الفهرس 
Biochemical Study of C-Reactive ProteinOnly 14 pages are availabe for public view
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Abstract
When used in conjunction with clinical assessment, C-reactive protein measurement is a useful tool for evaluating possible infective or inflammatory disease. However, as with any diagnostic test, false positives and false negatives can occur, and no test represents a replacement for thorough clinical review.
Venous thromboembolic disease is an evolving, multifactorial disease spectrum ranging from DVT to PE. It has been shown adequately in the published data that patients undergoing orthopedic procedures, particularly arthroplasty and trauma patients, are at increased risk for VTE. Virchow’s triad, as described over a century ago, includes venous stasis, a hypercoaguable state, and endothelial damage of the vessel wall. Under these circumstances, patients are at increased risk for VTE. Thus, with an understanding of the risk factors and pathophysiology of VTE, clinicians can adequately assess the risk of VTE, both in the preoperative setting to determine adequate preoperative testing, and to determine postoperative anticoagulation that would be appropriate for that patient’s risk profile.
A two- to six-fold increase in the risk of DVT is associated with increases in plasma concentrations of acute phase proteins including CRP, the nature of the relationship between inflammation and clinical venous thrombosis is not yet definitely established. Thus, measurement of CRP seems unjustified for predicting future venous thrombosis or diagnosing an acute venous thrombosis. The major drawback linking increased CRP concentrations and venous thrombosis is the need to further define the specific genetic, biochemical, and environmental determinants responsible for this association.
In fact, although some biological evidence seems to bestow a procoagulant role for CRP and support the hypothesis that CRP might not only be a marker, but also an active player in the development of venous thrombosis, further evidence is needed to establish which comes first between thrombosis and inflammation (e.g., several pathologies which increase CRP concentrations are also an incidental risk factor for VTE) . Taken together, the evidence linking CRP and VTE are still weak and circumstantial at best. Thus, it seems reasonable to conclude that increased CRP concentrations might be an epiphenomenon rather than a cause of venous thrombosis. As such, the use of statin therapy as a preventive measure for VTE appears unjustified at present, both because of the remarkably high number of patients that need to be treated for 5 years in order to prevent one case of VTE and also, as with use of other medications, the use of statins is not without risk of adverse effects, such as rhabdomyolysis and abnormalities in liver function tests.