C-Reactive Protein (CRP)

An acute-phase reactant produced by the liver in response to the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha.

The prototypic acute-phase protein, C-reactive protein, was originally described as a molecule that was present in the circulation of patients with infections and that was capable of recognizing the C-type polysaccharides of Streptococcus pneumoniae.

CRP is released by hepatocytes to coactivate the complement system in response to antigenic and other stimuli, and is widely available, and a highly sensitive marker of the inflammatory state.
 Systemic inflammation is involved in the pathogenesis of atherosclerosis and is measured by high sensitivity C reactive proteins, a marker for future risk of cardiovascular disease.                                                                       

A sensitive indicator of systemic inflammation.

Strongly induced by interleukin-6.

CRP can be increased 10,000- to 50,000-fold during acute responses to serious infection or major tissue damage, and usually peaks within 48 hours.

Acute rises in CRP may be attributed to exercise, burns, trauma, or acute bacterial or viral infections.

Chronic elevations in CRP levels include: hypertension, elevated BMI, cigarette smoking, cancer, metabolic syndrome, diabetes mellitus, decreased high-density lipoprotein (HDL), elevated triglycerides, estrogen and progesterone hormone use, chronic bacterial or viral infections, autoimmune conditions, and chronic inflammatory conditions.

Chronic CRP elevations may effect endothelial function, coagulation, fibrinolysis, oxidation of low-density lipoprotein (LDL), and atherosclerotic plaque stability.

The atherosclerotic plaque might be considered to be an inflammatory response to injury, including plaque rupture and resultant thrombosis as hs-CRP predicts new coronary events in patients with unstable angina and acute myocardial infarction.

Responds slowly to inflammatory stimuli.

Has a half-life approaching 19 hours.

Levels rise slowly and fall slowly.

C-Reactive Protein an acute-phase reactant synthesized by the liver in response to infection or inflammation.

C-reactive protein (CRP) is a measure of inflammation that got its name from the pneumococcal emphasis on “c”occal bacteria.

Treating serious bacterial infection needs to happen quickly before CRP has time to rise.

There are also multiple causes for CRP elevation so it has low specificity.

Synthesized in the liver.

Produced in the liver in response to elevated cytokine levels after an inflammatory stimulus.

Sensitive biomarker of subclinical inflammation.

CRP measured with prealbumin can differentiate a low prealbumin due to nutritional depletion versus low prealbumin from an acute phase process.

hsCRP (high-sensitivity CRP) value as a predictor for CV disease events controversial suggesting it is a marker, rather than a causal factor for such events (Helfand M).traditional rsik factors

A meta-analysis of 54 prospective studies reported a mosest associated between hsCRP and cardiovascular risk compared to traditional risk factors (Kaptoge S).

hsCRP predictive value is only 1.35% in the JUPITER trial.

JUPITER trial examined the effects of statin therapy in patients without CV disease, with normal LDL and higher than average CRP concentrations: reduction in clinical events with a relative risk reduction of 44%.

Plasma levels of high sensitivity CRP strong predictor of risk of future myocardial infarction, stroke, peripheral arterial disease and vascular deaths among individuals without known cardiovascular disease.

Among patients with acute coronary ischemia, stable angina and history of myocardial infarction levels of high sensitivity CRP associated with increased vascular event rates.

Independent predictor of first acute coronary events.

Plasma levels under genetic influence, so that CRP gene haplotypes associated with plasma levels.

The best predictor of first myocardial infarction in healthy middle-aged men.

Levels are elevated in patients with type I diabetes without macrovascular disease, which suggests I that inflammation may precede atherosclerosis in diabetic patients.

Elevated levels associated with poorer performance in executive functions, suggesting it may be a sensitive assay for cerebral small blood vessel disease.

High cardiovascular risk associated with elevations of CRP can be negated by treatment with statins or aspirin in nondiabetic patients.

Risk of recurrent coronary heart disease events among post-myocardial infarction patients is highest in placebo-treated patients with elevated CRP plasma levels.

Levels increase beginning 6 hours after the onset of ischemia in myocardial infarction and peaking at about 50 hours.

Values after myocardial infarction predict outcomes including death and congestive heart failure.

Elevated among persons who subsequently develop colon cancer.

Elevated levels in cancer free patients associated with increased risk of cancer.

Elevated levels at baseline associated with an early death after the diagnosis of cancer, particularly in patients without metastases (Allin K).

Elevated levels not associated with risk of developing breast cancer (Allin K).

Increased levels predicts for all-cause and cardiovascular mortality in patients on hemodialysis.

Generally made in the liver, but can be produced in smooth muscle cells within diseased coronary arteries.

Implicated in promoting endothelial cell activation.

Predictive value decreases with advancing age.

During infection, inflammation and tissue injury serum levels may rise by a factor of several thousands.

May contribute to innate immunity and suppression of autoimmunity.

Baseline levels moderately increased in obesity and smokers and those with hypertension.

Associated with systemic inflammation response to tumor proliferation and renal cell carcinoma specific mortality.

Elevated levels predict survival for localized and metastatic renal cell cancer.

Elevation a strong predictor of survival in men with prostate cancer (Beer).

Elevated levels associated with increased values of PSA in patients undergoing PSA screening.

Systemic inflammation elevates the C reactive protein and changes the proportion of white blood cells, increasing the neutrophil count and decreasing the lymphocyte count.

High sensitivity C reactive protein (CRP) levels is an inflammatory biomarker.

In healthy patients with high sensitivity C-reactive protein (hsCRP) without elevated low density lipoproteins levels, using a statin reduced the levels of the LDL-C and significantly reduced risk of myocardial infarction, stroke and death.

hsCRP may improve cardiovascular risk stratification beyond conventional factors.

Hs-CRP testing may improve risk stratification, particularly among intermediate cardiovascular risk patients

In patients with stable coronary disease or acute coronary syndromes, hs-CRP measurement may be useful as an independent marker for assessing the likelihood of recurrent events.

An association exists between elevated hs-CRP and sudden death and peripheral arterial disease.

hs-CRP has not been shown to predict the extent of atherosclerotic disease.

Traditional testing measures CRP within the range of 10 to 1,000 mg/L, whereas hs-CRP values range from 0.5 to 10 mg/L.

hs-CRP measures trace amounts of CRP in the blood.

Hs-CRP is the analyte of choice for cardiovascular risk assessment.

Low risk for cardiovascular disease is defined as hs-CRP <1 mg/L, average risk as 1 to 3 mg/L, and high risk as >3 mg/L.

An hs-CRP level >10 mg/L has been observed in acute plaque rupture, which may lead to arterial thrombosis.

The only known factor to interfere with CRP production is liver failure.

hs-CRP assay should be performed in a metabolically stable person without obvious inflammatory or infectious conditions, and it recommended to check two separate levels approximately 2 weeks apart and use the average of the readings for cardiovascular risk assessment and screening purposes.

Patients presenting with an hs-CRP level >2 mg/L with additional cardiovascular risk factors, classified as intermediate cardiovascular risk patients, should undergo repeat testing in 2 weeks to rule out an acute inflammatory response.

Patients with a persistently unexplained, marked elevation of hs-CRP >10 mg/L after repeat testing should be evaluated for noncardiovascular etiologies, such as infection, active arthritis, or concurrent illness.

If the hs-CRP level remains elevated, the patient may be reclassified as being at high cardiovascular risk based on clinical judgment, which would justify initiating therapy for primary cardiovascular prevention.

Risk of cardiovascular disease based on hs-CRP levels: low less than 1 mg/L, average 1-3 mg/L come in high grade it in 3 mg/L.

A high CRP level with a low erythrocyte sedimentation rate can occur in the presence of bacterial infections, thromboembolic disease, DIC, or early in the course of an inflammatory process, but is a non-specific finding.

CRP levels may be a guide to the use of antibiotics in patients with COPD exacerbation.

CRP guided treatment-seven day treatment are not inferior to 14 day antibiotic treatments in patients with uncomplicated gram-negative bacteremia.

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