Inflammation: A pivotal link between autoimmune diseases and atherosclerosis

Abou‐Raya, A.; Abou‐Raya, S.

doi:10.1016/j.autrev.2005.12.006

Cited by 236 publications

(158 citation statements)

References 35 publications

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“…However, a number of studies of gout, systemic lupus erythematous, rheumatoid arthritis (RA), and ankylosing spondylitis reviewed elsewhere have demonstrated an increased frequency of metabolic syndrome in patients with rheumatologic disease. 18 In addition, the association between the metabolic syndrome and psoriasis (PsO), a chronic infl ammatory disorder of the skin involving immune-mediated disease involving T lymphocytes, has also been examined in 1 VA Medical Center, Mather, California. …”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4] Studies have demonstrated that cardiovascular disease is accelerated in this patient population, but the cause remains unclear. 3 Whereas cardiovascular risk factors such as age, gender, smoking, hypertension (HTN), and dyslipidemia have been shown to play a role in atherosclerosis, they do not appear to fully account for the increased risk of cardiovascular disease in rheumatologic patients.…”

Section: Introductionmentioning

confidence: 99%

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Increased Prevalence of the Metabolic Syndrome in Patients with Psoriatic Arthritis

Raychaudhuri

Chatterjee

Nguyen

et al. 2010

Metabolic Syndrome and Related Disorders

104

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Objectives: Psoriasis (PsO) is a common chronic T cell-mediated infl ammatory disorder traditionally thought to manifest in the skin and joints (psoriatic arthritis, PsA). Recently, it has been shown that these patients have an increased risk for myocardial infarction and this was greater with increasing severity of psoriasis. Patients with psoriasis have reported to have cardiometabolic disturbances including obesity, insulin resistance, and dyslipidemia. This constellation of risk factors, referred to as the metabolic syndrome, increases the risk for atherosclerotic cardiovascular disease (ASCVD) and type 2 diabetes mellitus. The aim of this study was to determine the prevalence of metabolic syndrome in PsA. Methods: In our study, we examined the records of 105 patients with PsA to determine the prevalence of metabolic syndrome in PsA. This was a retrospective analysis of the Sacramento Veterans Affairs database. Results: Our results demonstrated an increased prevalence of the metabolic syndrome in patients with PsA (61/105 patients or 58.1%) compared to the 35.2 % reported for the Third National Health and Nutrition Examination Survery (NHANES III) data. Conclusions: Thus, patients with PsA have a very high prevalence of metabolic syndrome, which predisposes them to an increased risk of both diabetes and ASCVD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased Prevalence of the Metabolic Syndrome in Patients with Psoriatic Arthritis

Raychaudhuri

Chatterjee

Nguyen

et al. 2010

Metabolic Syndrome and Related Disorders

104

View full text Add to dashboard Cite

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“…Inflammation could deplete the antioxidant reserves that protect endothelial integrity, also altering lipid metabolism. Likewise, inflammation accounts for the activation of circulating leukocytes and facilitates their recruitment to sites of injury (1,2,12). Some experimental models have been used to address premature atherosclerosis associated with SLE (10,14).…”

mentioning

confidence: 99%

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

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Objective. To determine whether systemic inflammation induced by chronic antigen-induced arthritis (AIA) accelerates vascular lesions in rabbits with atherosclerosis.Methods. Two models of atherosclerosis and chronic AIA were combined. Atherosclerosis was induced by coupling a hyperlipemic diet with an endothelial lesion at the femoral arteries, while chronic AIA was induced by ovalbumin injection. Markers in sera and peripheral blood mononuclear cells (PBMCs) as well as vessels and synovial membranes from the rabbits with the double phenotype (both chronic AIA and atherosclerosis) were compared with those from rabbits with each disease alone.Results. Serum levels of interleukin-6, C-reactive protein, and prostaglandin E 2 increased in rabbits with both chronic AIA and atherosclerosis as compared with healthy animals or animals with either chronic AIA alone or atherosclerosis alone. NF-B binding and CCL2 and cyclooxygenase 2 (COX-2) expression were higher in PBMCs from rabbits with both chronic AIA and atherosclerosis than in PBMCs from healthy rabbits. The intima-media thickness ratio of femoral arteries was equally increased in rabbits with atherosclerosis alone and in rabbits with both chronic AIA and atherosclerosis, but the latter group showed a higher level of macrophage infiltration. Femoral CCL2 and COX-2 expression was increased in rabbits with both chronic AIA and atherosclerosis as compared with rabbits with atherosclerosis alone. In the aortas, vascular lesions were found in 27% of rabbits with atherosclerosis alone and in 60% of rabbits with both chronic AIA and atherosclerosis. Rabbits with both chronic AIA and atherosclerosis exhibited more severe synovitis and higher synovial expression of CCL2 than did rabbits with chronic AIA alone.Conclusion. The onset of chronic AIA in animals with atherosclerosis resulted in the local and systemic up-regulation of mediators of tissue inflammation and plaque instability associated with a higher incidence of aortic lesions. This model could represent a novel approach to the study of inflammation-associated atherosclerosis.

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“…Si è ammesso che possa esservi una risposta immunitaria crociata tra antigeni posti sulla superficie di organismi patogeni e le cellule endoteliali stesse. L'attivazione delle cellule endoteliali determinerebbe un reclutamento di cellule proinfiammatorie, un'attivazione delle molecole (ICAM-1,VCAM-1) che promuovono l'adesione dei monociti e un'iperproduzione di citochine infiammatorie con innesco della disfunzione endoteliale [10,11]. In tal senso, la mai confermata ipotesi di una genesi infettiva dell'AR troverebbe un sostegno in questo percorso comune nella via dell'aterosclerosi.…”

Section: Patogenesi Dell'aterosclerosiunclassified

Rheumatoid arthritis: prototype of accelerated atherosclerosis

Bruzzese¹

2013

Ital J Med

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IntroduzioneNumerose osservazioni e approfonditi studi hanno ormai ampiamente dimostrato che pazienti affetti da malattie autoimmuni sistemiche hanno un rischio cardiovascolare (CV) molto più alto rispetto alla popolazione sana, anche in assenza dei tradizionali fattori di rischio [1,2]. In particolare, nei soggetti con artrite reumatoide (AR) la patologia CV è la più frequente causa di morte, con un'incidenza doppia di infarto miocardico, tanto da indurre a ritenere la malattia un fattore indipendente di rischio CV [3]. Patogenesi dell'aterosclerosiNella patogenesi dell'aterosclerosi entrano in gioco numerosi fattori e, tra essi, svolge un ruolo non secondario un persistente stato infiammatorio (Fig. 1). Interessante è l'osservazione che l'infiammazione può interagire con un altro tradizionale fattore di rischio per l'aterosclerosi, l'insulino-resistenza [4], attraverso un'inibizione periferica dell'attività dell'insulina mediata dalle citochine infiammatorie, soprattutto dal fattore di necrosi tumorale-α (Tumour Necrosis Factor-α, TNF-α) [5]. Un'infiammazione cronica può quindi determinare insulino-resistenza periferica, che è fondamentale, insieme all'obesità centrale, nel determinismo della sindrome metabolica.È ormai certo, comunque, che l'infiammazione cronica ha un'azione proaterogena indipendente, che trova il suo momento iniziale nella primitiva disfunzione endoteliale (Fig. 2). Nelle malattie autoimmuni, e in particolare in corso di AR, esiste sempre disfunzione endoteliale a prescindere dall'età dei pazienti, dalla durata della malattia e dalla presenza/assenza del fattore reumatoide. I meccanismi patogenetici che innescano un danno endoteliale nell'AR sono molteplici (Fig. 3). È indubbio che fattori genetici entrino prepotentemente nel determinismo dell'aterosclerosi in soggetti con AR. Sembra ormai dimostrato che in presenza dell'allele HLA-DRB1 la disfunzione endoteliale e Summary The rheumatoid arthritis, as other rheumatic chronic inflammatory illnesses, is accompanied by an increased risk of cardio-vascular pathology. The primitive endothelial dysfunction is the principal moment of the primer of the atherosclerosis. This is mediated by various factors, the principals of which result to be genetic factors, the production of inflammatory cytokines, among which particularly the Tumour Necrosis Factor-α, an oxidative-stress, probable viral agents and a reduction of the endothelial ancestor cells. The smoke of cigarette can be a factor of independent risk for the rheumatoid arthritis and for the atherosclerosis.

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Inflammation: A pivotal link between autoimmune diseases and atherosclerosis

Cited by 236 publications

References 35 publications

Increased Prevalence of the Metabolic Syndrome in Patients with Psoriatic Arthritis

Increased Prevalence of the Metabolic Syndrome in Patients with Psoriatic Arthritis

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Rheumatoid arthritis: prototype of accelerated atherosclerosis

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