Thrombin time assay

V Mucosal tract bleeding Prolonged PT and aPTT Normal thrombin time Specific factor V assay... 

XIII Umbilical cord, intracranial, and joint bleeding recurrent miscarriages, impaired wound healing Normal PT, aPTT, thrombin time, bleeding time Specific factor XIII assay... 

The physiological expression of oral anticoagulant action is an increase in the time required for clotting in the prothrombin time assay. The slowing of all of the reactions that lead to the formation of thrombin is the direct result of the reduced concentrations of the vitamin K-related proteins in the reaction complexes on the membrane surface. The effects of oral anticoagulant blockage on the carboxylation reaction are common to all vitamin K-related proteins. 

Heparin therapy may be monitored by its increases in clotting time in the APTT, although this method for measuring heparin is difficult to standardize. Heparin is more specifically assayed by its effect on factor Xa inactivation by antithrombin. Such factor Xa-based heparin assays usually employ purified factor Xa as a reagent and factor X-deficient substrate plasma as the source of antithrombin. The prolongation of the clotting time that results from the heparin in the patient s plasma is compared with pooled normal plasma that is known to be free of heparin. Many variations of this heparin assay are available. Heparin assays can use thrombin rather than factor Xa, however, the low-molecular-weight heparins are not reliably measured in thrombin-based assays. 

Accepting the above limitations of our knowledge of the true in vivo reaction sequence, a series of clot-endpoint tests has been used for many years to determine the hemostatic balance in any patient. The first, known as the thrombin time test, can be used to measure the concentration of fibrinogen (B15). The second assay, the activated partial thromboplastin time test (APTT), measures the components of the intrinsic pathway (M4). These include the serine proteases (Factors XII, XI, X, and II), the cofactors (Factors VIII and V) and again, fibrinogen. Most of the hereditary deficiencies... 

Displacement by plasma of radiolabeled thrombin and radio-labeled thrombin-antithrombin III inactive complex from a heparinized surface was measured and found to be significant for example, removing 63% of the thrombin and 90% of the complex that could not be removed by phosphate-buffered saline alone. Heparin-poly(vinyl alcohol) (PVA) gel beads with a very low heparin release rate, prepared by acetal coupling of the heparin to the PVA, adsorbed thrombin and potentiated the inactivation of thrombin by antithrombin 111, as measured by both thrombin time and chromogenic substrate assays. 

In Vitro Activity of Bound Heparin. The prolongation of the thrombin time caused by the addition of heparin-PVA beads to plasma is contrasted with the negligible effect of PVA beads without heparin in Figure la. A similar prolongation was observed for the plasma recalcification time (Figure lb). In both cases, clumping or adhesion of the beads caused presumably by fibrin was the end point of the assay. 

In healthy volunteers orally administered garlic capsules at the manufacturer s recommended dose (amount not specified) daily for two weeks, no effects on platelet function or other hematological parameters were observed, including prothrombin time, partial thromboplastin time, thrombin time, bleeding time, the collagen/epinephrine assay, or the collagen/adenosine diphosphate assay. Aspirin was used as a positive control and markedly inhibited platelet function (Beckert et al. 2007). 

Lab test abnormalities In general, adjust the dosage (infusion rate) according to the aPTT ratio (patient aPTT at a given time over an aPTT reference value, usually the median of the laboratory normal range for aPTT see Administration and Dosage). Other thrombin-dependent coagulation assays are affected by lepirudin. 

The roles of Factors V and VIII in the reaction sequence leading to thrombin formation have slowly become known. Both these proteins are very large in size, serve as cofactors in this cascade reaction sequence, and increase by approximately 100 times their cofactor activity upon exposure to minimal concentrations of thrombin. Likewise, both factors are inactivated by a similar mechanism when attacked by activated protein C (Fll). Tans and coworkers utilized synthetic substrate assays specific for Factor Xa and thrombin to demonstrate that both these factors act predominantly by increasing... 

A PF3 indirect assay using a synthetic substrate was developed in 1979 by Sandberg and Anderson (S2). This test monitored thrombin production with the substrate S-2238 and claimed to be 10 times more sensitive than the above assay and to be free of EDTA interference. Later Harsialvi and coworkers claimed to improve the technique by adding soybean trypsin inhibitor to better control the reaction (H2). These workers believe this assay can be used for diagnosis of platelet disorders. 

Bioluminescence and Bioluminescence Resonance Energy Transfer Assays in Mkrofluidks, Fig. 6 (a) Time-dependent BRET ratio of the control assay and the positive (27 pM) assay, (b) Dose response curve for thrombin assay a limit of detection of 19.8 pM and a sensitivity of... 

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