الوصف
CRP was first described in the sera of patients infected with Streptococcus pneumonia and got its name because it could precipitate the “C” polysaccharide derived from pneumococcal cell wall. CRP is an acute phase reactant (non-specific biochemical response to most forms of tissue damage, infection, inflammation and neoplasia) that can activate the classical complement pathway, stimulate phagocytosis, and bind to immunoglobulin receptors (FcgR) as well as a variety of ligands including chromatin, histones, phosphoethanolamine, fibronectin, small nuclear ribonucleoproteins, laminin, and polycations. CRP induction, which is regulated by IL-6 and enhanced by IL-1b, is part of a larger picture of re-orchestration of liver gene expression during inflammatory states, the acute phase response, in which synthesis of many plasma proteins is increased. CRP has pleiotropic effects; both pro-inflammatory and anti-inflammatory activities have been described.
دواعي الإستعمال
CRP may rise rapidly and markedly after an acute inflammatory stimulus, largely reflecting increased synthesis by hepatocytes. Therefore, it is useful in screening for organic disease, monitoring response to treatment of inflammation and infection and detecting inter-current infection in a few specific diseases characterised by modest or absent acute phase response to those diseases themselves such as SLE. Historically, levels below 10 mg/dL have been regarded as clinically insignificant. However, recent studies have demonstrated an association between slight increases in CRP levels (3 - 10 mg/dL) and risk for cardiovascular disease. Liver failure is the only pathological condition in which CRP levels are reduced.
نوع العينة والكمية والشروط
1 ml Serum 1 ml Li-Heparin and K2-EDTA Plasma Stability: 11 Days at 15-25 °C 2 Months at 2-8 °C 3 Years at (-15)-(-25) °C
إحتياطات خاصة
المعدل الطبيعي
< 5 mg/L < 0.5 mg/dL
