C-reactive protein
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, the ability of the CRP to add to other methods of predicting heart disease such as the Framingham risk tool is limited.[4] Regardless, the CRP molecule itself does not seem to directly cause cardiac disease.[5]
Risk factor modification, particularly the use of aspirin and the Hydroxymethylglutaryl-coenzyme A reductase inhibitors (i.e., statins, may reduce plaque inflammation.[6] 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).[7][8] 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.
References
- ↑ Husain TM, Kim DH (Spring 2002), "C-Reactive Protein and Erythrocyte Sedimentation Rate in Orthopaedics", University of Pennsylvania Orthopedic Journal 15: 13-16
- ↑ Giant cell arteritis, Merck Manual for Healthcare Professionals
- ↑ Microscoping polyangiitis, Merck Manual for Healthcare Professionals
- ↑ 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
- ↑ 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.
- ↑ F Brian Boudi, Chowdhury H Ahsan, James L Orford, Andrew P Selwyn (Aug 10, 2006), "Atherosclerosis", eMedicine
- ↑ 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.
- ↑ 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.