Joint Bone Spine

2008

DOI: 10.1016/j.jbspin.2008.01.022

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Auto-antibodies do not influence development of atherosclerotic plaques in rheumatoid arthritis

Ivânio Alves Pereira

¹

,

Iêda Maria Magalhães Laurindo

²

,

Rufus W. Burlingame

³

et al.

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Rheumatoid Arthritis1

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Rheumatology1

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Cited by 26 publications

(14 citation statements)

References 41 publications

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“…A strong correlation between the presence of RF and decreased endothelial function has been reported in patients with longstanding RA ( 29 ). Similar correlations have been made between anti-CCP antibodies and decreased endothelial function ( 37 ), presence of atherogenic risk factors ( 38 ), and increased carotid intima media thickness ( 39 ), though not in every study ( 29 , 40 ). Anti-citrullinated vimentin antibodies have been associated with systemic inflammation and proatherogenic lipid profiles in RA ( 38 ).…”

Section: Rheumatoid Arthritissupporting

confidence: 63%

Mechanisms of Premature Atherosclerosis in Rheumatoid Arthritis and Lupus

¹

,

²

2013

Annu. Rev. Med.

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Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), the two most common systemic autoimmune disorders, have both unique and overlapping manifestations. One feature they share is a significantly enhanced risk of atherosclerotic cardiovascular (CV) disease that significantly contributes to morbidity and mortality. The primary mechanisms that drive CV damage in these diseases remain to be fully characterized, but recent discoveries indicate that distinct inflammatory pathways and immune dysregulation characteristic of RA and SLE likely play prominent roles. This review focuses on analyzing the major mechanisms and pathways potentially implicated in the acceleration of atherothrombosis [**AU: Should this be atherosclerosis for consistency?**] and CV risk in SLE and RA, as well as in the identification of putative preventive strategies that may mitigate vascular complications in systemic autoimmunity.

“…A strong correlation between the presence of RF and decreased endothelial function has been reported in patients with longstanding RA ( 29 ). Similar correlations have been made between anti-CCP antibodies and decreased endothelial function ( 37 ), presence of atherogenic risk factors ( 38 ), and increased carotid intima media thickness ( 39 ), though not in every study ( 29 , 40 ). Anti-citrullinated vimentin antibodies have been associated with systemic inflammation and proatherogenic lipid profiles in RA ( 38 ).…”

Section: Rheumatoid Arthritissupporting

confidence: 63%

Mechanisms of Premature Atherosclerosis in Rheumatoid Arthritis and Lupus

¹

,

²

2013

Annu. Rev. Med.

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Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), the two most common systemic autoimmune disorders, have both unique and overlapping manifestations. One feature they share is a significantly enhanced risk of atherosclerotic cardiovascular (CV) disease that significantly contributes to morbidity and mortality. The primary mechanisms that drive CV damage in these diseases remain to be fully characterized, but recent discoveries indicate that distinct inflammatory pathways and immune dysregulation characteristic of RA and SLE likely play prominent roles. This review focuses on analyzing the major mechanisms and pathways potentially implicated in the acceleration of atherothrombosis [**AU: Should this be atherosclerosis for consistency?**] and CV risk in SLE and RA, as well as in the identification of putative preventive strategies that may mitigate vascular complications in systemic autoimmunity.

“…This supports evidence from a large population-based study demonstrating association between CVD and the presence of RF but not anti-CCP,58 but does not support the findings of extensive subclinical atherosclerosis observed in patients with RA who are anti-CCP-positive versus negative,59 or the observed independent association of anti-CCP antibodies with the development of ischaemic heart disease 60. These conflicting results from various studies of autoantibodies and CVD in RA61 62 indicate that the exact role played by autoantibodies in accelerated atherosclerosis in RA is still undefined.…”

Section: Discussionmentioning

confidence: 59%

Interleukin 17 as a novel predictor of vascular function in rheumatoid arthritis

¹

,

²

,

³

et al. 2011

Annals of the Rheumatic Diseases

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Objectives Rheumatoid arthritis (RA) is associated with enhanced cardiovascular (CV) risk and subclinical vascular disease. The proinflammatory milieu has been linked to premature atherosclerosis and endothelial dysfunction in RA. While IL-17 is considered pathogenic in RA, its role in determining vascular dysfunction in this disease has not been systematically assessed. We analyzed candidate variables that could determine endothelial function in various vascular territories in a cohort of RA patients on biologic therapy, with minimal traditional CV risk factors and low disease activity score. Methods RA patients (n=51) on stable biologic therapy underwent measurement of conduit artery endothelial function by brachial artery flow-mediated dilatation (FMD); arterial compliance by pulse wave velocity (PWV) assessment; and endothelium-dependent microvascular testing with Endo-PAT2000 device to assess reactive hyperemia index (RHI). IL-17 was quantified by ELISA and disease activity was assessed by DAS-28. Results IL-17 and high sensitivity CRP were the main determinants of lower RHI in univariate (p=0.004, <0.001) and multivariate (p=0.004, <0.0001) analysis, respectively. Traditional and non-traditional CV risk variables determined PWV, with a significant positive association with IL-17 in univariate and multivariate analysis (p=0.02, 0.01, respectively). In contrast, conduit endothelial function was mainly determined by rheumatoid factor titers (p=0.003). Anti-CCP titers and disease activity did not determine vascular function. Conclusion In RA patients treated with biologics, IL-17 is a main predictor of microvascular function and arterial compliance. This study suggests IL-17 may play a significant role in development of endothelial dysfunction and CVD in RA.

“…Anti-Hsp 60, anti-Hsp 65, anti-β2GPI1, anticardiolipin (aCL), anti-CCP, or anti-lipoprotein lipase (anti-)LPL were studied, with only anti-CCP being elevated in RA. Patients positive to these antibodies did not show elevated IMT [53], CRP, and ESR levels.…”

Section: Dyslipidemiamentioning

confidence: 88%

Atherosclerosis in Autoimmune Rheumatic Diseases—Mechanisms and Clinical Findings

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,

²

,

³

2008

Clinic Rev Allerg Immunol

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Atherosclerosis is one of the major entities leading to morbidity and mortality in the western world. It is known now that atherosclerosis cannot be explained merely by the presence of the Framingham traditional risk factors and that autoimmunity takes a significant role in its pathogenesis. It is also known that individuals with autoimmune diseases demonstrate increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. The mechanisms for the assumed accelerated atherosclerosis in diseases such as systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, and systemic sclerosis include the classical risk factors, but may also be due to chronic inflammatory processes and immune dysregulation. Autoantibodies, autoantigens, pro-inflammatory cytokines, and infectious agents play a role in that process. Involvement of autoimmunity in the pathogenesis of accelerated atherosclerosis in rheumatic diseases and the common pathway that leads to this condition may lead to significant change in prevention of treatment.

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