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Technical Briefs |
Divisions of
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Environmental Hazards and Health Effects and
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Laboratory Sciences, National Center for Environmental Health, and
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Division of Adult and Community Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA 30341
aaddress correspondence to this author at: Centers for Disease Control and Prevention, 4770 Buford Hwy., MS K66, Atlanta, GA 30341; fax 770-488-8150, e-mail esf2@cdc.gov
| The first 300 words of the full text of this article appear below. |
C-reactive protein, an acute-phase reactant, is produced in the liver and belongs to the pentraxin family of proteins (1). This protein is very sensitive to inflammation, and its concentration can increase rapidly in response to a wide range of stimuli. Originally described in 1930 (2), C-reactive protein measurements served mostly in a diagnostic, albeit a nonspecific one, and in a monitoring role in such fields as infectious diseases and rheumatology. In the past decade, as the role of inflammation in cardiovascular disease became appreciated, interest turned to C-reactive protein as a possible risk marker for cardiovascular disease. Since then, studies have shown that the C-reactive protein concentration is positively associated with cardiovascular disease incidence and mortality (3) even when the concentration is <3.0 mg/L, which was previously thought to be "normal" (4).
As these research findings have reached the medical community, the use of C-reactive protein measurements has increased, but guidelines addressing the role of C-reactive protein testing in the primary and secondary prevention of cardiovascular disease have not been developed. To facilitate the development of such guidelines, several issues must be addressed, including population distributions of C-reactive protein concentrations and thresholds for interventions.
A key piece of missing information has been the population distribution of C-reactive protein in the US, especially the distribution of C-reactive protein concentrations <3.0 mg/L. This information is helpful in calculating the fraction of cardiovascular disease attributable to increased C-reactive protein concentrations. The National Health and Nutrition Examination Survey (NHANES) III provided information only on the upper ranges of the C-reactive protein distribution (5)(6) because the C-reactive protein test used in that survey had a lower detection limit of 3.0 mg/L.
Another missing piece of information is whether Creactive protein concentration distributions differ
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S-S. Lee, S. Singh, L. Magder, and M. Petri Predictors of high sensitivity C-reactive protein levels in patients with systemic lupus erythematosus Lupus, February 1, 2008; 17(2): 114 - 123. [Abstract] [PDF] |
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D. E. Laaksonen, L. Niskanen, K. Nyyssonen, K. Punnonen, T.-P. Tuomainen, and J. T. Salonen C-reactive protein in the prediction of cardiovascular and overall mortality in middle-aged men: a population-based cohort study Eur. Heart J., September 1, 2005; 26(17): 1783 - 1789. [Abstract] [Full Text] [PDF] |
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A. Khera, D. K. McGuire, S. A. Murphy, H. G. Stanek, S. R. Das, W. Vongpatanasin, F. H. Wians Jr, S. M. Grundy, and J. A. de Lemos Race and Gender Differences in C-Reactive Protein Levels J. Am. Coll. Cardiol., August 2, 2005; 46(3): 464 - 469. [Abstract] [Full Text] [PDF] |
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M. Di Napoli, M. Schwaninger, R. Cappelli, E. Ceccarelli, G. Di Gianfilippo, C. Donati, H. C.A. Emsley, S. Forconi, S. J. Hopkins, L. Masotti, et al. Evaluation of C-Reactive Protein Measurement for Assessing the Risk and Prognosis in Ischemic Stroke: A Statement for Health Care Professionals From the CRP Pooling Project Members Stroke, June 1, 2005; 36(6): 1316 - 1329. [Abstract] [Full Text] [PDF] |
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B. J. Nicklas, T. You, and M. Pahor Behavioural treatments for chronic systemic inflammation: effects of dietary weight loss and exercise training Can. Med. Assoc. J., April 26, 2005; 172(9): 1199 - 1209. [Abstract] [Full Text] [PDF] |
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G. L. Myers, N. Rifai, R. P. Tracy, W. L. Roberts, R. W. Alexander, L. M. Biasucci, J. D. Catravas, T. G. Cole, G. R. Cooper, B. V. Khan, et al. CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Report From the Laboratory Science Discussion Group Circulation, December 21, 2004; 110(25): e545 - e549. [Full Text] [PDF] |
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E. S. Ford, W. H. Giles, A. H. Mokdad, and G. L. Myers Distribution and Correlates of C-Reactive Protein Concentrations among Adult US Women Clin. Chem., March 1, 2004; 50(3): 574 - 581. [Abstract] [Full Text] [PDF] |
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T. B. Ledue and N. Rifai Preanalytic and Analytic Sources of Variations in C-reactive Protein Measurement: Implications for Cardiovascular Disease Risk Assessment Clin. Chem., August 1, 2003; 49(8): 1258 - 1271. [Abstract] [Full Text] [PDF] |
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