Laura Durcan1, Deborah A Winegar2, Margery A Connelly2, James D Otvos2, Laurence S Magder2, Michelle Petri2. 1. From the Johns Hopkins University School of Medicine, Baltimore; Department of Epidemiology and Public Health, University of Maryland, College Park, Maryland; LipoScience, Laboratory Corporation of America Holdings, Raleigh, North Carolina, USA.L. Durcan, MD, Johns Hopkins University School of Medicine; D.A. Winegar, PhD, LipoScience, Laboratory Corporation of America Holdings; M.A. Connelly, PhD, MBA, LipoScience, Laboratory Corporation of America Holdings; J.D. Otvos, PhD, LipoScience, Laboratory Corporation of America Holdings; L.S. Magder, MPH, PhD, Department of Epidemiology and Public Health, University of Maryland; M. Petri, MD, MPH, Johns Hopkins University School of Medicine. laurajanedurcan@hotmail.com. 2. From the Johns Hopkins University School of Medicine, Baltimore; Department of Epidemiology and Public Health, University of Maryland, College Park, Maryland; LipoScience, Laboratory Corporation of America Holdings, Raleigh, North Carolina, USA.L. Durcan, MD, Johns Hopkins University School of Medicine; D.A. Winegar, PhD, LipoScience, Laboratory Corporation of America Holdings; M.A. Connelly, PhD, MBA, LipoScience, Laboratory Corporation of America Holdings; J.D. Otvos, PhD, LipoScience, Laboratory Corporation of America Holdings; L.S. Magder, MPH, PhD, Department of Epidemiology and Public Health, University of Maryland; M. Petri, MD, MPH, Johns Hopkins University School of Medicine.
Abstract
OBJECTIVE: Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerotic cardiovascular disease. Patients with SLE have adverse lipoprotein variables, but little is known about how these change with treatment and disease activity. The nuclear magnetic resonance LipoProfile test contains a glycoprotein signal-termed GlycA, an inflammatory marker, which has not been evaluated in SLE. We assessed patients longitudinally to determine how lipoproteins and GlycA change with active SLE. METHODS: Sera from selected clinical visits of patients in the Hopkins Lupus Cohort were analyzed for lipoprotein and GlycA levels. Univariate and multivariate analyses were performed to evaluate lipoprotein variables and their relationship to ethnicity, disease activity, prednisone use, and hydroxychloroquine (HCQ) therapy. RESULTS: Fifty-two patients were included over 229 visits. Adverse changes in lipoprotein variables with disease activity were demonstrated. For each point increase in the Systemic Lupus Erythematosus Disease Activity Index, there was a decrease in high-density lipoprotein (HDL) even after adjusting for corticosteroid use. Prednisone was associated with higher very low-density lipoprotein, low-density lipoprotein, HDL, and triglycerides. HCQ was associated with more favorable variables. GlycA levels were higher than in normal populations and increased with disease activity. CONCLUSION: Adverse changes in lipoprotein profiles were associated with SLE activity and prednisone therapy. This gives insight into mechanisms of atherosclerosis in SLE. Favorable lipoprotein variables occurred in those taking HCQ. GlycA increased with disease activity and was higher than in healthy populations.
OBJECTIVE:Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerotic cardiovascular disease. Patients with SLE have adverse lipoprotein variables, but little is known about how these change with treatment and disease activity. The nuclear magnetic resonance LipoProfile test contains a glycoprotein signal-termed GlycA, an inflammatory marker, which has not been evaluated in SLE. We assessed patients longitudinally to determine how lipoproteins and GlycA change with active SLE. METHODS: Sera from selected clinical visits of patients in the Hopkins Lupus Cohort were analyzed for lipoprotein and GlycA levels. Univariate and multivariate analyses were performed to evaluate lipoprotein variables and their relationship to ethnicity, disease activity, prednisone use, and hydroxychloroquine (HCQ) therapy. RESULTS: Fifty-two patients were included over 229 visits. Adverse changes in lipoprotein variables with disease activity were demonstrated. For each point increase in the Systemic Lupus Erythematosus Disease Activity Index, there was a decrease in high-density lipoprotein (HDL) even after adjusting for corticosteroid use. Prednisone was associated with higher very low-density lipoprotein, low-density lipoprotein, HDL, and triglycerides. HCQ was associated with more favorable variables. GlycA levels were higher than in normal populations and increased with disease activity. CONCLUSION: Adverse changes in lipoprotein profiles were associated with SLE activity and prednisone therapy. This gives insight into mechanisms of atherosclerosis in SLE. Favorable lipoprotein variables occurred in those taking HCQ. GlycA increased with disease activity and was higher than in healthy populations.
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