Rheumatoid arthritis versus diabetes as a risk factor for cardiovascular disease: a cross-sectional study, the CARRÉ Investigation

Halm, Vokko P. van; Peters, Mike J L; Voskuyl, Alexandre E.; Boers, Maarten; Lems, Willem F.; Visser, Marjolein; Stehouwer, Coen D.A.; Spijkerman, Annemieke M.W.; Dekker, J.M.; Nijpels, Giel; Heine, R.J.; Bouter, Lex M.; Smulders, Yvo M.; Dijkmans, Ben A. C.; Nurmohamed, Michael T.

doi:10.1136/ard.2008.094151

Cited by 335 publications

(223 citation statements)

References 36 publications

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“…Rheumatoid arthritis (RA) is the most common systemic autoimmune disease and is associated with excessive cardiovascular mortality (1,2). There is a decrease of 10-15 years in life expectancy in these patients compared with that in the general population, particularly in patients with severe disease (3).…”

mentioning

confidence: 99%

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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Objective. To investigate whether arginase pathway abnormalities occur in vessels from rats with adjuvant-induced arthritis (AIA), and to determine whether the up-regulation of arginase, which reciprocally regulates nitric oxide synthase (NOS) by competing for the same substrate, L-arginine, contributes to endothelial dysfunction in AIA.Methods. We performed vascular reactivity experiments on thoracic aortic rings from AIA rats and control rats, and we investigated the response of rings to norepinephrine (NE), sodium nitroprusside (SNP), and acetylcholine (ACh). ACh-induced relaxation was evaluated in the presence (or not in the presence) of the NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME), the arginase inhibitor N -hydroxy-nor-Larginine (nor-NOHA), or both. Aortic arginase activity was measured using a spectrophotometric method, and the expression of arginase and endothelial NOS (eNOS) was evaluated by Western blotting.Results. ACh-induced vasodilation was significantly impaired in AIA rats, while the responses to NE and to SNP did not differ from those in control rats. L-NAME reduced ACh-induced vasodilation to a lesser extent in AIA rats than in control rats. Incubation of aortic rings with nor-NOHA enhanced the vascular response to ACh in AIA rats and reversed the effects of L-NAME. Compared with control rats, AIA rats exhibited increased vascular expression of arginase II (by 22%) (P < 0.05) as well as increased arginase activity (by 49%) (P < 0.05), whereas eNOS expression was unchanged. Finally, arginase activity and expression correlated positively with arthritis severity.Conclusion. Our results are consistent with the notion that arginase up-regulation plays a role in AIAassociated endothelial dysfunction. They suggest that arginase might be an attractive new target for treating endothelial dysfunction in arthritis.

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mentioning

confidence: 99%

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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“…Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus [7][8][9][10][11][12][13][14][15][16][17][18]. In these diseases, an increased prevalence of atherosclerosis and, consequently, increased cardiovascular morbidity and mortality has been observed.…”

Section: Introductionmentioning

confidence: 99%

Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Tervaert

2009

Clinical and Experimental Immunology

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SummaryPremature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible.

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“…Toms et al 73 have reported a lower prevalence of MS in elderly patients using MTX; on the other hand, a subanalysis of the CARRE Investigation has not confi rmed those fi ndings. 13 …”

Section: Metabolic Syndromementioning

confidence: 99%

“…5 Individuals diagnosed with RA have greater likelihood of having other diseases associated, such as those of autoimmune etiology, 6,7 and comorbidities, such as systemic arterial hypertension (SAH), dyslipidemia, and diabetes mellitus (DM). [8][9][10][11][12][13][14] The understanding and adequate management of the comorbidities of patients with RA are fundamental, because those diseases contribute to an increased cardiovascular risk and to the greater mortality observed in that group. 15 The present study aimed at elaborating recommendations for the diagnosis and management of comorbidities in patients with RA, emphasizing the most frequent conditions.…”

Section: Introductionmentioning

confidence: 99%

Consenso 2012 da Sociedade Brasileira de Reumatologia sobre o manejo de comorbidades em pacientes com artrite reumatoide

Pereira¹,

Mota²,

Cruz³

et al. 2012

Rev. Bras. Reumatol.

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Objective: To elaborate recommendations of the Rheumatoid Arthritis Committee of the Brazilian Society of Rheumatology (SBR) to manage comorbidities in rheumatoid arthritis (RA). Methods: To review the literature and the opinions of the SBR RA Committee experts. Results and conclusions: Recommendations: 1) Early diagnosis and proper treatment of comorbidities are recommended; 2) The specifi c treatment of RA should be adapted to the presence of comorbidities; 3) Angiotensin-converting-enzyme inhibitors or angiotensin II receptor blockers are preferred to treat systemic arterial hypertension; 4) In patients diagnosed with rheumatoid arthritis and diabetes mellitus, the continuous use of a high cumulative dose of corticoids should be avoided; 5) Statins should be used to maintain LDL cholesterol levels under 100 mg/dL and the atherosclerotic index lower than 3.5 in patients with RA who have other comorbidities; 6) Metabolic syndrome should be treated; 7) Performing non-invasive tests to investigate subclinical atherosclerosis is recommended; 8) Greater surveillance for the early diagnosis of occult malignancy is recommended; 9) Preventive measures of venous thrombosis are suggested; 10) Bone densitometry is recommended in RA patients over the age of 50 years and in younger patients on corticoid therapy at a dose greater than 7.5 mg for over three months; 11) Patients with RA and osteoporosis should be instructed to avoid falls, to increase their dietary calcium intake and sun exposure, and to exercise; 12) Calcium and vitamin D supplementation is suggested. Bisphosphonates are suggested for patients with T score < -2.5 on bone densitometry; 13) A multidisciplinary team, with the active participation of a rheumatologist, is recommended to treat comorbidities.

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Rheumatoid arthritis versus diabetes as a risk factor for cardiovascular disease: a cross-sectional study, the CARRÉ Investigation

Cited by 335 publications

References 36 publications

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Consenso 2012 da Sociedade Brasileira de Reumatologia sobre o manejo de comorbidades em pacientes com artrite reumatoide

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