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Arch Intern Med. 2002;162:389-392.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

HUMAN C-reactive protein (CRP) was originally observed in the plasma of patients with acute infections and was found to react with the C-polysaccharide of the pneumococcus.¹ It is an acute-phase reactant, because of the pronounced rise in concentration after tissue injury or inflammation. This diagnostically sensitive but nonspecific marker for inflammation is produced primarily by the liver but also by lymphocytes.² C-reactive protein appears to recognize both foreign pathogens and damaged host cells and can initiate their elimination by interacting with humoral and cellular effector systems in the blood.³ The work of Ross and others has clearly shown that arteriosclerosis involves a chronic inflammatory process.⁴ Thus, it is not surprising that a series of studies have now found a significant positive relationship between CRP concentration and coronary artery disease (CAD),^5-6 although it remains unclear that this relationship is independent of other inflammatory markers.⁷ Hence, a 70-year-old test used to detect . . . [Full Text of this Article]

DISEASE DISCRIMINATION AND REFERENCE INTERVALS


SPECIFICITY AND POSITIVE PREDICTIVE VALUE

UNSTABLE CORONARY SYNDROMES

CRP FUNCTION IN CAD

CONCLUSIONS


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