Background: Accelerated atherosclerosis has become an important cause of death in Systemic Lupus Erythematosus (SLE) patients. The protective role of HDL-C against atherosclerosis is believed to be mainly due to the enzyme paraoxonase1 (PON1) which functions to prevent LDL-C from peroxidation. Decreased PON1 activity has been observed in SLE patients.
Objectives: In the present study, we aimed to determine the PON1 activity and PON1 Q192R polymorphism in SLE patients and to study their relation to premature atherosclerosis. Methods: 40 SLE patients and 20 age & sex matched controls were included. PON1 activity was determined by paraoxon substrate. PON1 genotyping was conducted by PCR followed by polymorphism-specific restriction enzyme digestion and gel electrophoresis. Atherosclerosis was assessed by intima-media thickness (IMT). Results: Significantly lower PON1 activity and higher IMT was found in SLE patients compared to controls (p<0.05). Significant negative correlation was observed between PON1 activity and IMT, SLEDAI score, total cholesterol and LDL-C. There was no significant difference in the prevalence of any of the PON1 Q192R polymorphisms in SLE patients compared to controls. PON1 activity was lowest in the QQ, intermediate in QR and highest in RR group (p<0.05) and the mean IMT was highest in RR, intermediate in QR and lowest in QQ group (p<0.05). Conclusion: Although there was no association between any of the PON1Q192R polymorphism and SLE, PON1 activity was significantly decreased in SLE patients and was significantly correlated with the severity of atherosclerotic lesions. And thus, it might be involved in the pathogenesis of atherosclerosis in SLE patients.