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(Circulation. 2005;111:2414-2415.)
© 2005 American Heart Association, Inc.
Editorial |
From the Department of Medicine, University of Texas Health Science Center, San Antonio (A.F., S.M.H.), and Eli Lilly & Co, Area Medical Center, Vienna, Austria (A.F.).
Correspondence to Steven M. Haffner, Dept of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Drive, MC 7873, San Antonio, TX 782293900. E-mail haffner@uthscsa.edu
Key Words: Editorials cardiovascular diseases diabetes insulin C-reactive protein
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Cardiovascular disease (CVD) is a major cause of morbidity and mortality in patients with diabetes; in type 1 diabetes, CVD typically is related to diabetic nephropathy.1 In both type 1 (DCCT, the Diabetes Control and Complications Trial) and type 2 diabetes (UKPDS, the United Kingdom Prospective Diabetes Study), intensive glucose control affects macrovascular disease less than microvascular disease.2,3 The pathophysiology of CVD in patients with diabetes is complex. Insulin-resistance syndrome risk factors rather than hyperglycemia per se seem to affect the risk of CVD in patients with both type 14 and type 2 diabetes.5
See p 2446
Elevated levels of C-reactive protein (CRP) have been related to CVD risk mainly in nondiabetic populations6; data in diabetic populations are scarce. Much less is known about the relationship of adhesion molecules to insulin resistance, diabetes, and CVD, respectively. This commentary, therefore, focuses on CRP as a marker of chronic, subclinical inflammation related to CVD.
CRP levels are elevated in nondiabetic individuals with increased insulin resistance and the metabolic syndrome,7 in patients with type 2 diabetes,8 and less consistently so in patients with type 1 diabetes.9 Components of the insulin-resistance syndrome, including obesity, rather than hyperglycemia contribute significantly to elevated CRP levels.7,8 A proinflammatory state prevails also in prediabetic individuals 5 years before the actual onset of (type 2) diabetes.10 In prediabetic individuals, increased insulin resistance rather than impaired insulin secretion defines the proatherogenic state, as exemplified by elevated blood pressure and dyslipidemia,11 as well as inflammation.12
Given the strong correlation of
Related Article:
Circulation 2005 111: 2446-2453.
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