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The Role of Inflammation in Diabetes and Its Complications

Ali A. Rizvi, MD
Volume: 99 Issue: 1 January, 2006

Abstract:

The contribution of inflammation to morbidity in the closely related conditions of cardiovascular disease, obesity, the metabolic syndrome, and type 2 diabetes has been the focus of extensive research and intense speculation over the past decade.1,2 Many inflammatory markers such as C-reactive protein (CRP), fibrinogen, the interleukins, tumor necrosis factor-α, tissue-type plasminogen activator, and serum amyloid A have been included in the ever-expanding list of emerging or “nontraditional” risk factors for the atherosclerotic process,3 and they may represent underlying oxidative stress and generation of free radicals that promote damage to the vascular wall. Endothelial injury, plaque rupture, and atherothrombosis are believed to be related by a series of mutually-related cascades that lead to adverse macrovascular (coronary, cerebrovascular, and peripheral vascular) outcomes.4 Histologic and pathophysiologic studies have established a significant inflammatory component against the backdrop of a complex interplay of clinically recognizable risk factors (for example, hypertension, hyperglycemia, dyslipidemia, obesity, and smoking).5

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References:

1. Danesh J, Wheeler JG, Hirschfield GM, et al. C-reactive protein and other markers of inflammation in the prediction of coronary artery disease. N Engl J Med 2004;350:1387–1397.
 
2. Wannamethee SG, Lowe GD, Shaper AG, et al. Insulin resistance, haemostatic and inflammatory markers and coronary heart disease risk factors in type 2 diabetic men with and without coronary heart disease. Diabetalogia 2004;47(9):1557–1565.
 
3. Muntner P, He J, Chen J, Fonseca V, Whelton PK. Prevalence of non-traditional cardiovascular risk factors among persons with impaired fasting glucose, impaired glucose tolerance, diabetes, and the metabolic syndrome: analysis of the Third National Health and Nutrition Examination Survey (NHANES III). Ann Epidemiol 2004;14:686–695.
 
4. Hsueh WA, Quinones MJ. Role of endothelial dysfunction in insulin resistance. Am J Cardiol.2003;92:10J–17J.
 
5. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation2003;107:499–511.
 
6. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973–979. (Erratum, N Engl J Med1997;337:356).
 
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8. Mosca L. C-reactive protein – to screen or not to screen? N Engl J Med 2002;347:1615–1617.
 
9. Hackam DG, Anand SS. Emerging risk factors for atherosclerotic vascular disease: a critical review of the evidence. JAMA 2003;290:932–940.
 
10. Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arterioscler Thromb Vasc Biol 2004;24:816–823.
 
11. Freeman DJ, Norrie J, Caslake MJ, et al. C-reactive protein is an independent predictor of risk for the development of diabetes in the West of Scotland Coronary Prevention Study. Diabetes 2002;51:1596–1600.
 
12. Pradhan A, Manson J, Rifai N, et al. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001;286:327–334.
 
13. Asakawa H, Tokunaga K, Kawakami F. Elevation of fibrinogen and thrombin-antithrombin III complex levels of type 2 diabetes patients with retinopathy and nephropathy. J Diabetes Complications 2000;14 (3):121–126.
 
14. Saraheimo M, Teppo AM, Forsblom C, et al. Diabetic nephropathy is associated with low-grade inflammation in type 1 diabetic patients. Diabetalogia 2003;46:1402–1407.
 
15. Stehouwer CDA, Gall M, Twisk JWR, et al. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes. Progressive, interrelated, and independently associated with risk of death. Diabetes 2002;51:1157–1165.
 
16. Duncan BB, Schmidt MI, Pankow JI, et al. Low-grade systemic inflammation and the development of type 2 diabetes. The Atherosclerosis Risk in Communities study. Diabetes 2003;52:1799–1805.
 
17. Tall AR. C-reactive protein reassessed. N Engl J Med 2004;350:1450–1452.
 
18. Bruno G, Cavallo-Perin P, Bargero G, et al. Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study. Diabetes Metab Res Rev 2001;17(2):124–130.
 
19. Carr ME. Diabetes mellitus: a hypercoagulable state. J Diabetes Complications 2001;15(1):44–54.
 
20. Takebayashi, K, et al. High-sensitivity C-reactive protein & plasma fibrinogen show different specificities as markers of individual complications in patients with type 2 diabetes. South Med J2006;99:23–27.
 
21. Streja D, Cressey P, Rabkin SW. Associations between inflammatory markers, traditional risk factors, and complications in patients with type 2 diabetes mellitus. J Diabetes Complications2003;17:120–127.
 
22. Bhatt DL, Topol EJ. Need to test the inflammation hypothesis. Circulation 2002;106:136–140.
 
23. Gaede P, Vedel P, Larsen N, et al. Multufactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med 2003;348:383–393.
 

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