BACKGROUND: Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis but the mechanisms underlying this association are not understood. The role of endothelial dysfunction is hypothesized. METHODS: In predominantly non-Caucasian patients with SLE (N=119) and controls (N=71), carotid ultrasonography was performed and circulating endothelial cells (CECs), soluble endothelial protein C receptor and gene polymorphism at A6936G, soluble E-selectin (sE-selectin), and adiponectin were assessed. RESULTS: Carotid plaque was more prevalent among patients than controls (43% vs 17%, p=0.0002). Mean CCA IMT was greater in patients compared to controls (0.59+/-0.19 mm vs 0.54+/-0.11 mm, p=0.03). Among SLE patients, plaque was not associated with smoking, body-mass index, LDL, triglycerides, homocysteine, C-reactive protein, anti-ds DNA antibody, C3, C4, SLE activity, or medications. Age and levels of soluble E-selectin and adiponectin were significantly higher in the SLE patients with plaque compared to those without plaque in univariate and multivariate analyses. sE-selectin and adiponectin were found to serve as independent predictors of carotid plaque and that elevations were persistent over more than one visit. Unexpectedly, these biomarkers were present despite clinical quiescence. CONCLUSION: Premature atherosclerosis is a consistent feature of SLE and extends across ethnicities. Higher levels of adiponectin may represent a physiological attempt to limit further endothelial damage already reflected by the elevation in sE-selectin and the observed increase in plaque represents overwhelming of this reparative process by atherogenic stimuli. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
BACKGROUND:Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis but the mechanisms underlying this association are not understood. The role of endothelial dysfunction is hypothesized. METHODS: In predominantly non-Caucasian patients with SLE (N=119) and controls (N=71), carotid ultrasonography was performed and circulating endothelial cells (CECs), soluble endothelial protein C receptor and gene polymorphism at A6936G, soluble E-selectin (sE-selectin), and adiponectin were assessed. RESULTS: Carotid plaque was more prevalent among patients than controls (43% vs 17%, p=0.0002). Mean CCA IMT was greater in patients compared to controls (0.59+/-0.19 mm vs 0.54+/-0.11 mm, p=0.03). Among SLEpatients, plaque was not associated with smoking, body-mass index, LDL, triglycerides, homocysteine, C-reactive protein, anti-ds DNA antibody, C3, C4, SLE activity, or medications. Age and levels of soluble E-selectin and adiponectin were significantly higher in the SLEpatients with plaque compared to those without plaque in univariate and multivariate analyses. sE-selectin and adiponectin were found to serve as independent predictors of carotid plaque and that elevations were persistent over more than one visit. Unexpectedly, these biomarkers were present despite clinical quiescence. CONCLUSION:Premature atherosclerosis is a consistent feature of SLE and extends across ethnicities. Higher levels of adiponectin may represent a physiological attempt to limit further endothelial damage already reflected by the elevation in sE-selectin and the observed increase in plaque represents overwhelming of this reparative process by atherogenic stimuli. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
Authors: Jan Frystyk; Christian Berne; Lars Berglund; Karin Jensevik; Allan Flyvbjerg; Björn Zethelius Journal: J Clin Endocrinol Metab Date: 2006-11-21 Impact factor: 5.958
Authors: Cecilia P Chung; Annette Oeser; Paolo Raggi; Tebeb Gebretsadik; Ayumi K Shintani; Tuulikki Sokka; Theodore Pincus; Ingrid Avalos; C Michael Stein Journal: Arthritis Rheum Date: 2005-10
Authors: Naveed Sattar; Goya Wannamethee; Nadeem Sarwar; Julia Tchernova; Lynne Cherry; A Michael Wallace; John Danesh; Peter H Whincup Journal: Circulation Date: 2006-08-07 Impact factor: 29.690
Authors: H Ireland; C J Konstantoulas; J A Cooper; E Hawe; S E Humphries; H Mather; A H Goodall; J Hogwood; I Juhan-Vague; J S Yudkin; G di Minno; M Margaglione; A Hamsten; G J Miller; K A Bauer; Y T Kim; D J Stearns-Kurosawa; S Kurosawa Journal: Atherosclerosis Date: 2005-12 Impact factor: 5.162
Authors: Alka M Kanaya; Christina Wassel Fyr; Eric Vittinghoff; Peter J Havel; Matteo Cesari; Barbara Nicklas; Tamara Harris; Anne B Newman; Suzanne Satterfield; Steve R Cummings Journal: J Clin Endocrinol Metab Date: 2006-09-19 Impact factor: 5.958
Authors: Michelle Petri; Mimi Y Kim; Kenneth C Kalunian; Jennifer Grossman; Bevra H Hahn; Lisa R Sammaritano; Michael Lockshin; Joan T Merrill; H Michael Belmont; Anca D Askanase; W Joseph McCune; Michelene Hearth-Holmes; Mary Anne Dooley; Joan Von Feldt; Alan Friedman; Mark Tan; John Davis; Mary Cronin; Betty Diamond; Meggan Mackay; Lisa Sigler; Michael Fillius; Ann Rupel; Frederick Licciardi; Jill P Buyon Journal: N Engl J Med Date: 2005-12-15 Impact factor: 91.245
Authors: Maureen McMahon; Jennifer Grossman; John FitzGerald; Erika Dahlin-Lee; Daniel J Wallace; Bernard Y Thong; Humeira Badsha; Kenneth Kalunian; Christina Charles; Mohamad Navab; Alan M Fogelman; Bevra H Hahn Journal: Arthritis Rheum Date: 2006-08
Authors: Kelly J Shields; Emma Barinas-Mitchell; Matthew R Gingo; Ping Tepper; Bret H Goodpaster; Amy H Kao; Susan Manzi; Kim Sutton-Tyrrell Journal: Atherosclerosis Date: 2013-09-11 Impact factor: 5.162
Authors: M J Ormseth; L L Swift; S Fazio; M F Linton; P Raggi; J F Solus; A Oeser; A Bian; T Gebretsadik; A Shintani; C M Stein Journal: Lupus Date: 2012-10-11 Impact factor: 2.911