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Subject: C-Reactive Protein, High Sensitivity
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High-sensitivity C-reactive protein (hs-CRP or cardiac CRP) is an acute-phase reactant produced by hepatocytes and induced by the release of interleukin 1 and 6. It reflects activation of systemic inflammation. Blood levels of CRP are known to rise rapidly from normal baseline levels to as high as 50 mg/dL as part of the body's nonspecific inflammatory response to infection or injury. The hs-CRP test is more sensitive than the standard CRP test.
Normal range: <0.3 mg/dL (see Table 16.24).
Source: Pearson TA, Mensah GA, Alexander RW Markers of inflammation and cardiovascular disease. Application to clinical and public health practice. A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499–511.
Performing risk assessment for cardiovascular disease: Cardiac disease is believed to be the end result of interplay between minor changes in the cardiovascular endothelium and the corresponding inflammatory response to these changes.
hs-CRP is an independent risk factor for cardiovascular disease, stroke, and peripheral vascular disease. It adds to the predictive value of total cholesterol and HDL cholesterol for future events.
hs-CRP may be useful as an independent marker of prognosis for recurrent events in patients with stable coronary disease or acute coronary syndrome. Recent evidence supporting this potential application has shown that high baseline values of CRP in individuals without a history of cardiac disease were associated with an increased incidence of subsequent cardiac events.
Determining risk of hypotension: hs-CRP has been reported as a risk factor for hypotension.
hs-CRP appears within 24–48 hours, peaks at 72 hours, and becomes negative after 7 days; it correlates with peak CK-MB levels, but the CRP peak occurs 1–3 days later.
Failure of CRP to return to normal indicates tissue damage in the heart or elsewhere. The absence of a CRP increase raises the question of necrosis in prior 2–10 days. CRP is usually normal in patients with unstable angina in the absence of tissue necrosis and a normal troponin T (<0.1 ng/mL).
Peak hs-CRP correlates with peak CK-MB following AMI. CRP may remain increased for at least 3 months following AMI.
Acute or chronic inflammatory change
Tissue injury or necrosis
Ischemia or infarction of other tissues
Infections, inflammation, tissue injury, or necrosis (possible)
Elevated blood pressure
Malignant (but not benign) tumors, especially of the breast, lung, and GI tract
Leukemia: fever, blast crisis, or cytotoxic drugs
Hormone therapy, estrogen, and progesterone
Exercise and weight loss
Moderate alcohol consumption
Drugs (e.g., statins, fibrates, niacin)
Race and gender differences affect CRP levels. One study indicates that black patients have higher levels than white patients and women have higher levels than men.