Prevalence and relation to risk factors of carotid atherosclerosis and left ventricular hypertrophy in systemic lupus erythematosus and antiphospholipid antibody syndrome

Roman, Mary J.; Salmon, Jane E.; Sobel, Rachel E.; Lockshin, Michael D.; Sammaritano, Lisa R.; Schwartz, Joseph E.; Devereux, Richard B.

doi:10.1016/s0002-9149(00)01453-3

Cited by 90 publications

(53 citation statements)

References 19 publications

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“…However, the cellular and molecular mechanisms underlying this accelerated atherosclerosis are poorly understood and cannot be attributed to traditional CVD risk factors (3,17). Mechanistic studies of accelerated atherosclerosis in lupus are difficult due in part to the lack of an appropriate animal model.…”

Section: Discussionmentioning

confidence: 99%

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Stanic

Stein

Morgan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis. The underlying mechanisms are poorly understood, and investigations have been hampered by the absence of animal models that reflect the human condition of generalized atherosclerosis and lupus. We addressed this problem by transferring lupus susceptibility to low-density lipoprotein (LDL) receptordeficient (LDLr ؊/؊ ) mice, an established model of atherosclerosis, creating radiation chimeras with NZM2410-derived, lupus-susceptible, B6.Sle1.2.3 congenic or C57BL͞6 control donors (LDLr.Sle and LDLr.B6, respectively). LDLr.Sle mice developed a lupus-like disease characterized by production of double-stranded DNA autoantibodies and renal disease. When fed a Western-type diet, LDLr.Sle chimeras had increased mortality and atherosclerotic lesions. The plaques of LDLr.Sle mice were highly inflammatory and contained more CD3 ؉ T cells than controls. LDLr.Sle mice also had increased activation of CD4 ؉ T and B cells and significantly higher antibody to oxidized LDL and cardiolipin. Collectively, these studies demonstrate that the lupus-susceptible immune system enhances atherogenesis and modulates plaque composition.autoimmunity ͉ congenic mice

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Section: Discussionmentioning

confidence: 99%

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Stanic

Stein

Morgan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Both conditions have been found in patients with SLE (11,31), whereas a strong link between lipid peroxidation and IgG aCL titers has been demonstrated in APS (32). Furthermore, aCL antibodies have also been related to atherosclerosis (33,34). This may occur either via direct activation of the vascular endothelium or by the increased uptake of anti-oxidized LDL-LDL immune complexes by macrophages (35).…”

Section: Discussionmentioning

confidence: 99%

Antibodies to high‐density lipoprotein and β₂‐glycoprotein I are inversely correlated with paraoxonase activity in systemic lupus erythematosus and primary antiphospholipid syndrome

Alves

Ames

Donohue

et al. 2002

Arthritis & Rheumatism

187

129

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Objective. To determine the prevalence of antihigh-density lipoprotein (anti-HDL) antibodies and to establish a possible relationship between anti-HDL, anticardiolipin antibodies (aCL), anti-␤ 2 -glycoprotein I (anti-␤ 2 GPI), and paraoxonase (PON) activity in patients with systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (APS).Methods. Thirty-two patients with SLE and 36 with primary APS were enrolled in a cross-sectional study. Twenty age-and sex-matched healthy subjects were used as controls. Serum levels of IgG and IgM aCL, anti-␤ 2 GPI, and antiprothrombin antibodies and IgG anti-HDL were measured by enzyme-linked immunosorbent assay. Total cholesterol, HDL cholesterol, HDL 2 , and HDL 3 were determined by standard enzymatic techniques. PON activity was assessed by quantification of nitrophenol formation, and total antioxidant capacity (TAC) by chemiluminescence.Results. Levels of total HDL, HDL 2 , and HDL 3 were reduced in patients with SLE compared with controls (mean ؎ SD 0.51 ؎ 0.3, 0.37 ؎ 0.3, and 0.14 ؎ 0.1 mmoles/liter, respectively, versus 1.42 ؎ 0.9, 1.01 ؎ 0.7, and 0.40 ؎ 0.2). Patients with SLE and primary APS had higher titers of anti-HDL antibodies and lower PON activity than controls. In the SLE population, PON activity was inversely correlated with IgG anti-HDL titers (r ‫؍‬ ؊0.48, P ‫؍‬ 0.005) whereas in the primary APS population, IgG anti-␤ 2 GPI was the only independent predictor of PON activity (r ‫؍‬ ؊0.483, P ‫؍‬ 0.003). In the SLE group, anti-HDL was inversely correlated with TAC (r ‫؍‬ ؊0.40, P < 0.02), and PON activity was positively correlated with TAC (r ‫؍‬ 0.43, P < 0.02).Conclusion. IgG anti-HDL and IgG anti-␤ 2 GPI antibodies are associated with reduced PON activity in patients with SLE and primary APS. Since the physiologic role of PON is to prevent low-density lipoprotein oxidation with its attendant atherogenic effects, the reported interactions may be relevant to the development of atherosclerosis in SLE and primary APS.

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“…It is well known that patients with valvular disease are at higher risk of arterial thromboembolic events [ 39 ]. In a multicenter prospective study, AMI was the presenting manifestation in 2.8% and reached up to 5.5% during the follow-up period [ 40 ]. A large prospective study found that high titers of anti-CL antibodies are an independent risk factor for AMI or sudden cardiac death [ 41 ].…”

Section: Cardiovascular Manifestationsmentioning

confidence: 99%

Pathogenic Mechanisms of Thrombosis in Antiphospholipid Syndrome (APS)

Sikara¹,

Grika²,

Vlachoyiannopoulos³

2011

Thrombophilia

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Prevalence and relation to risk factors of carotid atherosclerosis and left ventricular hypertrophy in systemic lupus erythematosus and antiphospholipid antibody syndrome

Cited by 90 publications

References 19 publications

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Antibodies to high‐density lipoprotein and β₂‐glycoprotein I are inversely correlated with paraoxonase activity in systemic lupus erythematosus and primary antiphospholipid syndrome

Pathogenic Mechanisms of Thrombosis in Antiphospholipid Syndrome (APS)

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Prevalence and relation to risk factors of carotid atherosclerosis and left ventricular hypertrophy in systemic lupus erythematosus and antiphospholipid antibody syndrome

Cited by 90 publications

References 19 publications

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus

Antibodies to high‐density lipoprotein and β2‐glycoprotein I are inversely correlated with paraoxonase activity in systemic lupus erythematosus and primary antiphospholipid syndrome

Pathogenic Mechanisms of Thrombosis in Antiphospholipid Syndrome (APS)

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Antibodies to high‐density lipoprotein and β₂‐glycoprotein I are inversely correlated with paraoxonase activity in systemic lupus erythematosus and primary antiphospholipid syndrome