Abstract
SLE is associated with increased cardiovascular risk. The objective of this study was to determine the prevalence of asymptomatic carotid atherosclerosis to analyze its relationship with dyslipidemia and related genetic factors in a population of patients with SLE. Seventy-one SLE female patients were recruited. Carotid ultrasound, laboratory profiles, and genetic analysis of the ZPR1, APOA5, and GCKR genes were performed. SLE patients were divided into two groups according to the presence or absence of carotid plaques. Patients with carotid plaque had higher plasma TG (1.5 vs. 0.9 mmol/L, p = 0.001), Non-HDL-C (3.5 vs. 3.1 mmol/L, p = 0.025), and apoB concentrations (1.0 vs. 0.9 g/L, p = 0.010) and a higher prevalence of hypertension (80 vs. 37.5%, p = 0.003) than patients without carotid plaque. The GCKR C-allele was present in 83.3% and 16.7% (p = 0.047) of patients with and without carotid plaque, respectively. The GCKR CC genotype (OR = 0.026; 95% CI: 0.001 to 0.473, p = 0.014), an increase of 1 mmol/L in TG concentrations (OR = 12.550; 95% CI: 1.703 to 92.475, p = 0.013) and to be hypertensive (OR = 9.691; 95% CI: 1.703 to 84.874, p = 0.040) were independently associated with carotid atherosclerosis. In summary, plasma TG concentrations, CGKR CC homozygosity, and hypertension are independent predictors of carotid atherosclerosis in women with SLE.
Highlights
Systemic lupus erythematosus (SLE) patients may have characteristic dyslipidemia that is known as the “lupus pattern” consisting of hypertriglyceridemia and decreased levels of high-density lipoprotein cholesterol (HDL-C) [2]
These results are in agreement with current knowledge of the role of triglyceride-rich lipoproteins and their remnants in the origin and progression of atherosclerosis, which is strongly influenced by the number of circulating concentrations of apolipoprotein B (apoB)-containing lipoprotein particles [40]
This study shows that CGKR CC homozygosity for the CGKR gene, plasma triglyceride concentrations, and hypertension are independent predictive factors of carotid atherosclerosis in women with SLE
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by inflammation and tissue damage produced by an exaggerated response of the immune system, the binding of autoantibodies to different cells, and the deposition of antigenantibody complexes in tissues. SLE most commonly presents in women of reproductive age, has a highly variable clinical course, and is associated with a 3-fold increased risk of premature death, mainly due to infection, renal impairment, or cardiovascular disease [1]. SLE patients may have characteristic dyslipidemia that is known as the “lupus pattern” consisting of hypertriglyceridemia and decreased levels of high-density lipoprotein cholesterol (HDL-C) [2]. In active SLE, this “lupus pattern” may be aggravated by the presence of anti-lipoprotein lipase (LPL) antibodies and a consequent decrease in lipolysis that results in the accumulation of triglyceride-rich lipoproteins [3]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
