Gout, hyperuricemia, and the risk of cardiovascular disease: Cause and effect?

被引：46

作者：

Shah A. ^{[1
]}

Keenan R.T. ^{[1
]}

机构：

[1] Division of Rheumatology and Immunology, Duke University School of Medicine, DUMC 3544, Durham, NC 27710

来源：

Current Rheumatology Reports | 2010年 / 12卷 / 2期

关键词：

Cardiovascular disease; Gout; Hyperuricemia; Inflammation;

D O I：

10.1007/s11926-010-0084-3

中图分类号：

学科分类号：

摘要：

Gout and hyperuricemia have long been suspected to be risk factors for cardiovascular disease. However, studies have frequently failed to distinguish whether these entities have an independent effect on cardiovascular risk or serve as markers for other risk factors. In vitro and animal studies suggest that uric acid is a biologically active compound that can increase inflammatory mediators known to lead to vascular damage. In contrast, uric acid also has potentially protective effects as a strong antioxidant, approaching the potency of vitamin C. Large clinical trials demonstrate a consistent relationship between elevated serum uric acid and a variety of cardiovascular diseases, although the strength of association varies greatly. We review the evidence for and against an independent role for hyperuricemia and/or gout in cardiovascular pathology. © Springer Science+Business Media, LLC 2010.

引用

页码：118 / 124

页数：6

共 54 条

[1]

Watanabe S., Kang D.H., Feng L., Et al., Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity, Hypertension, 40, pp. 355-360, (2002)

[2]

So A., Developments in the scientific and clinical understanding of gout, Arthritis Res Ther, 10, (2008)

[3]

Hahn B.H., McMahon M., Atherosclerosis and systemic lupus erythematosus: The role of altered lipids and of autoantibodies, Lupus, 17, pp. 368-370, (2008)

[4]

Hahn B.H., Grossman J., Chen W., McMahon M., The pathogenesis of atherosclerosis in autoimmune rheumatic diseases: Roles of inflammation and dyslipidemia, J Autoimmun, 28, pp. 69-75, (2007)

[5]

Scott P., Ma H., Viriyakosol S., Et al., Engagement of CD14 mediates the inflammatory potential of monosodium urate crystals, J Immunol, 177, pp. 6370-6378, (2006)

[6]

Di Giovine F.S., Malawista S.E., Thornton E., Duff G.W., Urate crystals stimulate production of tumor necrosis factor alpha from human blood monocytes and synovial cells. Cytokine mRNA and protein kinetics, and cellular distribution, J Clin Invest, 87, pp. 1375-1381, (1991)

[7]

Kanellis J., Watanabe S., Li J.H., Et al., Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2, Hypertension, 41, pp. 1287-1293, (2003)

[8]

Rao G.N., Corson M.A., Berk B.C., Uric acid stimulates vascular smooth muscle cell proliferation by increasing platelet-derived growth factor A-chain expression, J Biol Chem, 266, pp. 8604-8608, (1991)

[9]

Corry D.B., Eslami P., Yamamoto K., Et al., Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system, J Hypertens, 26, pp. 269-275, (2008)

[10]

Sharma R., Coats A.J., Anker S.D., The role of inflammatory mediators in chronic heart failure: Cytokines, nitric oxide, and endothelin-1, Int J Cardiol, 72, pp. 175-186, (2000)

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