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Opinion |
1 Laboratory Service, Department of Veterans Affairs Medical Center, Louisville, KY
2 Department of Pathology and Laboratory Medicine, School of Medicine, University of Louisville, Louisville, KY
aAddress correspondence to this author at: Laboratory Service, Department of Veterans Affairs Medical Center, 800 Zorn Ave., Louisville, KY 40206. Fax 502-287-6265; e-mail levinson@louisville.edu.
| The first 20% of the full text of this article appears below. |
Inflammation appears to be an integral part of the process of atherosclerosis that leads to coronary artery disease (CAD) and acute ischemic syndromes (1)(2). Data indicate that high-sensitivity C-reactive protein (hs-CRP) and other inflammatory markers are associated with atherosclerosis and that hs-CRP decreases with statin treatment (3)(4). These are important findings that support the inflammatory disease hypothesis. Moreover, it was suggested that hs-CRP could be used to assess risk of CAD for clinical purposes (5), and several hs-CRP assays are commercially available (6).
In this Journal, Rifai and Ridker (7) suggested an algorithm for assessing risk of CAD based on hs-CRP in conjunction with the ratio of HDL-cholesterol to total cholesterol. The algorithm was later modified to use hs-CRP cutoffs of <1, 13, and >3 mg/L in conjunction with the LDL-cholesterol (LDLC) concentration or the Framingham 10-year risk assessment (8). Several editorials that have accompanied reports on hs-CRP cautioned that use of this test for clinical purposes was premature (9)(10)(11)(12). In spite of these warnings, an American Heart Association/CDC Scientific Statement (13) recommended the use of this test to enhance risk evaluation in certain population groups, although they noted that the benefits of this strategy or any treatment based on it remain uncertain. The clinical recommendations of others argued for even wider use of the test, suggesting that it should be an adjunct for initial screening for global risk assessment in conjunction with conventional lipid testing (8).
We contend that because of its poor predictive value, until its use is better demonstrated, hs-CRP should not be recommended for defining risk. As
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M. B. Pepys, P. N. Hawkins, M. C. Kahan, G. A. Tennent, J. R. Gallimore, D. Graham, C. A. Sabin, A. Zychlinsky, and J. de Diego Proinflammatory Effects of Bacterial Recombinant Human C-Reactive Protein Are Caused by Contamination With Bacterial Products, Not by C-Reactive Protein Itself Circ. Res., November 25, 2005; 97(11): e97 - e103. [Abstract] [Full Text] [PDF] |
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M. B. Pepys CRP or not CRP? That Is the Question Arterioscler Thromb Vasc Biol, June 1, 2005; 25(6): 1091 - 1094. [Full Text] [PDF] |
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N. Rifai High-Sensitivity C-Reactive Protein: A Useful Marker for Cardiovascular Disease Risk Prediction and the Metabolic Syndrome Clin. Chem., March 1, 2005; 51(3): 504 - 505. [Full Text] [PDF] |
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