The Stuart-Prower Factor Assay and its Clinical Significance

1958 ◽  
Vol 02 (01/02) ◽  
pp. 024-038 ◽  
Author(s):  
F Bachmann ◽  
F Duckert ◽  
F Koller

SummaryA simple one-stage test for the determination of the Stuart-Prower factor is described. The method is a modification of the classical Factor VII complex assay, using a Russell’s viper venom (Stypven)-cephalin reagent instead of brain thromboplastin. The optimal conditions for the assay system have been systematically investigated. A high dilution of RVV (1 : 200 000) has given the best results. The system is not influenced by different concentrations of fibrinogen, prothrombin, Factor V, Factor VII and plasma thromboplastin precursors other than Stuart-Prower factor. Variations of lipoid and/or platelet contents of the plasma do not alter the results. Stuart-Prower factor is not activated by glass contact. The method has proved most valuable in the detection of heterozygous Stuart-Prower factor deficiencies. Comparison with a specific Stuart-Prower factor assay using patient’s plasma deficient in Stuart-Prower factor gave variations not greater than 15%. If determined simultaneously with the Quick one-stage ‘prothrombin time’, the test may provide a better control of patients under treatment with dicoumarol derivatives.

1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.


PEDIATRICS ◽  
1961 ◽  
Vol 27 (2) ◽  
pp. 204-213
Author(s):  
Helen I. Glueck ◽  
James M. Sutherland

A case of factor-VII deficiency of a congenital nature in a Negro male child has been reported. As far as can be determined, this is the first case reported in this race. The defect was detected at 6 hours of age. Prothrombin, as contrasted to factor VII, after initially low levels normally found in infants, rose to adult levels. The patient's one-stage prothrombin time has ranged between 25 to 35 second (normal 11 to 12 seconds). In spite of this, he has never shown any manifestations of hemorrhage. The patient's family was studied and the findings indicate that the patient's defect represented a homozygous state and that both parents with a less severe deficiency were heterozygous for the trait. The defect is an autosomal disorder directly inherited. It is clinically apparent and easily detected only in the homozygous state. The heterozygous state is characterized by a very slight prolongation of the one-stage prothrombin time, the difference from the control value being so minimal as to be overlooked. In one subject studied, an aunt of the propositus, the quantitative defect (42% of normal) could not be regularly detected by the usual methods. Only by using the plasma of the propositus as the test plasma, was the defect in her plasma detected, thus explaining the transmission of the trait to her offspring. These findings explain the difficulties previously encountered in understanding the inheritance of the disorder.


PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1151-1151
Author(s):  
ARMAND J. QUICK

I wish to call your attention to a matter concerning the article of Fresh et al., "Blood Prothrombin, Proconvertin and Proaccelerin in Normal Infancy: Questionable Relationships of Vitamin K" which appeared in Pediatrics (19:241, 1957). On page 248 the following statement occurs: "Notwithstanding the insufficiently substantiated claims of Quick et al., that the simple `prothrombin time' determination is uninfluenced by an excess of factor V or factor VII,...." I consider such a statement inexcusable. While they could have said that "we regard the claims to be insufficiently substantiated, etc.," they made their statement to appear as a fact, which is not justified.


1980 ◽  
Vol 2 (3) ◽  
pp. 185-190
Author(s):  
J. MONASTERIO ◽  
J. JUNCÁ ◽  
J. TORRAS ◽  
B. CLOTET ◽  
M. CERVANTES ◽  
...  

1981 ◽  
Author(s):  
A P Bode ◽  
H Sandberg ◽  
F A Dombrose ◽  
B R Lentz

Reconstitution of membrane-associated Factor V-like activity (PF1) in human platelets isolated from severe F.V-deficient donors was assessed following incubations in citrated normal platelet free plasma. Coagulant activities were measured using: a one-stage prothrombin time, the Stypven time and a modified KAPTT in which the kaolin particles were removed from the plasma prior to recalcification. The supernatant from 3x frozen-and-thawed lysed normal platelets was used as a standard for 100% PF1 and 100% PF3. Normal platelets gel filtered or centrifuge-washed in the presence of adenosine, theophylline and PGEj had <1% available PFI and PF3, whereas platelets from severe F.V-deficient donors isolated by the same procedure had no PF1 and the same amount of PF3. The supernatant from 3x frozen-and-thawed lysed F.V-deficient platelets also had no PF1 but had 100% total PF3. When gel filtered, PFl-deficient platelets were incubated in normal plasma, they acquired about 1% PF1 which did not change following freezing-and-thawing. By contrast, PFI-deficent platelets washed in the absence of these inhibitors had 15-20 times more available PF3 and acquired about 15-20 times more total PFI after incubation in normal plasma. When either the crude frozen-and-thawed lysed membrane supernatant from these PFl-deficient platelets (100% available PF3) or a partially purified membrane-rich fraction from this supernatant was incubated with normal plasma, then 100% reconstitution of PFI was achieved. PF1 was also reconstituted in a purified system using all-or-none binding when the PF3-containing lipid-protein particles secreted by platelets, upon collagen induced aggregation, were incubated with purified human F.Va. Following incubation, these particles had the same amount of PFI as the PF3-containing particles from normal platelets. It is apparent that in human platelets a correlation exists between the amount of available PF3 and the capacity to reconstitute PFI.


1979 ◽  
Vol 42 (04) ◽  
pp. 1115-1127 ◽  
Author(s):  
E A Loeliger ◽  
L P van Halem-Visser

SummaryThe fourteen types of thromboplastin included in the ICTH/ICSH Collaborative Study on Prothrombin Time Standardization were investigated with respect to their sensitivity for factor VII, activation products, and PIVKAs. All of these thromboplastins displayed sufficient factor VII sensitivity, and all were sensitive to activation products. After correction for the overall sensitivity slope, rabbit plain thromboplastins were the most sensitive preparations and human as well as rabbit diluted the least sensitive; bovine brain thromboplastin lost its exceptional position. Sensitivity to activation products explains why factors II, VII, and X present in artificially prepared abnormal plasmas may be difficult to assess accurately. Also, all thromboplastins appear to be sensitive for both PIVKA VII and PIVKA X. PIVKA VII acts as a procoagulant which increases the amount of factor VII measured by the one-stage assay technique. PIVKA X inhibits and thus reduces the activity of factor X. The procoagulant activity of PIVKA VII is particulary pronounced for the two lung-brain rabbit thromboplastins (Lyoplastin and Simplastin), whereas the anticoagulant action of PIVKA X is strongest with bovine brain thromboplastin (Thrombotest). Considered as a group, rabbit thromboplastins appear to be less sensitive for PIVKA X and more sensitive for PIVKA VII.As judged from thromboplastin calibration results, all three types of lyophilized reference plasmas are to some degree distinguishable from fresh patient plasmas. Primary calibration of a thromboplastin must therefore still be performed with freshly prepared normal as well as patient plasmas.


1959 ◽  
Vol 197 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey ◽  
John Harris ◽  
Kenneth Peters

On infusing a dilute solution of thrombin intravenously into a dog at a constant and carefully regulated rate, no massive thrombosis occurs and no evidence of a thrombo-embolic state is obtained. An occult type of intravascular clotting is produced which is characterized by a progressive decrease of the level of fibrinogen, thrombocytopenia, a prolonged prothrombin time and a poor consumption of prothrombin. Labile factor (factor V) and thromboplastinogen (factor VIII) are strikingly diminished. Prothrombin is moderately decreased while stable factor (factor VII) and PTC (factor IX) are not significantly affected. It is postulated that the adsorption of thrombin to the fibrin fibrils which are filtered off in the capillary network and destroyed, constitutes the principal means for preventing dangerous accumulation of thrombin in the blood.


1958 ◽  
Vol 36 (9) ◽  
pp. 953-958 ◽  
Author(s):  
L. G. Israels ◽  
E. Friesen ◽  
C. Sinclair

The adsorption of beef plasma on asbestos markedly shortens the one-stage prothrombin time of the plasma when tissue thromboplastin is used as the throm boplastic agent. This adsorption on asbestos does not affect the Russell viper venom time of the plasma. The adsorbed plasma exhibits increased factor VII activity over that of the original plasma. An eluate can be prepared from the asbestos which prolongs the one-stage prothrombin time sof beef and human plasma.


1978 ◽  
Vol 39 (03) ◽  
pp. 592-599 ◽  
Author(s):  
Neville W Spurling ◽  
Janet Savory

SummaryOne-stage prothrombin times of normal and of factor VII-deficient beagle plasma were determined with two types of beagle brain thromboplastin, one prepared from normal beagles and the other from factor VII-deficient beagles. There was little difference between the reagents in the prothrombin times obtained for normal plasma. However, when factor VII-deficient plasma was tested, reagent prepared from factor VII-deficient beagles gave considerably longer prothrombin times than were obtained with the normal reagent and the difference increased with increasing reagent concentration to a maximum at 140 mg/ml.Prothrombin times of a series of mixtures of normal and factor VII-deficient plasma indicated that the presence of only 1/90 part of normal plasma was necessary to compensate for the difference between the two reagents. Determination of the iron content of the reagent suggested that the microcirculation of an average brain contained some 1.8 g of whole blood.The finding that brain thromboplastin prepared from factor VII-deficient beagles is more sensitive to a deficiency of factor VII in plasma, presumably a result of the smaller quantity of factor VII present in the reagent, is compatible with the known kinetics of extrinsic coagulation.


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