for overall hemostatic function. Whole citrated blood is recalcified in the instrument, which then measures the increase in the elastic shear modulus of the clot as it forms over the period of an hour. The width of the graph at any point is the clot strength or elasticity. Five graph parameters are measured when the TEG is complete. The “r” value is a measure of the time it takes for clotting to begin, it is similar to a whole blood clotting time. If the “r” value is prolonged, it indicates a possible coagulation deficiency that could be followed up with PT, PTT and factor assays. The “k” value and angle (a) indicate how fast clot strength is increasing once clotting starts. Reduced “k” or angle may be due to any combination of coagulation deficiencies, reduced platelet function and reduced platelet count. The maximum amplitude (MA) or maximum width of the graph is an indication of the maximum attainable clot strength. Decreases in MA are associated with reduced platelet function or number and with reduced fibrinogen levels. The amplitude after 60 minutes (A60) is a measure of fibrinolysis. If the A60 is significantly less than the MA it indicates in vivo clot lysis may be occurring. THROMBOPHILIA DNA SCREEN The panel consists of two DNA based tests for inherited venous thrombotic disorders, the Factor V DNA Screen (1691G->A, R506Q, factor V Leiden) and the Prothrombin (Factor II) DNA Screen (base 20210 G->A double check). VENOUS THROMBOSIS PANEL Tests included in the panel are APCR, protein C activity, protein S free antigen, antithrombin and lupus inhibitor. The tests should not be performed during an ongoing thrombosis. The only tests that can be run during this period are the APCR and lupus inhibitor assays. The patient should be off oral anticoagulant therapy for a minimum of 7 days. See page 13 for a detailed description of venous thrombosis. VON WILLEBRAND DISEASE PANEL This is a comprehensive panel for the diagnosis of von Willebrand disease including most common subtypes (type 1, type 2 and type 3). Panel consists of von Willebrand factor antigen, factor VIII activity, von Willebrand factor multimer analysis and interpretive report. See page 9 for detailed description of von Willebrand disease and different subtypes. 25 Individual Tests ACTIVATED PARTIAL THROMBOPLASTIN TIME (APTT) Method: Clot-based assay. The activated partial thromboplastin time (APTT) is a screening assay used to detect abnormalities in the intrinsic pathway of coagulation with specific sensitivity to factors VIII, IX, XI and XII. Direct thrombin inhibitors, such as Argatroban and Lepirudin, will falsely prolong the clotting time. ACTIVATED PARTIAL THROMBOPLASTIN TIME (APTT) 1:1 MIX Method: Clot-based assay. The APTT may be prolonged due to factor deficiencies or an inhibitor. A 1:1 mix is used to differentiate between the two. Equal parts of patient plasma and normal plasma pool are combined and an APTT is performed on the mixture. Correction of the prolonged APTT on the mixture indicates a factor deficiency. No correction or partial correction indicates an inhibitor. An interpretive report is given with the result. Direct thrombin inhibitors, such as Argatroban and Lepirudin, will prolong the clotting time. ACTIVATED PROTEIN C RESISTANCE (APCR) Method: Clot-based factor V degradation assay. Activated protein C (APC) resistance is inherited in an autosomal dominant manner. The abnormality is a point mutation in the gene encoding for coagulation factor V and is commonly called the factor V Leiden mutation. This mutation prevents APC from cleaving a peptide bond at ARG-506 that is required to inactivate factor Va. This abnormality occurs in 5% of the normal population and may occur in 20-40% of patients with thrombophilia. A patient with this mutation has a lifelong increased risk of thrombosis. If the disorder is combined with another genetic defect such as a deficiency of protein C, protein S or antithrombin, the risk of thrombosis is further increased. This assays evaluates the degradation of factor Va by APC during coagulation activation. Clotting times are typically prolonged by addition of exogenous APC. If the prolongation is reduced it indicates reduced factor V degradation