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====== Test: C-Reactive Protein (CRP) ====== | ====== Test: C-Reactive Protein (CRP) ====== | ||
- | C-reactive protein (CRP) is an important and evolutionarily ancient component of the innate immune response.(({{pubmed> | + | C-reactive protein (CRP) is an important and evolutionarily ancient component of the innate immune response.(({{pmid> |
- | The fact that CRP is an independent predictor of stroke and coronary artery disease but also a key contributor to effective bacterial clearance, | + | The fact that CRP is an independent predictor of stroke and coronary artery disease but also a key contributor to effective bacterial clearance, |
- | CRP's name comes from its capacity to bind the C-polysaccharide of // | + | CRP's name comes from its capacity to bind the C-polysaccharide of // |
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===== Function ===== | ===== Function ===== | ||
- | [{{ : | + | [{{ : |
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* **innate host defense** – promotes phagocytosis by opsonizing bacteria (i.e. coating the microbe with antibodies or a complement protein so as to make it palatable to phagocytes) | * **innate host defense** – promotes phagocytosis by opsonizing bacteria (i.e. coating the microbe with antibodies or a complement protein so as to make it palatable to phagocytes) | ||
* **clearance of damaged cells** – binds phosphocholine expressed on the surface of dead or dying (i.e. apoptotic, necrotic) human and bacterial cells | * **clearance of damaged cells** – binds phosphocholine expressed on the surface of dead or dying (i.e. apoptotic, necrotic) human and bacterial cells | ||
- | * **regulation of the inflammatory response** – may act through Fcgamma receptors to reduce inflammation and protect from certain autoimmune diseases(({{pubmed> | + | * **regulation of the inflammatory response** – may act through Fcgamma receptors to reduce inflammation and protect from certain autoimmune diseases(({{pmid> |
- | During the acute phase response, levels of CRP rapidly increase up to 1000-fold, reaching a peak at 48 hours. With resolution of the acute phase response, CRP declines with a relatively short half-life of 18 hours.((// | + | During the acute phase response, levels of CRP rapidly increase up to 1000-fold, reaching a peak at 48 hours. With resolution of the acute phase response, CRP declines with a relatively short half-life of 18 hours.((// |
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CRP has been shown to be generated in response to several gram-negative species of bacteria including: | CRP has been shown to be generated in response to several gram-negative species of bacteria including: | ||
- | * **// | + | * **// |
- | * **// | + | * **// |
Of course, one of the structural components of gram-negative bacteria are endotoxins, the bioavailability of which leads to the immunopathological reaction as described by the Marshall Pathogenesis. | Of course, one of the structural components of gram-negative bacteria are endotoxins, the bioavailability of which leads to the immunopathological reaction as described by the Marshall Pathogenesis. | ||
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C-reactive protein is a predictor of: | C-reactive protein is a predictor of: | ||
- | * long-term risk of heart attack and stroke in apparently healthy men and women(({{pubmed> | + | * long-term risk of heart attack and stroke in apparently healthy men and women(({{pmid> |
- | * risk of cardiovascular events in patients with coronary artery disease(({{pubmed> | + | * risk of cardiovascular events in patients with coronary artery disease(({{pmid> |
- | * development of hypertension(({{pubmed> | + | * development of hypertension(({{pmid> |
- | The association between serum C-reactive protein levels and subsequent risk of stroke, heart attack, and death from cardiac causes supports the importance of inflammation and chronic infection in the pathogenesis of cerebrovascular and coronary artery disease.(({{pubmed> | + | The association between serum C-reactive protein levels and subsequent risk of stroke, heart attack, and death from cardiac causes supports the importance of inflammation and chronic infection in the pathogenesis of cerebrovascular and coronary artery disease.(({{pmid> |
- | Because there are a large number of disparate conditions that can induce CRP production, an elevated CRP level does not have diagnostic specificity.(({{pubmed> | + | Because there are a large number of disparate conditions that can induce CRP production, an elevated CRP level does not have diagnostic specificity.(({{pmid> |
A more sensitive CRP test, called a highly sensitive C-reactive protein (hs-CRP) assay, is available to determine heart disease risk. | A more sensitive CRP test, called a highly sensitive C-reactive protein (hs-CRP) assay, is available to determine heart disease risk. | ||
===== Other diseases ===== | ===== Other diseases ===== | ||
- | In addition to the blood serum, CRP has also been detected in the cerebrospinal fluid,(({{pubmed> | + | In addition to the blood serum, CRP has also been detected in the cerebrospinal fluid,(({{pmid> |
- | CRP also tends to be associated with other chronic inflammatory diseases including rheumatoid arthritis, ankylosing spondylitis, | + | CRP also tends to be associated with other chronic inflammatory diseases including rheumatoid arthritis, ankylosing spondylitis, |
Ultimately, the absence of CRP as a sensitive marker for inflammatory disease may parallel the inconsistency with which any one species of pathogen is found in chronic disease. It would appear that the body employs a variety of mechanisms for responding to infection, only one of which is the production of CRP. | Ultimately, the absence of CRP as a sensitive marker for inflammatory disease may parallel the inconsistency with which any one species of pathogen is found in chronic disease. It would appear that the body employs a variety of mechanisms for responding to infection, only one of which is the production of CRP. | ||
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===== Read more ===== | ===== Read more ===== | ||
- | * [[http:// | + | * [[https:// |
+ | {{tag> | ||
+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
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- | //July 13, 2011// -- [[http:// | + | //July 13, 2011// -- [[https:// |
- | ===== References ===== | + | |
+ | |||
+ | < | ||
+ | Relation Between Serum 25-Hydroxyvitamin D and C-Reactive Protein in Asymptomatic Adults (From the Continuous National Health and Nutrition Examination Survey 2001 to 2006). | ||
+ | Amer M, Qayyum R. | ||
+ | Source | ||
+ | Johns Hopkins University School of Medicine, Baltimore, Maryland. | ||
+ | Abstract | ||
+ | The inverse relation between vitamin D supplementation and inflammatory biomarkers among asymptomatic adults is not settled. We hypothesized that the inverse relation is present only at lower levels and disappears at higher serum levels of vitamin D. We examined the relation between 25-hydroxyvitamin D [25(OH)D] and C-reactive protein (CRP) using the continuous National Health and Nutrition Examination Survey data from 2001 to 2006. Linear spline [single knot at median serum levels of 25(OH)D] regression models were used. The median serum 25(OH)D and CRP level was 21 ng/ml (interquartile range 15 to 27) and 0.21 mg/dl (interquartile range 0.08 to 0.5), respectively. On univariate linear regression analysis, CRP decreased [geometric mean CRP change 0.285 mg/dl for each 10-ng/ml change in 25(OH)D, 95% confidence interval [CI] -0.33 to -0.23] as 25(OH)D increased ≤21 ng/ml. However, an increase in 25(OH)D to >21 ng/ml was not associated with any significant decrease [geometric mean CRP change 0.05 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI -0.11 to 0.005) in CRP. The inverse relation between 25(OH)D below its median and CRP remained significant [geometric mean CRP change 0.11 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.16 to -0.04] on multivariate linear regression analysis. Additionally, | ||
+ | Copyright © 2011 Elsevier Inc. All rights reserved. | ||
+ | |||
+ | PMID: 21996139 | ||
+ | </ | ||
+ | ===== References =====</ |