Antibodies against oxidized low-density lipoprotein are associated with subclinical atherosclerosis in recent-onset rheumatoid arthritis

Ahmed, Hosam F.; Youssef, Mahmoud; Mosaad, Youssef M.

doi:10.1007/s10067-010-1436-0

Cited by 39 publications

(24 citation statements)

References 30 publications

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“…A younger RA group might also be responsible for the lower mean IMT than in other reports [25]. Although Ahmed et al analyzed an equally young group of RA patients, severe atherosclerosis was more frequent in their cohort [27]. This might be due to the fact that in 12.5% of the RA patients assessed by Ahmed et al were diabetic, as opposed to none in the present study; and in 22.5% of the RA patients in those authors' study reported a significant family history of CV diseases, while patients with a significant family history of CVD were excluded from the present study.…”

Section: Discussioncontrasting

confidence: 45%

Disease Activity, Oxidized-LDL Fraction and Anti-Oxidized LDL Antibodies Influence Cardiovascular Risk in Rheumatoid Arthritis

Nowak¹,

Madej²,

Łuczak³

et al. 2015

Adv Clin Exp Med

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Section: Discussioncontrasting

confidence: 45%

Disease Activity, Oxidized-LDL Fraction and Anti-Oxidized LDL Antibodies Influence Cardiovascular Risk in Rheumatoid Arthritis

Nowak¹,

Madej²,

Łuczak³

et al. 2015

Adv Clin Exp Med

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“…Two studies showed that plaques were more prevalent in early RA cohorts than among healthy controls,30 32 whereas one study found the prevalence to be similar among early RA cases and controls 31. As an aggregate, it seems that enhanced atherogenesis occurs soon after RA symptom onset (figure 1) and that this is subsequently ongoing.…”

Section: Subclinical CV Changesmentioning

confidence: 99%

“…In early RA, antibodies against oxidised LDL30 and anti-modified citrullinated vimentin levels67 have been demonstrated to correlate positively with subclinical atherosclerosis. However, in the 5-year prospective study already mentioned, the incidence of overt CV events did not correlate with immunological mediators such as RF, anti-citrullinated peptide antibody and antinuclear antibodies during the first years of RA 48…”

Section: Risk Factorsmentioning

confidence: 99%

How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?

et al. 2012

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Rheumatoid arthritis (RA) is a chronic inflammatory disease which is associated with an increased cardiovascular (CV) burden. Whether the risk is already present at the time of RA diagnosis remains a key area of debate. The aim of this review was to evaluate the existence of both subclinical CV changes, including endothelial dysfunction and atherosclerosis, CV risk factors, as well as CV disease manifestations such as coronary heart disease, myocardial infarction, congestive heart failure and CV death prior to RA diagnosis and during the first few years of the disease. The state of the endothelial function remains controversial in patients with newly diagnosed RA. Studies with impaired brachial artery vasodilatory responses at baseline showed a reversal of the dysfunction after 6-12 months of anti-inflammatory therapy. Morphological evidence of arterial wall atherosclerosis, measured by carotid artery intima-media thickness or the prevalence of carotid plaques, was already present during the first year following RA diagnosis. The risk of coronary heart disease and myocardial infarction is increased even prior to and, at the latest, within 1 year of the clinical onset of RA. The prevalence of hypertension was similar among patients with RA and controls. CV mortality may not increase within the first years of RA diagnosis. In conclusion, the CV risk seems to increase sooner after the RA diagnosis than previously thought. In addition to systematic CV risk assessment, patients with early RA might benefit from being targeted with stricter than conventional CV risk prevention and intervention.

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“…Anticyclic citrullinated peptide antibodies (anti-CCP), IgM rheumatoid factor, circulating immune complexes, proinflammatory cytokines including TNF α and IL-6, Th0/Th1 cells, decreased folate and vitamin B12 productions, and impaired paraoxonase activity, among others, may all be further involved in the development of vascular disease in RA [85–87]. Epigenetic data indicate that defective DNA methylation might also be relevant to CVD and AT development in RA, so that it has been shown hypomethylation of IL-6 promoter [35].…”

Section: Epigenetic Alterations Inflammation and Cardiovascular mentioning

confidence: 99%

Cardiovascular Risk in Systemic Autoimmune Diseases: Epigenetic Mechanisms of Immune Regulatory Functions

López‐Pedrera

Pérez-Sánchez

Ramos-Casals

et al. 2012

Clinical and Developmental Immunology

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Autoimmune diseases (AIDs) have been associated with accelerated atherosclerosis (AT) leading to increased cardio- and cerebrovascular disease risk. Traditional risk factors, as well as systemic inflammation mediators, including cytokines, chemokines, proteases, autoantibodies, adhesion receptors, and others, have been implicated in the development of these vascular pathologies. Yet, the characteristics of vasculopathies may significantly differ depending on the underlying disease. In recent years, many new genes and signalling pathways involved in autoimmunity with often overlapping patterns between different disease entities have been further detected. Epigenetics, the control of gene packaging and expression independent of alterations in the DNA sequence, is providing new directions linking genetics and environmental factors. Epigenetic regulatory mechanisms comprise DNA methylation, histone modifications, and microRNA activity, all of which act upon gene and protein expression levels. Recent findings have contributed to our understanding of how epigenetic modifications could influence AID development, not only showing differences between AID patients and healthy controls, but also showing how one disease differs from another and even how the expression of key proteins involved in the development of each disease is regulated.

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Antibodies against oxidized low-density lipoprotein are associated with subclinical atherosclerosis in recent-onset rheumatoid arthritis

Cited by 39 publications

References 30 publications

Disease Activity, Oxidized-LDL Fraction and Anti-Oxidized LDL Antibodies Influence Cardiovascular Risk in Rheumatoid Arthritis

Disease Activity, Oxidized-LDL Fraction and Anti-Oxidized LDL Antibodies Influence Cardiovascular Risk in Rheumatoid Arthritis

How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?

Cardiovascular Risk in Systemic Autoimmune Diseases: Epigenetic Mechanisms of Immune Regulatory Functions

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