase activity and erythrocyte sedimentation rate were independent predictors of total HDL antioxidant capacity.ConclusionsInduced by the systemic inflammation, altered composition and antioxidant activity may diminish the anti-atherogenic effect of HDL and therefore may contribute to the increased cardiovascular risk of SLE patients.
Highlights
The causes of increased cardiovascular risk in systemic lupus erythematosus (SLE) are not understood thoroughly, presence of traditional cardiovascular risk factors and disease-specific agents were proposed
The glucose level was significantly higher in SLE patients compared to controls, it was still in the normal range
Lower high-density lipoprotein (HDL) and apolipoprotein A1 (ApoA1) levels, as well as significantly higher triglyceride and ApoB100 levels were found in SLE patients compared to controls
Summary
The causes of increased cardiovascular risk in systemic lupus erythematosus (SLE) are not understood thoroughly, presence of traditional cardiovascular risk factors and disease-specific agents were proposed. We investigated the quantitative changes in the lipid profile, as well as qualitative characteristics of high-density lipoprotein (HDL) and markers of inflammation and disease activity in SLE patients. Previous data suggest that the direct anti-oxidant effect of HDL on LDL oxidation, measured as a reduction in lipid peroxides, is likely mediated by HDL-linked paraoxonase-1 (PON1) [7, 8]. This major antioxidant effect might be mitigated in inflammatory conditions. Altered lipoprotein metabolism may indirectly influence the composition and function of HDL Both of these mechanisms may be responsible for the decrease in the ApoA1 levels. Reverse cholesterol transport is impaired during acute phase reaction [9]
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