![]() ![]() The intraindividual coefficient of variation (CV) can vary as much as 46% over a 2 to 3 week period. The biggest challenge to interpreting CRP elevation is the large variability in measurement that occurs in following an individual over time. Overweight (BMI 25-29) and obese (BMI >30) men and women have higher CRP values than normal-weight (BMI 5 mg/L to avoid misclassification because of clinically silent infection. Estrogen replacement therapy increases CRP levels. Median CRP levels are lower in men than in women. Individuals 80 years and older have CRP levels that are almost two times higher than individuals in their 40s. Many factors can influence baseline CRP levels including ethnicity, age, gender, body weight and smoking status. Increased CRP is additive to the predictive value of total and HDL cholesterol in determining cardiovascular risk. ![]() They also concluded that there was moderate evidence for using CRP to further stratify the risk of patients with intermediate risk (10-20%) of having a cardiovascular event in the next decade. Preventive Services Task Force concluded that there was strong evidence that CRP is associated with cardiovascular disease events (Buckley DI, et al. The lower limit of quantification should be significantly below 1.0 mg/L.Ĭurrent 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. The coefficient of variation for hsCRP assays should be 10% of less near the medical decision point of 1.0 mg/L. HS-CRP assays reliably measure levels between 1.0 mg/L and 10.0 mg/L. More sensitive CRP assays, called high-sensitivity CRP (hs-CRP), have been developed to detect lower levels of inflammation that accompany cardiovascular disease. Sequential measurement of CRP is important for effective monitoring of inflammation. The upper limit of quantification is approximately 500 mg/L. When using CRP to evaluate infection, inflammation or tissue injury, a CRP level less than 5 mg/L is considered negative and a value greater than 10 mg/L is considered positive. Historically, CRP has been used clinically to monitor inflammatory disease activity, detect postoperative and neonatal infections and assess transplant rejection. CRP concentration peaks at 48 hours and then decreases with a half-life of 48 hours. CRP also increases to much higher levels than other acute phase proteins, making it the most sensitive indicator of small inflammatory stimuli. This is much earlier than other acute phase reactants, which do not begin to increase until 24 hours or more. It is a general marker of inflammation that begins to rise four to six hours after tissue injury. CRP also binds C1q and activates the classical complement cascade.ĬRP is synthesized in hepatocytes and alveolar macrophages in response to cytokines, particularly IL-6. CRP acts as an opsonin by binding to bacterial or damaged human cells and the immunoglobulin receptors on phagocytes, thereby promoting phagocytosis. C reactive protein (CRP) is an acute phase reactant that plays a role in innate immunity. ![]()
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