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C-reactive protein (CRP) is an acute phase protein synthesized in the liver. It is a general marker of inflammation that begins to rise four to six hours after tissue injury. This is much earlier than other acute phase reactants, which do not begin to increase until 24 hours or more. CRP also increases to much higher levels than other acute phase proteins, making it the most sensitive indicator of small inflammatory stimuli. CRP concentration peaks at 48 hours and then decreases with a half-life of 48 hours. Generally, a CRP level above 10 mg/L indicates significant inflammatory disease. Historically, CRP has been used clinically to monitor inflammatory disease activity, detect postoperative and neonatal infections and assess transplant rejection. Recently, more sensitive methods for measurement of CRP have become available. They have been referred to as high-sensitivity CRP (hs-CRP) because they can accurately measure very low levels of CRP. Current evidence indicates that inflammation plays a central role in the pathogenesis of atherosclerosis and thrombosis and that CRP is a marker of low-grade vascular inflammation that is predictive of future cardiovascular events. All prospective studies reported to date have indicated that basal CRP values in the highest quartile or quintile of data are associated with a 2.3 to 4.8-fold increased relative risk of developing cardiovascular disease. These studies have convincingly demonstrated that hs-CRP is a risk factor for future myocardial infarction, ischemic stroke, peripheral arterial disease and coronary heart disease mortality in apparently healthy men and women. In addition, elevated CRP is predictive of cardiac complications in patients with unstable angina or myocardial infarction. Increased CRP is additive to the predictive value of total and HDL cholesterol in determining cardiovascular risk. Aspirin decreases the relative risk of future myocardial infarction most effectively in patients with the highest CRP. This observation raises the possibility that the beneficial effect of aspirin is due to its anti-inflammatory effect rather than its anti-platelet effect. Pravastatin has also been shown to reduce the relative risk of recurrent coronary events most effectively in patients with the highest CRP levels. Statin drugs may have anti-inflammatory as well as lipid-lowering properties. In contrast, estrogen replacement therapy, which is associated with increased risk of thrombosis, increases CRP levels, suggesting that it may promote pro-inflammatory events. Overweight (BMI 25-29) and obese (BMI >30) men and women have higher hs-CRP values than normal-weight (BMI < 25) individuals. CRP should not be ordered for cardiac risk assessment if a patient has had recent inflammation, infection or trauma. A period of 2 weeks is usually adequate for CRP concentrations to return to basal levels. The predictive value of CRP is greatly improved if two measurements are made approximately 1 month apart and the lowest of these values is used to determine the appropriate quintile for cardiovascular risk assessment. It is especially important to repeat CRP values >5 mg/L to avoid misclassification because of clinically silent infection.
Sequential measurement of CRP is important for effective monitoring of inflammation. Specimen requirement is a minimum of 0.5 mL of serum (one SST tube). Gross lipemia or hemolysis interferes with this test. |
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