C-Reactive Protein (CRP), named for its capacity to precipitate the somatic C-polysaccharide of Streptococcus pneumoniae, was the first acute phase protein to be described . CRP is required for the activation of complement (via its interaction with Fc? receptors), the acceleration of phagocytosis and the detoxification of substances released from damaged tissue, to which it binds specifically. After an inflammatory stimulus, a significant rise in CRP may be detected in the serum within 6 hours. As such, CRP was for many years thought of as a sensitive, but non-specific, passive indicator of inflammation. More recent studies have shown that, although CRP also has an anti-inflammatory role in autoimmune diseases such as systemic lupus erythematosus (SLE), it can also initiate or exacerbate the development of inflammatory lesions; for example, it is now thought that CRP is a not only a marker of atherosclerotic disease, but plays a role in its pathogenesis . It has also been reported that CRP inhibits endothelial nitric oxide synthase (eNOS) activity [3,4]. A subsequent study demonstrated the molecular mechanism by which CRP inhibits eNOS , and resulting in decreased eNOS activity, an increase in the production of reactive oxygen species, and the impairment of in vivo vasoreactivity .
No special preparation is required and the patient can continue to take nutritional supplements and medication before the collection of the sample.
Included in Profiles:
Health Risk Profile
CRP production is part of the nonspecific acute-phase response to inflammation, infection, and tissue damage. CRP values are non specific and can never be diagnostic on their own, but can contribute to the evaluation of the inflammatory response, including the cardiovascular disease risk of an individual patient. Furthermore, since trace element levels in the serum may change during inflammation, CRP levels are of relevance in the evaluation of the micronutrient status of patients with an on-going inflammatory response.
Normal baseline serum concentrations of CRP are less than 0.3 mg/dL , but hepatic synthesis is rapidly induced in the acute-phase response. CRP concentrations are often in the range of 5.0-10.0 mg/dL and may reach 500 mg/dL . The half-life of CRP is approximately 19 hours  and is constant under all conditions of health and disease, so the rate of synthesis of CRP is the sole determinant of its serum concentration, reflecting the intensity of the pathological processes stimulating its production.
Please note that this reference interval was amended in May 2015.
Gold (SST). Must reach Biolab within 24 hours of collection
Postal Samples Acceptable:
1. Tillett WS, Francis T. Serological reactions in pneumonia with a non-protein fraction of pneumococcus. J Exp Med 1930;52:561-571.
2. Pepys MB. C-reactive protein fifty years on. Lancet. 1981;8221:653-657.
3. Verma S, Wang CH, Li SH, Dumont AS, Fedak PW, Badiwala MV. A self-fulfilling prophecy: C-reactive protein attenuates nitric oxide production and inhibits angiogenesis. Circulation 2002;106:913-9.
4. Venugopal SK, Devaraj S, Yuhanna I, Shaul P, Jialal I. Demonstration that C-Reactive protein decrease eNOS expression and bioactivity in human aortic endothelial cells. Circulation 2002;106:1439-41.
5. Singh U, Devaraj S, Vasquez-Vivar J, Jialal I. CRP decreases endothelial nitric oxide synthase via uncoupling. J Mol Cell Cardiol 2007;43:780-91.
6. Otsuji S, Shibata H, Umeda M. Turbidimetric immunoassay of serum C-reactive protein. Clin Chem 1982;28:2121-2124.
7. Hutchinson WL, Koenig W, Fröhlich M, Sund M, Lowe GD, Pepys MB. Immunoradiometric assay of circulating C-reactive protein: age-related values in the adult general population. Clin Chem 2000;46:934-938.
8. Vigushin DM, Pepys MB, Hawkins PN. Metabolic and scintigraphic studies of radioiodinated human C-reactive protein in health and disease. J Clin Invest 1993;91:1351-1357.
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