C-reactive protein (CRP) is a protein (alpha-globulin) that belongs to the pentraxin family, calcium-binding proteins consisting of five identical subunits that aggregate to form a ring-shaped pentameric molecule. It was discovered in 1930 due to its ability to bind and precipitate pneumococcal polysaccharide C. This phenomenon is due to the calcium- dependent reaction between the phosphatidylcholine residues of polysaccharide C in the bacterial wall and CRP. It can also bind other molecules that contain phosphatidylcholine residues, such as phospholipids, lipoproteins, or damaged cell membranes. Finally, CRP can activate the classical complement pathway and bind to chromatin, histones, and small riboprotein particles; CRP binding to cells or nuclear debris helps to eliminate mate rial that could cause persistent inflammation and produce specific autoimmune reactions against nuclear antigens. Thus, CRP acts as an opsonin, capable of binding to many substances, both exogenous and endogenous, and facilitating their removal from the circulation by promoting their phagocytosis by leukocytes (opsonization).

CRP increases more markedly than other acute phase proteins during inflammation, bacterial infection, and trauma. Viral infections generally do not cause a significant CRP increase; therefore, in the absence of trauma, an increase in CRP indicates bacterial infection. However, if the viral infection is very “inflammatory,” as in the case of adenovirus tonsillitis or mononucleosis, an increase in CRP may be observed.

CRP is synthesized by the liver mainly in response to IL-6; its levels increase within 4–8 hours after the onset of an inflammatory process, peaking within 48–72 hours and decreasing rapidly once the inflammatory state is resolved.

Increased CRP values are indicative of acute or chronic inflammation, autoimmune disease or disease caused by immune complexes, tissue necrosis, and neoplasms; however, normal values do not exclude the presence of small inflammatory foci, or systemic lupus erythematosus (SLE), progressive systemic sclerosis, dermatomyositis, and ulcerative colitis, in which the acute phase response is minimal. The increase in CRP, although indicating the presence of an inflammatory state, does not provide any information on the etiology and, therefore, it is not helpful for diagnostic purposes.

The CRP assay is, however, useful for:

• Assessing the course and severity of the inflammatory process (infections, acute myocardial infarction [AMI], deep vein thrombosis, rheumatic diseases, neoplasms)

• Determining the effectiveness of an anti-inflammatory therapy

• Checking the healing process of surgical wounds, burns, or organ transplantation

• Diagnosing and/or monitoring infection when it is necessary to have this information early, before the results of microbiological investigations (post-operative infectious complications, intensive care, neonatology, infections due to neutropenia from chemotherapy or post- transplantation, monitoring of response to antibiotic therapy).

Table 1 shows the normal and pathological CRP values.

Table1. Interpretation of circulating levels of C-reactive protein

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مواضيع ذات صلة

Procalcitonin

Erythrocyte Sedimentation Rate

plasminogen (Fibrinolysin)

placental growth factor (PGF)

PI-linked antigen (Phosphatidylinositol antigen)

Pre-implantation Diagnosis

Pepsinogen

Parkinson disease testing

Papanicolaou smear (Pap smear, Pap test, Cytologic test for cancer, Liquid-based cervical cytology [LBCC], ThinPrep)

Carrier Diagnosis

oximetry (Pulse oximetry, Oxygen saturation)

5′-nucleotidase