C-reactive protein— Part I

C-reactive protein— Part I

The very first response of living cells to injury or a noxious stimulus, anywhere in human body is inflammation. The inflammation is then followed by secrection of cytokines, mostly interlukines IL-1, IL-6, IL-8 and TNFα. The liver responds by means of releasing acute phase reactants. One of the most sensitive markers among the acute phase proteins is the C-reactive protein. Other acute phase proteins are proteinase inhibitors, coagulation factors, complement factors, transport proteins and miscellaneous proteins like the serum amyloid A protein.

C-reactive protein (CRP) derived its name from its ability to precipitate the somatic C-polysaccharide of Streptococcus pneumoniae. It is a member of the pentraxin family of proteins. CRP was originally discovered by Tillett and Francis in 1930 as a substance in the serum of patients with acute inflammation. The CRP gene is located on the first chromosome (1q21-q23). Human CRP is a calcium-dependent ligand binding protein, which binds with highest affinity to phosphocholine (PC) residues, as well as a variety of other autologous and extrinsic ligands, and aggregates or precipitates the cellular, particulate or molecular structures bearing these ligands.

In a healthy individual, the median concentration of CRP is 0.8mg/l, but following a stimulus it could rapidly increase by as much as 10,000 fold, with de novo hepatic synthesis, serum concentrations beginning to rise by about 6h, and peaking around 48h. The CRP levels also vary in relation to age and sex (females having slightly higher concentration). CRP levels accurately reflect the ongoing inflammatory process than any other biochemical parameters, in most if not all diseases. The CRP value is thus a very useful non-specific biochemical marker of inflammation, measurement of which contributes importantly to: (i) screening for organic disease; (ii) monitoring the response to treatment of inflammation and infection; and (iii) detecting intercurrent infection in the few specific diseases characterized by modest or absent acute-phase responses to those diseases themselves.


CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. It is thought to assist in complement binding to foreign and damaged cells and affect the humoral response to disease. It is also believed to play an important role in innate immunity, as an early defense system against infections. CRP is also thought to stimulate tissue factor production.

Measuring CRP:

CRP measurements are used to asses the active inflammation in sepsis or arthritis. High sensitive methods which allow detection of low level states of inflammation are important in CVD risk.

The following types of CRP assays have been cleared: by U.S. Department of Health and Human Services Food and Drug Administration

  • Conventional C-Reactive Protein (CRP)
  • High sensitivity CRP (hsCRP)
  • Cardiac C-Reactive Protein (cCRP)

The American Heart Association (AHA) has set a parameter for what is considered as normal hsCRP level:

  • If hs-CRP level is lower than 1.0 mg/L, a person has a low risk of developing cardiovascular disease.
  • If hs-CRP is between 1.0 and 3.0 mg/L, a person has an average risk.
  • If hs-CRP is higher than 3.0 mg/L, a person is at high risk.

If, after repeated testing, patients have persistently unexplained, markedly elevated hs-CRP (greater than 10.0 mg/L), other evaluation should be considered to exclude noncardiovascular causes.

As for getting ones CRP level measured this is what AHA has to say: “If a person’s cardiovascular risk score — judged by global risk assessment — is low (the possibility of developing cardiovascular disease is less than 10 percent in 10 years, no test is immediately warranted. If the risk score is in the intermediate range (10-20 percent in 10 years), such a test can help predict a cardiovascular and stroke event and help direct further evaluation and therapy. However, the benefits of such therapy based on this strategy remain uncertain. A person with a high risk score (greater than 20 percent in 10 years) or established heart disease or stroke should be treated intensively regardless of hs-CRP levels.”

(The next post will discuss about the various disease and in specific relation of CRP to cardio vascular disease)

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