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C Reactive Protein (CRP)

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C Reactive Protein (CRP)

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10/08/2020 C Reactive Protein (CRP) Article - StatPearls

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Article Author:
Sara Nehring
Article Author:
Amandeep Goyal
Article Author:
Pankaj Bansal
Article Editor:
Bhupendra Patel
Updated:
6/5/2020 9:08:53 PM
PubMed Link:
C Reactive Protein (CRP) (https://www.ncbi.nlm.nih.gov/books/n/statpearls/article-
18744)

Introduction
C-reactive protein (CRP) was discovered by Tillett and Francis in 1930. The name CRP
arose because it was rst identi ed as a substance in the serum of patients with
acute in ammation that reacted with the "c" carbohydrate antibody of the capsule of
pneumococcus.

CRP is a pentameric protein synthesized by the liver, whose level rises in response
to in ammation. CRP is an acute-phase reactant protein that is primarily induced by
the IL-6 action on the gene responsible for transcription of CRP during the acute
phase of an in ammatory/infectious process. There is some question of whether
dysregulation of the role of CRP in the clearance of apoptotic cells and cellular debris
plays a role in the pathogenesis of systemic lupus erythematosus (SLE), but this has
not been de nitively demonstrated. It has been demonstrated to have
some protective properties in animal studies on lung tissue in alveolitis by reducing
neutrophil-mediated damage to the alveoli and protein leakage into the lung.

CRP has both proin ammatory and anti-in ammatory properties. It plays a role in
the recognition and clearance of foreign pathogens and damaged cells by binding to
the phosphocholine, phospholipids, histone, chromatin, and bronectin. It can
activate the classic complement pathway and also activates phagocytic cells via Fc
receptors to expedite the removal of cellular debris and damaged or apoptotic cells
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and foreign pathogens. This can become pathologic, however, when it is activated by
autoantibodies displaying the phosphocholine arm in auto-immune processes, such
as idiopathic thrombocytopenic purpura (ITP). It can also worsen tissue damage in
certain cases by activation of the complement system and thus in ammatory
cytokines.[1][2][3]

As compared to the erythrocyte sedimentation rate, which is an indirect test for


in ammation, the levels of CRP rise and fall rapidly with the onset and removal of the
in ammatory stimulus respectively. Persistently elevated CRP levels can be seen in
chronic in ammatory conditions such as chronic infections or in ammatory
arthritides such as rheumatoid arthritis.

There are numerous causes of an elevated C-reactive protein. These include acute
and chronic conditions, and these can be infectious or non-infectious in etiology.
However, markedly elevated levels of CRP are most often associated with an
infectious cause[4] (an example of pathogen-associated molecular pattern
recognition). Trauma can also cause elevations in CRP (alarmin response). More
modest elevations tend to be associated with a broader spectrum of etiologies,
ranging from sleep disturbances to periodontal disease.

Specimen Collection
A blood specimen is taken from a peripheral venous draw. A phlebotomist performs
the procedure in most cases. The phlebotomist secures a snug, rubber band around
the upper arm, and the patient pumps his or her st several times.
The phlebotomist palpates the vein to con rm the location and cleanses the area
with an alcohol prep pad. Once the area air dries, the practitioner introduces a
needle into the vein and draws a vial of blood. He or she removes the band from the
patient's arm, and then removes the needle and applies pressure to the
venipuncture site until hemostasis occurs, usually within one minute. A bandage is
applied over the site.

The patient's medications should be reviewed, as these can a ect the outcome of the
test. Fasting is not required before the blood draw. There are no special procedures
required. Complications include oozing at the draw site, bruising or mild tenderness
at the site, or very rarely, infection at the venipuncture site. Other bodily uids, such
as synovial uid, can be tested for in this manner, but frequently are not.

Immunoassays and laser nephelometry are the methods to quantify CRP levels and
are cheap, accurate and fast. To detect lower levels of CRP (0.3 to 1.0 mg/dL), high-
sensitivity CRP methods are recommended as the usual CRP detection tests are less
precise. High-sensitivity CRP only denotes the assay process used, allowing for
detection of lower levels of CRP, and not a di erent, or more speci c, di erential
diagnosis.

Indications
This test is performed when the physician suspects acute or chronic in ammation
(e.g, SLE or rheumatoid arthritis (RA)) or infection. The utility of the hs-CRP for cardiac
screening is debatable. There is some correlation between cardiovascular risk and

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elevated hs-CRP, but the application of this is still controversial especially given the
poor speci city of this test, and it is currently undergoing more evaluation.[5][6][7]

Normal and Critical Findings


Lab values vary, and there is no standard at present. However, in general, the result
is reported in either mg/dL or mg/L. Hs-CRP is usually reported in mg/L. When used
for cardiac risk strati cation, hs-CRP levels less than 1 mg/dL are considered low risk.
Levels between 1 mg/dL and 3 mg/dL are considered a moderate risk and a level
greater than 3 mg/dL is considered high risk for the development of cardiovascular
disease.[8][9]

Interpretation of CRP levels:

Less than 0.3 mg/dL: Normal (level seen in most healthy adults).

0.3 to 1.0 mg/dL: Normal or minor elevation (can be seen in obesity, pregnancy,
depression, diabetes, common cold, gingivitis, periodontitis, sedentary lifestyle,
cigarette smoking, and genetic polymorphisms).

1.0 to 10.0 mg/dL: Moderate elevation (Systemic in ammation such as RA, SLE or
other autoimmune diseases, malignancies, myocardial infarction, pancreatitis,
bronchitis).

More than 10.0 mg/dL: Marked elevation (Acute bacterial infections, viral infections,
systemic vasculitis, major trauma).

More than 50.0 mg/dL: Severe elevation (Acute bacterial infections).

Interfering Factors
Certain medications, such as non-steroidal anti-in ammatory drugs (NSAIDs) will
falsely decrease CRP levels. Statins, as well, have been known to reduce CRP levels
falsely. Recent injury or illness can falsely elevate levels, particularly when using this
test for cardiac risk strati cation. Magnesium supplementation also can decrease
CRP levels.

As mentioned above, mild elevations in CRP can be seen without any systemic or
in ammatory disease. Females and elderly patients have higher levels of CRP.
Obesity, insomnia, depression, smoking, and diabetes can all contribute to mild
elevations in CRP, and the results shall be interpreted with caution in individuals with
these comorbidities.

Complications
Given the highly variable causality of elevated CRP, marginal elevations in the CRP
can be di cult to interpret and should not be used as an isolated test result
interpreted as appropriate for the clinical picture. It is useful in suggesting infection
versus in ammation if the levels are extremely high, but levels between 1 mg/dL and
10 mg/dL can be di cult to interpret accurately. Chronic conditions, such as

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in ammatory arthritis or SLE, can make these levels elevated chronically, making it
harder to determine if there is any signi cance to an elevated hs-CRP level when
using it as a predictive marker for cardiovascular disease.

Clinical Signi cance


Very high levels of CRP, greater than 50 mg/dL, are associated with bacterial
infections about 90% of the time. In multiple studies, CRP has been used as a
prognostic factor in acute and chronic infections, including hepatitis C, dengue, and
malaria. [10][11][12] On the other hand, mild elevations may or may not be clinically
relevant. Clinical correlation is strongly recommended while interpreting the results
of the CRP test.

We recommend

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2019-nCoV infection (third edition)
Author links open overlay panelBureau of
Disease Prevention and Control, National
Health Commission of People's Republic of
China, Biosafety and Health, 2020

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