C-reactive protein as a novel biomarker - Essay Example

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Preview: C-reactive protein (CRP) is a relatively nonspecific marker of inflammation. However, it can be used to monitor the severity and progression of some well-defined cardiovascular diseases. For example, it can predict serious events in patients with coronary artery disease (CAD) who are hospitalized with acute coronary syndrome, myocardial infarction (MI), or advanced peripheral vascular disease…
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C-reactive protein as a novel biomarker
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Download file to see previous pages This process leads to the formation of foamy macrophages and atheromatous plaques and, finally, to atherothrombotic disease. Atherosclerosis is associated with high morbidity and mortality.
Although measurement of lipid levels, stress testing, and coronary angiography are effective indicators of the extent and severity of the disease, circulating markers that could be easily and noninvasively measured would be powerful tools to diagnose, monitor, and intervene in this disease process. One promising marker is CRP, a major acute phase response protein synthesized in the liver in response to the elaboration of acute phase response cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) (figure 1). Other associated acute phase proteins include serum amyloid A protein, fibrinogen, and mannan-binding lectin.
CRP is a member of the pentraxin protein family, which is so named because these proteins possess five identical subunits. CRP, which is elaborated dramatically during acute inflammation, augments the immune response to certain antigens, activates complement, and increases the monocytic production of tissue factors (1).
CRP binds to phosphoryl choline on bacterial surfaces, acting as an opsonin and playing a pivotal role in host defense. Interestingly, CRP also appears to bind low-density lipoprotein cholesterol (LDL-C) in vitro, which suggests a direct interaction with the atherogenic lipids (2).

Why use CRP as an indicator
Atherogenesis is initiated by endothelial injury, which is followed by activation of endothelial cells, up-regulation of cytokines and adhesion molecules (eg, soluble intercellular adhesion molecules, E-selectin), and migration of inflammatory cells into the subendothelium (see figure 1). In this scenario, IL-1, IL-6, and TNF-alpha stimulate CRP synthesis by inducing hepatic gene expression (3).

Because atherosclerosis is now considered an inflammatory disease and an elevated level of CRP in ...Download file to see next pagesRead More
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