Genetic polymorphisms of hypertriglyceridemia and asymptomatic atherosclerosis in women with Systemic Lupus Erythematosus: A case-control study

Background and Aims : Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that predominantly affects adult women and is associated with increased cardiovascular risk. The increase in triglyceride-rich lipoproteins and particles containing apolipoprotein B constitute the characteristic dyslipidemia of SLE. The objective of this study was to determine the relationship between the genetic variants of polygenic hypertriglyceridemia, asymptomatic atherosclerosis and lipoprotein disturbances in a population of patients with SLE.Methods: Seventy-three SLE female patients were recruited and age-sex matched with a control group. Carotid ultrasound, laboratory profiles, and genetic analysis of the ZPR1, APOA5, and GCKR genes were performed.Results: The prevalence of carotid plaque, hypertension and dyslipidemia was higher in patients with SLE, compared with the control group (20.5% vs 6.9%, p=0.028; 45.2% vs 5.5%, p<0.001; 52.1% vs 34.2%, p=0.030, respectively). SLE patients had higher triglyceride concentrations (1.0 mmol/L vs 0.8 mmol/L, p=0.008) than control group. The GCKR rs1260326 CC genotype (OR=0.111; 95% CI: 0.015 to 0.804, p=0.030) was independently associated with carotid atherosclerosis. In addition, the increase of 1 mmol/L of triglycerides was associated with an increase of 7.5 times in the risk of presenting carotid plaque (OR=7.576; 95% CI: 2.415 to 23.767, p=0.001).Conclusions: In conclusion, the GCKR rs1260326 CC genotype and serum triglyceride concentration were independent predictors of carotid atherosclerosis in women with SLE. These data suggest that adequate control of hypertriglyceridemia and diagnosis of genetic variants related to hypertriglyceridemia may be useful to better stratify and prevent cardiovascular risk in patients with SLE. Background and Aims : Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that predominantly affects adult women and is associated with increased cardiovascular risk. The increase in triglyceride-rich lipoproteins and particles containing apolipoprotein B constitute the characteristic dyslipidemia of SLE. The objective of this study was to determine the relationship between the genetic variants of polygenic hypertriglyceridemia, asymptomatic atherosclerosis and lipoprotein disturbances in a population of patients with SLE. Methods: Seventy-three SLE female patients were recruited and age-sex matched with a control group. Carotid ultrasound, laboratory profiles, and genetic analysis of the ZPR1, APOA5, and GCKR genes were performed. Results: The prevalence of carotid plaque, hypertension and dyslipidemia was higher in patients with SLE, compared with the control group (20.5% vs 6.9%, p=0.028; 45.2% vs 5.5%, p<0.001; 52.1% vs 34.2%, p=0.030, respectively). SLE patients had higher triglyceride concentrations (1.0 mmol/L vs 0.8 mmol/L, p=0.008) than control group. The GCKR rs1260326 CC genotype (OR=0.111; 95% CI: 0.015 to 0.804, p=0.030) was independently associated with carotid atherosclerosis. In addition, the increase of 1 mmol/L of triglycerides was associated with an increase of 7.5 times in the risk of presenting carotid plaque (OR=7.576; 95% CI: 2.415 to 23.767, p=0.001). Conclusions: In conclusion, the GCKR rs1260326 CC genotype and serum triglyceride concentration were independent predictors of carotid atherosclerosis in women with SLE. These data suggest that adequate control of hypertriglyceridemia and diagnosis of genetic variants related to hypertriglyceridemia may be useful to better stratify and prevent cardiovascular risk in patients with SLE.