Dyslipidemia in systemic lupus erythematosus.
Cardiovascular disease is one of the major causes of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Accelerated atherosclerosis is related to traditional (age, hypertension, diabetes mellitus, dyslipidemia, obesity, smoking, and positive family history) and non-traditional, disease-related factors. Traditional risk factors are still more prominent in patients with lupus, as both hypertension and hypercholesterinemia were independently associated with premature atherosclerosis in several SLE cohorts. In this work, the authors summarize the epidemiology of dyslipidemia in lupus patients and review the latest results in the pathogenesis of lipid abnormalities. The prevalence of dyslipidemia, with elevations in total cholesterol (TC), low-density lipoprotein (LDL), triglyceride (TG), and apolipoprotein B (ApoB), and a reduction in low-density lipoprotein (LDL) levels are about 30% at the diagnosis of SLE rising to 60% after 3 years. Multiple pathogenetic mechanism is included, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) can suppress HDL and increase TG, auto-antibodies can cause the injury of the endothelium, lipoprotein lipase (LPL) activity can be reduced by circulating inflammatory mediators and antibodies, and increased oxidative stress may trigger a wide range of pro-atherogenic lipid modifications. As a major risk factor, dyslipidemia should be treated aggressively to minimize the risk of atherosclerosis and cardiovascular events. Randomized controlled trials with statins are controversial in the detention of atherosclerosis progression, but can be favorable by inhibiting immune activation that is the arterial wall and by decreasing lupus activity.
Department of Clinical Immunology, Adult and Pediatric Rheumatology, National Institute of Rheumatology and Physiotherapy, Budapest, Hungary. szabo.melinda@orfi.hu.
Melinda Zsuzsanna
MZ
Szabó
Institute of Immunology, Rikshospitalet, Oslo University, Oslo, Norway.
Peter
P
Szodoray
Department of Clinical Immunology, Adult and Pediatric Rheumatology, National Institute of Rheumatology and Physiotherapy, Budapest, Hungary.|IIIrd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Emese
E
Kiss
D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000453:epidemiology*; D001323:Autoantibodies / Q000097:blood; D002784:Cholesterol / Q000378:metabolism; D050171:Dyslipidemias / Q000188:drug therapy / Q000453:epidemiology*; D042783:Endothelial Cells / Q000276:immunology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D056747:Immunomodulation; D050356:Lipid Metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy / Q000453:epidemiology*; D018384:Oxidative Stress; D016032:Randomized Controlled Trials as Topic; D014280:Triglycerides / Q000378:metabolism
D001323:Autoantibodies; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol
Accelerated atherosclerosis; Dyslipidemia; Reverse cholesterol transport; Systemic lupus erythematosus