C-reactive protein: Difference between revisions

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===Predicting risk of atherosclerosis===
===Predicting risk of atherosclerosis===
Abnormal high sensitivity CRP values may assist in assessing lipid measurements in apparently healthy people due to the theory that chronic inflammation precedes [[atherosclerosis]].<ref name="pmid16818927">Lloyd-Jones DM, Liu K, Tian L, Greenland P. [http://annals.org/cgi/content/full/145/1/35 Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease]. Ann Intern Med. 2006 Jul 4;145(1):35-42. PMID 16818927</ref> However, the ability of the CRP to add to other methods of predicting heart disease such as the [http://hp2010.nhlbihin.net/atpiii/calculator.asp Framingham risk tool] is limited.<ref name="pmid16818927"/> Regardless, the CRP molecule itself does not seem to directly cause cardiac disease.<ref name="pmid18971492">{{cite journal |author=Zacho J, Tybjaerg-Hansen A, Jensen JS, Grande P, Sillesen H, Nordestgaard BG |title=Genetically elevated C-reactive protein and ischemic vascular disease |journal=N. Engl. J. Med. |volume=359 |issue=18 |pages=1897–908 |year=2008 |month=October |pmid=18971492 |doi=10.1056/NEJMoa0707402 |url=http://content.nejm.org/cgi/content/full/359/18/1897 |issn=}}</ref>
Abnormal high sensitivity CRP values may assist in assessing lipid measurements in apparently healthy people due to the theory that chronic inflammation precedes [[atherosclerosis]].<ref name="pmid16818927">Lloyd-Jones DM, Liu K, Tian L, Greenland P. [http://annals.org/cgi/content/full/145/1/35 Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease]. Ann Intern Med. 2006 Jul 4;145(1):35-42. PMID 16818927</ref> However, a review found that the ability of the CRP to add to other methods of predicting heart disease such as the [http://hp2010.nhlbihin.net/atpiii/calculator.asp Framingham risk tool] is limited<ref name="pmid16818927"/> except in one study ([[Receiver operating characteristic curve|AUC]] increased from 0.735 to 0.750)<ref name="pmid15023871">{{cite journal |author=Koenig W, Löwel H, Baumert J, Meisinger C |title=C-reactive protein modulates risk prediction based on the Framingham Score: implications for future risk assessment: results from a large cohort study in southern Germany |journal=Circulation |volume=109 |issue=11 |pages=1349–53 |year=2004 |month=March |pmid=15023871 |doi=10.1161/01.CIR.0000120707.98922.E3 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15023871 |issn=}}</ref>. More recently, an analysis of Framingham data from small improvement from using the log of the CRP ([[Receiver operating characteristic curve|AUC]] increased from 0.795 to 0.799).<ref>{{Cite journal | doi = 10.1161/CIRCOUTCOMES.108.831198 | volume = 1 | issue = 2 | pages = 92-97 | last = Wilson | first = Peter W.F. | coauthors = Michael Pencina, Paul Jacques, Jacob Selhub, Ralph D'Agostino, Christopher J. O'Donnell | title = C-Reactive Protein and Reclassification of Cardiovascular Risk in the Framingham Heart Study | journal = Circ Cardiovasc Qual Outcomes | accessdate = 2008-12-08 | date = 2008-11-01
| url = http://circoutcomes.ahajournals.org/cgi/content/abstract/1/2/92 }}</ref> Regardless, the CRP molecule itself does not seem to directly cause cardiac disease.<ref name="pmid18971492">{{cite journal |author=Zacho J, Tybjaerg-Hansen A, Jensen JS, Grande P, Sillesen H, Nordestgaard BG |title=Genetically elevated C-reactive protein and ischemic vascular disease |journal=N. Engl. J. Med. |volume=359 |issue=18 |pages=1897–908 |year=2008 |month=October |pmid=18971492 |doi=10.1056/NEJMoa0707402 |url=http://content.nejm.org/cgi/content/full/359/18/1897 |issn=}}</ref>


Risk factor modification, particularly the use of [[aspirin]] and the [[Hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (i.e., statins, may reduce plaque inflammation.<ref name=EM-CR{>{{citation  | journal = eMedicine  | title =Atherosclerosis | date =  Aug 10, 2006  | author = F Brian Boudi, Chowdhury H Ahsan, James L Orford, Andrew P Selwyn  | url =http://www.emedicine.com/med/topic182.htm}}</ref> [[Statin]] therapy benefited about 1 of every 170 patients with [[LDL cholesterol]] less than 130 mg per deciliter (3.4 mmol per liter), [http://hp2010.nhlbihin.net/atpiii/calculator.asp Framingham risk score] of 10%, and high-sensitivity [[C-reactive protein]] levels of 2.0 mg per liter or higher who took [[rosuvastatin]] 20 mg daily for 2 years if they are similar to the patients in the JUPITER [[randomized controlled trial]] ([[number needed to treat]] for two years is 170).<ref name="pmid18997196">{{cite journal |author=Ridker PM, Danielson E, Fonseca FA, ''et al'' |title=Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein |journal=N. Engl. J. Med. |volume= |issue= |pages= |year=2008 |month=November |pmid=18997196 |doi=10.1056/NEJMoa0807646 |url=http://content.nejm.org/cgi/content/full/NEJMoa0807646 |issn=}}</ref><ref name="pmid14609996">{{cite journal |author=Ridker PM |title=Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial |journal=Circulation |volume=108 |issue=19 |pages=2292–7 |year=2003 |month=November |pmid=14609996 |doi=10.1161/01.CIR.0000100688.17280.E6 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=14609996 |issn=}}</ref> The frequency of death from any cause fell from 2.8% to 2.2% ([[number needed to treat]] for two years is 180). However, this trial was stopped early afer an interim analysis so it is likely that the results are exaggerated.
Risk factor modification, particularly the use of [[aspirin]] and the [[Hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (i.e., statins, may reduce plaque inflammation.<ref name=EM-CR{>{{citation  | journal = eMedicine  | title =Atherosclerosis | date =  Aug 10, 2006  | author = F Brian Boudi, Chowdhury H Ahsan, James L Orford, Andrew P Selwyn  | url =http://www.emedicine.com/med/topic182.htm}}</ref> [[Statin]] therapy benefited about 1 of every 170 patients with [[LDL cholesterol]] less than 130 mg per deciliter (3.4 mmol per liter), [http://hp2010.nhlbihin.net/atpiii/calculator.asp Framingham risk score] of 10%, and high-sensitivity [[C-reactive protein]] levels of 2.0 mg per liter or higher who took [[rosuvastatin]] 20 mg daily for 2 years if they are similar to the patients in the JUPITER [[randomized controlled trial]] ([[number needed to treat]] for two years is 170).<ref name="pmid18997196">{{cite journal |author=Ridker PM, Danielson E, Fonseca FA, ''et al'' |title=Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein |journal=N. Engl. J. Med. |volume= |issue= |pages= |year=2008 |month=November |pmid=18997196 |doi=10.1056/NEJMoa0807646 |url=http://content.nejm.org/cgi/content/full/NEJMoa0807646 |issn=}}</ref><ref name="pmid14609996">{{cite journal |author=Ridker PM |title=Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial |journal=Circulation |volume=108 |issue=19 |pages=2292–7 |year=2003 |month=November |pmid=14609996 |doi=10.1161/01.CIR.0000100688.17280.E6 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=14609996 |issn=}}</ref> The frequency of death from any cause fell from 2.8% to 2.2% ([[number needed to treat]] for two years is 180). However, this trial was stopped early afer an interim analysis so it is likely that the results are exaggerated.

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Template:TOC-right C-reactive protein (CRP) is one of the circulating blood proteins that help the host defense system begin immune defense by phagocytosis performed my macrophage. Its opsonization of target cells is much less precise than from immunoglobulin generated by B-lympocytes for T8 lymphocytes. When activated, it binds, with the antigen, to a surface receptor on macrophages and opsonize the threatening cells.

Diagnostic use

Detecting inflammation

Along with the erythrocyte sedimentation rate, when laboratory results are elevated, the clinician has warning an an acute inflammatory disorder exists.[1] CRP is a better predictor inflammatory disease than the erythrocyte sedimentation rate in a vasculitis such as giant cell arteritis, also called temporal arteritis; cranial arteritis; or Horton's disease [2] or microscopic polyangiitis[3]

Predicting risk of atherosclerosis

Abnormal high sensitivity CRP values may assist in assessing lipid measurements in apparently healthy people due to the theory that chronic inflammation precedes atherosclerosis.[4] However, a review found that the ability of the CRP to add to other methods of predicting heart disease such as the Framingham risk tool is limited[4] except in one study (AUC increased from 0.735 to 0.750)[5]. More recently, an analysis of Framingham data from small improvement from using the log of the CRP (AUC increased from 0.795 to 0.799).[6] Regardless, the CRP molecule itself does not seem to directly cause cardiac disease.[7]

Risk factor modification, particularly the use of aspirin and the Hydroxymethylglutaryl-coenzyme A reductase inhibitors (i.e., statins, may reduce plaque inflammation.[8] Statin therapy benefited about 1 of every 170 patients with LDL cholesterol less than 130 mg per deciliter (3.4 mmol per liter), Framingham risk score of 10%, and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher who took rosuvastatin 20 mg daily for 2 years if they are similar to the patients in the JUPITER randomized controlled trial (number needed to treat for two years is 170).[9][10] The frequency of death from any cause fell from 2.8% to 2.2% (number needed to treat for two years is 180). However, this trial was stopped early afer an interim analysis so it is likely that the results are exaggerated.

Lowering the C-reactive protein

Both aspirin[11] and statins (lovastatin[12] and rosuvastatin[9]) can lower the C-reactive protein with a synergistic effect from combining both drugs[13]. Aspirin is especially effect in reducing coronary heart disease among people with eleveate C-reactive proteins.[14]

References

  1. ↑ Husain TM, Kim DH (Spring 2002), "C-Reactive Protein and Erythrocyte Sedimentation Rate in Orthopaedics", University of Pennsylvania Orthopedic Journal 15: 13-16
  2. ↑ Giant cell arteritis, Merck Manual for Healthcare Professionals
  3. ↑ Microscoping polyangiitis, Merck Manual for Healthcare Professionals
  4. ↑ 4.0 4.1 Lloyd-Jones DM, Liu K, Tian L, Greenland P. Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease. Ann Intern Med. 2006 Jul 4;145(1):35-42. PMID 16818927
  5. ↑ Koenig W, Löwel H, Baumert J, Meisinger C (March 2004). "C-reactive protein modulates risk prediction based on the Framingham Score: implications for future risk assessment: results from a large cohort study in southern Germany". Circulation 109 (11): 1349–53. DOI:10.1161/01.CIR.0000120707.98922.E3. PMID 15023871. Research Blogging.
  6. ↑ Wilson, Peter W.F.; Michael Pencina, Paul Jacques, Jacob Selhub, Ralph D'Agostino, Christopher J. O'Donnell (2008-11-01). "C-Reactive Protein and Reclassification of Cardiovascular Risk in the Framingham Heart Study". Circ Cardiovasc Qual Outcomes 1 (2): 92-97. DOI:10.1161/CIRCOUTCOMES.108.831198. Retrieved on 2008-12-08. Research Blogging.
  7. ↑ Zacho J, Tybjaerg-Hansen A, Jensen JS, Grande P, Sillesen H, Nordestgaard BG (October 2008). "Genetically elevated C-reactive protein and ischemic vascular disease". N. Engl. J. Med. 359 (18): 1897–908. DOI:10.1056/NEJMoa0707402. PMID 18971492. Research Blogging.
  8. ↑ F Brian Boudi, Chowdhury H Ahsan, James L Orford, Andrew P Selwyn (Aug 10, 2006), "Atherosclerosis", eMedicine
  9. ↑ 9.0 9.1 Ridker PM, Danielson E, Fonseca FA, et al (November 2008). "Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein". N. Engl. J. Med.. DOI:10.1056/NEJMoa0807646. PMID 18997196. Research Blogging.
  10. ↑ Ridker PM (November 2003). "Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial". Circulation 108 (19): 2292–7. DOI:10.1161/01.CIR.0000100688.17280.E6. PMID 14609996. Research Blogging.
  11. ↑ Solheim S, Arnesen H, Eikvar L, Hurlen M, Seljeflot I (October 2003). "Influence of aspirin on inflammatory markers in patients after acute myocardial infarction". Am. J. Cardiol. 92 (7): 843–5. PMID 14516890. [e]
  12. ↑ Ridker PM, Rifai N, Clearfield M, et al (June 2001). "Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events". N. Engl. J. Med. 344 (26): 1959–65. PMID 11430324. [e]
  13. ↑ Fisher M, Cushman M, Knappertz V, Howard G (July 2008). "An assessment of the joint associations of aspirin and statin use with C-reactive protein concentration". Am. Heart J. 156 (1): 106–11. DOI:10.1016/j.ahj.2007.12.035. PMID 18585504. Research Blogging.
  14. ↑ Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH (April 1997). "Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men". N. Engl. J. Med. 336 (14): 973–9. PMID 9077376. [e]
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