Coagulation factor measurements

Quantification was developed by measuring the relationship between the shortening of the clotting time of the plasma from the patient with the bleeding disorder (deficient plasma) and the amount of normal plasma added to the deficient plasma. This approach remains the basis for specific factor assays however, the deficient plasmas are depleted of individual factors by immunoprecipitation and separation of the antibody-factor complex from the plasma. 

The term coagulation factor deficiency is frequently ambiguous. Previously, it implied a deficit in the functional activity of a component because the clotting time tests measured only the ability of the component to support normal coagulation. The reference for normal functionality is the response of dilutions of plasma from pooled 

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Many of the coagulation factors measured by global coagulation tests have limited stability, and the time and temperature of storage of sample will affect their measurements. Concepts of analyte stability and half-life in plasma extend to markers measured by immunoassay. Markers of platelet activation are affected by artifactual activation in vitro upon collection of the blood specimen. This section will highlight some of the nonanalytical variables that, if uncontrolled, can lead to spurious results and thus affect the interpretation of laboratory data. 

Isaacs, B.S., Husten, E.J., Esmon, C.T., and Johnson, A.E. (1986) A domain of membrane-bound blood coagulation factor Va is located far from the phospholipid surface. A fluorescence energy transfer measurement. Biochemistry 25, 4958-4969. 

Controls were a sample of 723 postmenopausal women without MI who were matched to cases by age, calendar year, and hypertension status. The main outcome measure was risk of hrst nonfatal MI based on current use of HRT and the presence or absence of coagulation factor V Leiden and prothrombin 20210 G A variants among cases and controls, stratihed by hypertension. 

I7(x-Methyl-17 -hydroxy-estra-4,9,l l-trien-3-one (Methyltrienolone, N-99). In the course of a steroid total synthesis [293] this compound (Methyltrienolone, N-99) was prepared it was reported [55] to possess 6000% of the androgenic (ventral prostate index), 7500% of the androgenic (seminal vesicles index), and 12,000% of the anabolic (levator ani index) activity of methyltestosterone. Later the anabolic activity was reported [74] to be 30,000% of that of methyltestosterone. As measured by multiple parameters methyltrienolone turned out to be the most hepatotoxic steroid, causing biochemical symptoms of intrahepatic cholestasis [75]. It was also reported [74] to reduce the excretion of 17-ketosteroids and 17-hydroxycorticosteroids and to cause enhancement of the blood coagulation factors V, VII, and X. It also increases the prothrombin content of the plasma [74]. 

Acute renal tubular damage occurs in association with the liver damage, together with muscle necrosis and hyperkalemia. The muscle necrosis, as demonstrated at autopsy in fatal cases (82), can itself exacerbate the severe electrolyte derangement, particularly marked hyperkalemia, that occurs in liver failure. The measurement of serum concentrations of coagulation factors V (below 10%) and VIII (VIII/V ratio over 30) can have predictive value and can thus be helpful in selecting patients who require hver transplantation (SEDA-17, 99). 

The liver synthesizes coagulation factors I, II, V, VII, IX, and X. ° The prothrombin time is prolonged when any of these factors are absent. In acute liver disease the prothrombin time can be used as an outcome measurement in acetaminophen overdose and acute alcoholic hepatitis In chronic liver disease, the prothrombin time is employed as a marker of decreased synthetic capacity. 

Liver disease may cause a decreased synthesis of coagulation factors, and the subsequent abnormal laboratory results can be difficult to differentiate from DlC. Increased levels of PDFs are not specific to DlC, but elevated levels occur in 85% to 100% of patients with DICT Because PDFs are metabolized in the liver and excreted by the kidney, organ damage may increase the level of PDFs. However, an increased PDF level may help to identify compensated DlC, as it may be the only abnormal laboratory result. D-dimer is formed when plasmin digests cross-linked fibrin thus the level of D-dimer is a more specific measure of PDFs and should be elevated only in Die. ... 

The prothrombin time, which is a measure of the activities of certain coagulation factors made by (he liver, is sometimes used as an indicator of hepatic synthetic function. Prothrombin has a very short half-life, and an increased prothrombin time may be the earliest indicator of hepatocellular damage. 

UF has also been used to concentrate antihemophilic coagulation factor VIII (AHF) with no measurable loss in activity it is particularly susceptible to thermal and shear denaturation. All of the other plasma proteins, including antithrombin III have been concentrated as well. 

Both aPTT and PTT measure the coagulation factors of the intrinsic system during a defined activation time until clotting occurs. The difference between both tests resides in the fact that in aPTT kaolin is added to provoke an additional contact activation of factor XII. 

As for coagulation factors, the findings on the fibrinolytic effects of saturates are still inconclusive and need to be examined by more specific assays, measuring the activities of the separate fibrinolytic factors such as tPA and PAI-1. 

Prothrombin time (PT) is a coagulation assay, which measures the time for plasma to clot upon activation by thromboplastin (a mixture of tissue factor and phospholipids). 

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