by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Dr Glenn Reeves, Immunology HAPS (Hunter Area Pathology Service, New South Wales, Australia), has written an excellent article about CRP. Here is an excerpt...
“Inflammation is a protective reaction of vascular connective tissue to damaging stimuli, including infection. The inflammatory response is associated with vasodilatation, increased vascular permeability, recruitment of inflammatory cells (especially neutrophils in acute inflammation), the release of inflammatory mediators from these cells (including vasoactive amines, prostanoids, and reactive oxygen intermediates), and cytokine release. The macrophage-derived cytokines IL-1 and IL-6 are primarily responsible for the acute phase response, a protective change in plasma protein production by hepatocytes...
...C-Reactive Protein (CRP) belongs to the pentraxin family of proteins, so-called because it has five identical subunits, encoded by a single gene on chromosome 1, which associate to form a stable disc-like pentameric structure. It was so named because it reacts with the somatic C polysaccharide of Streptococcus pneumonia, and was first discovered in 1930 by Tillet and Frances. In the presence of calcium, CRP specifically binds to phosphocholine moieties. This gives CRP a host-defensive role, as phosphocholine is found in microbial polysaccharides (where CRP-binding activates the classical complement pathway and opsonises ligands for phagocytosis), the pro-inflammatory platelet-activating factor (PAF) (which is neutralized), and polymorphs (which are down-regulated)...
...CRP is exclusively made in the liver and is secreted in increased amounts within 6 hours of an acute inflammatory stimulus. The plasma level can double at least every 8 hours, reaching a peak after about 50 hours. After effective treatment
or removal of the inflammatory stimulus, levels can fall almost as rapidly as the 5-7-hour plasma half-life of labeled exogenous CRP. The only condition that interferes with the "normal" CRP response is severe hepatocellular impairment...
Clinical Utility of CRP
Screening for inflammatory disease
While an elevated CRP value is not specific for any condition, it is a very sensitive index of ongoing inflammation, and so provides a valuable adjunct to a careful clinical assessment. In differentiating between bacterial and viral infections, the CRP level is of some use. A very high CRP (>100 mg/L) is more likely to occur in bacterial than viral infection, and a normal CRP is unlikely in the presence of bacterial infection. However, intermediate CRP levels (10-50 mg/L) may be seen in both bacterial and viral conditions.
Monitoring the extent and activity of disease
Once a diagnosis has been established, CRP may be used to monitor the patient's response to therapy. The possiblity of intercurrent infection must always be kept in mind, especially when immunosuppressants are being administered. Infections usefully monitored by CRP levels include pyelonephritis, pelvic infections, meningitis, and endocarditis. Serial CRP measurements are important adjuncts to the use of temperature charts in clinical practice, as CRP levels are not affected by drug therapy or thermoregulatory factors. In rheumatoid arthritis, CRP levels correspond well to disease activity and treatment efficacy.
Detection and management of intercurrent infection
In conditions such as lupus and ulcerative colitis, where a major diagnostic dilemma is often posed between a disease flare and super-infection, elevation of the CRP above usual baseline levels for a particular patient may provide a valuable clue to the presence of infection.
CRP or ESR?
CRP is superior to ESR in terms of rapidity of response and specificity for inflammation. The CRP is also more precise and reproducible and a quicker test to perform than the ESR. However, ESR measurements remain helpful in certain clinical situations:
Detection of paraproteinemias, which often don't elicit an acute phase response; and Monitoring of disease activity in Hodgkin's disease and the Polymyalgia Rheumatica-Giant Cell Arteritis syndrome.”
The median normal concentration of CRP is 0.8mg/L, with 90% of apparently healthy individuals having a value less than 3mg/L and 99% less than 12mg/L. Higher values are abnormal and indicate the presence of organic disease. In pregnancy, the normal range is < 20mg/L.
Serum (5mL) should be collected in a non-anticoagulated tube...
1. Pepys MB. The acute phase response and C-reactive protein. The Oxford Textbook of Medicine 1996 Ed. 3, Vol. 2. pp. 1527-1533
2. Young B, Gleeson M, Cripps AW. C-reactive protein: A critical review. Pathology 1991; 23: pp. 118-124
3. Janeway C, Travers P. Immunobiology. 1994; 9:18
4. Seldon M. Erythrocyte Sedimentation Rate. HAPS Newsletter September 1995.
Get more information about immunology crp and related issues as well as...
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