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C-reactive protein (CRP) is a plasma protein, an acute phase protein produced by the liver. It is a member of the pentraxin family of proteins. It should not be confused with C-peptide or Protein C.
C-reactive protein was originally discovered by Tillett and Francis in 1930 as a substance in the serum of patients with acute inflammation that reacted with the C polysaccharide of pneumococcus [1].
The CRP gene is located on the first chromosome (1q21-q23). CRP is a 224 residue protein [2] with a monomer molar mass of 25106 Da, and native cyclic pentamer mass of 125530.
CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis. It is also believed to play an important role in innate immunity, as an early defense system against infections.
CRP is used mainly as a marker of inflammation. Measuring and charting C-reactive protein values can prove useful in determining disease progress or the effectiveness of treatments. Blood, usually collected in a serum-separating tube, is analysed in a medical laboratory or at the point of testing.
Various analytical methods are available for CRP determination, such as ELISA, immunoturbidimetry, rapid immunodiffusion and visual agglutination.
Viral infections tend to give a lower CRP level than bacterial infection.
C-reactive protein blood test[3] Low risk: <1mg/L High risk: >3mg/L How to lower: Exercise, stop smoking, flaxseed, aspirin, niacin, statins, alcohol, clean teeth
Recent research suggests that patients with elevated basal levels of CRP are at an increased risk for diabetes[4], hypertension and cardiovascular disease. A study of over 700 nurses showed that those in the highest quartile of trans fat consumption had blood levels of C-reactive protein (CRP, a pro-inflammatory cytokine which is a cardiovascular disease risk factor) that was 73% higher than those in the lowest quartile[5] Although one group of researchers indicated that CRP may only be a moderate risk factor for cardiovascular disease [6], this study (known as the Reykjavik Study) was found to have some problems for this type of analysis related to the characteristics of the population studied, and there was an extremely long follow-up time which may have attenuated the association between CRP and future outcomes [7]. Others have shown that CRP can exacerbate ischemic necrosis in a complement-dependent fashion and that CRP inhibition can be a safe and effective therapy for myocardial and cerebral infarcts[8].
To measure the CRP level, a "high-sensitivity" CRP or hs-CRP test needs to be performed and analyzed by a laboratory. This is an automated blood test designed for greater accuracy in measuring low levels of CRP, which allows the physician to assess cardiovascular risk. If a result in the low-risk range is found ( < 1 mg/L), it does not need repeating. Higher levels need repeating, and clinical evaluation as necessary.
The role of inflammation in cancer is not well known. Some organs of the body show greater risk of cancer when they are chronically inflamed.
Blood samples of persons with colon cancer have an average CRP concentration of 2.69 milligrams per liter. Persons without colon cancer average 1.97 milligrams per liter. The difference was statistically significant [9]. These findings concur with previous studies that indicate that anti-inflammatory drugs could lower colon cancer risk [10].