C-reactive protein (CRP) has an MW of 118 kD and is a member of the pentraxin family, its molecule being com posed of five protomers containing 206 amino acids each, arranged with cyclic symmetry. The PCR gene has been mapped to chromosome 1, but no genetic defects are known, which supports the hypothesis that it is essential for life. Its synthesis by hepatocytes is under the control of proinflammatory cytokines, mainly IL-6. When stimulation by IL-6 ceases, CRP production by hepatocytes normalizes within 2–4 hours; the half-life of the protein in blood is ~24 hours. Functionally, CRP can bind a wide group of exogenous and endogenous substances, facilitating their elimination from the bloodstream. Removal of the CRP/ligand complex occurs through the activation of several biological systems, such as activation of the classical complement pathway, binding to phagocyte receptors, and binding to the lymphocyte receptor of the Fc fragment of IgG. CRP is considered the marker of inflammation par excellence, as its concentration increases during both acute and chronic inflammation. A value of  <5  mg/L is considered normal; however, this value should be considered indicative as the parameter has not yet been included in international standardization. Its plasma concentration reflects the degree of inflammation and the mass of tissue involved, particularly in acute situations. However, plasma concentrations of CRP within the reference range do not allow the exclusion of a mild or localized inflammatory state in which the magnitude of the acute-phase response is modest. Serial determinations of CRP allow monitoring of disease progression and response to therapy, whereas a single determination may be uninformative due to the high intraindividual biological variability of the protein (CV 26%), and its rapid kinetics. PCR measurement is indicated in rheumatoid arthritis, at first detection, to identify patients at higher risk of progression and for monitoring therapy. In chronic inflammatory bowel disease (e.g., Crohn’s disease), the demonstration of an inflammatory picture is a primary criterion for differential diagnosis from other noninflammatory diseases (such as irritable bowel disease), evaluation of disease activity, and monitoring of therapy. PCR must also be measured when the existence of a possible inflammatory state must be taken into account for correct interpretation of results of other laboratory tests (e.g., in the measurement of AAT, CER, HPT).

It has long been known that chronic inflammation plays a fundamental role in the development of cardiovascular dis ease, and that the persistence of the inflammatory phenome non represents an important prognostic and risk stratification factor. CRP measurement with methods characterized by high analytical sensitivity (detection limit, ~0.3 mg/L) is the marker that best meets the requirements of practicability, due to the adaptability of measurement in automation. Therefore, PCR can currently be considered the parameter of choice in this diagnostic field.

مواضيع ذات صلة

Transthyretin (Prealbumin)

growth hormone (GH,Human growth hormone [HGH],Somatotropin hormone [SH])

glycosylated hemoglobin (GHb, GHB, Glycohemoglobin, Glycolated hemoglobin, Hemoglobin [Hb A1c ], Diabetic control index)

Cultivation of Streptococcus, Enterococcus, and Similar Organisms

Direct Detection Methods of Streptococcus, Enterococcus, and Similar Organisms

Immunoglobulins

Complement

Ceruloplasmin

glucose tolerance test (GTT, Oral glucose tolerance test [OGTT])

glucose, postprandial (2-Hour postprandial glucose [2-Hour PPG], 1-Hour glucose screen)

α1-antitrypsin

Albumin