Oxidized low-density lipoprotein and β2-glycoprotein I in patients with systemic lupus erythematosus and increased carotid intima-media thickness: Implications in autoimmune-mediated atherosclerosis

Luis R. Lopez, M. Salazar-Paramo, C. Palafox-Sanchez, B. L. Hurley, Eiji Matsuura, I. Garcia-De La Torre

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

Oxidative stress and LDL modification (oxLDL) are early pro-atherogenic events. OxLDL binds β2GPI producing immunogenic oxLDL/β2GPI complexes. Antibodies to these complexes have been associated with arterial thrombosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Circulating oxLDL/β2GPI complexes, IgG and IgM antibodies to these complexes were measured by ELISA in 30 SLE patients asymptomatic for cardiovascular disease (mean age 31 years) and 27 age/sex matched healthy controls. Carotid intima-media thickness (IMT) was measured by ultrasound in all patients and controls. Forty-seven percent of SLE presented plaques (median IMT of 0.65 ± 0.12 mm) while only 7% of the controls had plaques (median IMT of 0.50 ± 0.04 mm, P <0.001). Median optical density (OD 450nm) for oxLDL/β2GPI complexes in SLE was 0.244 ± 0.07, higher than controls (0.174 ± 0.09, P <0.001). Median OD for IgG anti-oxLDL/β2GPI antibodies was also higher in SLE (0.297 ± 0.26) compared to controls (0.194 ± 0.07, P <0.001) while the median OD for IgM antibodies in SLE (0.444 ± 0.46) was not different than controls (0.326 ± 0.22, P = 0.267). There was no correlation between IMT and oxLDL/β2GPI complexes, IgG or IgM antibodies, possibly reflecting the complex interrelationship between these serologic elements and tissue factors in the arterial wall. These results support the hypothesis that oxLDL/β2GPI complexes and IgG (not IgM) anti-oxLDL/β2GPI antibodies contribute to the development of autoimmune-mediated atherosclerosis.

Original languageEnglish
Pages (from-to)80-86
Number of pages7
JournalLupus
Volume15
Issue number2
DOIs
Publication statusPublished - 2006

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Carotid Intima-Media Thickness
LDL Lipoproteins
Systemic Lupus Erythematosus
Atherosclerosis
Glycoproteins
Antibodies
Immunoglobulin M
Immunoglobulin G
oxidized low density lipoprotein
Asymptomatic Diseases
Antiphospholipid Syndrome
Thromboplastin
Oxidative Stress
Thrombosis
Cardiovascular Diseases
Enzyme-Linked Immunosorbent Assay

Keywords

  • β2-glycoprotein I
  • Autoimmune-mediated atherosclerosis
  • Intima-media thickness
  • Oxidized low-density lipoprotein
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

Oxidized low-density lipoprotein and β2-glycoprotein I in patients with systemic lupus erythematosus and increased carotid intima-media thickness : Implications in autoimmune-mediated atherosclerosis. / Lopez, Luis R.; Salazar-Paramo, M.; Palafox-Sanchez, C.; Hurley, B. L.; Matsuura, Eiji; Garcia-De La Torre, I.

In: Lupus, Vol. 15, No. 2, 2006, p. 80-86.

Research output: Contribution to journalArticle

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abstract = "Oxidative stress and LDL modification (oxLDL) are early pro-atherogenic events. OxLDL binds β2GPI producing immunogenic oxLDL/β2GPI complexes. Antibodies to these complexes have been associated with arterial thrombosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Circulating oxLDL/β2GPI complexes, IgG and IgM antibodies to these complexes were measured by ELISA in 30 SLE patients asymptomatic for cardiovascular disease (mean age 31 years) and 27 age/sex matched healthy controls. Carotid intima-media thickness (IMT) was measured by ultrasound in all patients and controls. Forty-seven percent of SLE presented plaques (median IMT of 0.65 ± 0.12 mm) while only 7{\%} of the controls had plaques (median IMT of 0.50 ± 0.04 mm, P <0.001). Median optical density (OD 450nm) for oxLDL/β2GPI complexes in SLE was 0.244 ± 0.07, higher than controls (0.174 ± 0.09, P <0.001). Median OD for IgG anti-oxLDL/β2GPI antibodies was also higher in SLE (0.297 ± 0.26) compared to controls (0.194 ± 0.07, P <0.001) while the median OD for IgM antibodies in SLE (0.444 ± 0.46) was not different than controls (0.326 ± 0.22, P = 0.267). There was no correlation between IMT and oxLDL/β2GPI complexes, IgG or IgM antibodies, possibly reflecting the complex interrelationship between these serologic elements and tissue factors in the arterial wall. These results support the hypothesis that oxLDL/β2GPI complexes and IgG (not IgM) anti-oxLDL/β2GPI antibodies contribute to the development of autoimmune-mediated atherosclerosis.",
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AU - Garcia-De La Torre, I.

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AB - Oxidative stress and LDL modification (oxLDL) are early pro-atherogenic events. OxLDL binds β2GPI producing immunogenic oxLDL/β2GPI complexes. Antibodies to these complexes have been associated with arterial thrombosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Circulating oxLDL/β2GPI complexes, IgG and IgM antibodies to these complexes were measured by ELISA in 30 SLE patients asymptomatic for cardiovascular disease (mean age 31 years) and 27 age/sex matched healthy controls. Carotid intima-media thickness (IMT) was measured by ultrasound in all patients and controls. Forty-seven percent of SLE presented plaques (median IMT of 0.65 ± 0.12 mm) while only 7% of the controls had plaques (median IMT of 0.50 ± 0.04 mm, P <0.001). Median optical density (OD 450nm) for oxLDL/β2GPI complexes in SLE was 0.244 ± 0.07, higher than controls (0.174 ± 0.09, P <0.001). Median OD for IgG anti-oxLDL/β2GPI antibodies was also higher in SLE (0.297 ± 0.26) compared to controls (0.194 ± 0.07, P <0.001) while the median OD for IgM antibodies in SLE (0.444 ± 0.46) was not different than controls (0.326 ± 0.22, P = 0.267). There was no correlation between IMT and oxLDL/β2GPI complexes, IgG or IgM antibodies, possibly reflecting the complex interrelationship between these serologic elements and tissue factors in the arterial wall. These results support the hypothesis that oxLDL/β2GPI complexes and IgG (not IgM) anti-oxLDL/β2GPI antibodies contribute to the development of autoimmune-mediated atherosclerosis.

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