Antithrombin III contribution to cholestasis differential diagnosis: its correlation with one stage prothrombin time and factor V

1980 ◽  
Vol 2 (3) ◽  
pp. 185-190
Author(s):  
J. MONASTERIO ◽  
J. JUNCÁ ◽  
J. TORRAS ◽  
B. CLOTET ◽  
M. CERVANTES ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Prothrombin Time ◽  
Antithrombin Iii ◽  
Factor V ◽  
One Stage

Perioperative Evaluation of Bleeding Diathesis

Hematology ◽  
2006 ◽  
Vol 2006 (1) ◽  
pp. 457-461 ◽  
Author(s):  
Lawrence L.K. Leung
Keyword(s):  
Differential Diagnosis ◽  
Prothrombin Time ◽  
Bypass Surgery ◽  
Clotting Factor ◽  
Factor V ◽  
Bleeding Diathesis ◽  
Factor Deficiency ◽  
Cardiac Bypass

AbstractThe differential diagnosis of a long APTT with a normal prothrombin time can be due to either a clotting factor deficiency or the presence of an inhibitor, which can be distinguished by using a plasma-mixing study. The various clotting factor deficiency states are reviewed. Clinical bleeding following cardiac bypass surgery due to acquired factor V and thrombin antibodies is also reviewed.

Reconstitution Of PF1 In Platelets From Factor V-Deficient Donors As A Function Of Available PF3

1981 ◽  
Author(s):  
A P Bode ◽  
H Sandberg ◽  
F A Dombrose ◽  
B R Lentz
Keyword(s):  
Prothrombin Time ◽  
Human Platelets ◽  
Factor V ◽  
Freezing And Thawing ◽  
One Stage ◽  
Normal Platelet ◽  
Normal Plasma ◽  
Protein Particles ◽  
Induced Aggregation ◽  
Free Plasma

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.

Effect of heparin on chronically induced intravascular coagulation in dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 449-454 ◽  
Author(s):  
Owen CA ◽  
EJ Bowie
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Antithrombin Iii ◽  
Plasma Fibrinogen ◽  
Factor V ◽  
Thrombin Time ◽  
Turnover Rates ◽  
Clotting Factors ◽  
Intravascular Coagulation ◽  
Absolute Concentrations

When intermediate-strength thromboplastin was continuously infused into dogs for 10 days or more, platelet counts decreased sharply and factor VIII concentrations decreased by more than 50%. There was little change in plasma fibrinogen, prothrombin, factor V, antithrombin III, plasminogen, prothrombin time, and thrombin time values. When heparin was infused (25-50 U/kg per h) along with the same thromboplastin, there was no change in onset or degree of thrombocytopenia. However, the decrease in factor VIII was abolished and there were significant increases in fibrinogen, prothrombin, and factor V. The absolute concentrations of the various clotting factors seemed to give no indication of their turnover rates. Unexplained is the remarkable heparin tolerance that developed in these dogs.

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
Keyword(s):  
Prothrombin Time ◽  
Clinical Significance ◽  
Assay System ◽  
Factor Vii ◽  
Factor V ◽  
Optimal Conditions ◽  
High Dilution ◽  
One Stage ◽  
Factor Assay

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.

PARAHEMOPHILIA (OWREN'S DISEASE)

PEDIATRICS ◽  
1953 ◽  
Vol 12 (1) ◽  
pp. 5-10
Author(s):  
BERNARD REDNER ◽  
HOWARD SCALETTAR ◽  
MURRAY WEINER
Keyword(s):  
Prothrombin Time ◽  
Fibrinolytic Activity ◽  
Hemorrhagic Disease ◽  
Factor V ◽  
Clotting Time ◽  
Laboratory Findings ◽  
Prothrombin Activity ◽  
One Stage ◽  
The One ◽  
Free Plasma

A case of parahemophilia in a five year old child has been presented. This case follows the pattern first described by Owren, namely, a congenital hemorrhagic disease with deficient prothrombin activity by the one-stage method correctable by the addition of prothrombin-free plasma. The positive laboratory findings consisted of a prolonged prothrombin time and a slightly prolonged clotting time. Ac globulin deficiency was confirmed both by Dr. Seegers and by Dr. Stefanini. There was no abnormal fibrinolytic activity or fibrinogen deficiency. Serum prothrombin activity indicated that a deficiency of Factor V was accompanied by decreased prothrombin consumption. There was no response to prolonged vitamin K therapy. Blood and plasma transfusions temporarily controlled bleeding, although at no time was a normal one-stage plasma prothrombin time obtained.

Plasma Factor V Activation Is Prevented by Activated Protein C in the Presence of Phospholipid Vesicles, Not Platelets

1993 ◽  
Vol 69 (02) ◽  
pp. 124-129 ◽  
Author(s):  
Susan Solymoss ◽  
Kim Thi Phu Nguyen
Keyword(s):  
Western Blotting ◽  
Protein C ◽  
Thrombin Generation ◽  
Blood Platelets ◽  
Activated Protein C ◽  
Phospholipid Vesicles ◽  
Factor V ◽  
Two Stage ◽  
One Stage ◽  
Plasma Factor

SummaryActivated protein C (APC) is a vitamin K dependent anticoagulant which catalyzes the inactivation of factor Va and VIIIa, in a reaction modulated by phospholipid membrane surface, or blood platelets. APC prevents thrombin generation at a much lower concentration when added to recalcified plasma and phospholipid vesicles, than recalcified plasma and platelets. This observation was attributed to a platelet associated APC inhibitor. We have performed serial thrombin, factor V one stage and two stage assays and Western blotting of dilute recalcified plasma containing either phospholipid vesicles or platelets and APC. More thrombin was formed at a given APC concentration with platelets than phospholipid. One stage factor V values increased to higher levels with platelets and APC than phospholipid and APC. Two stage factor V values decreased substantially with platelets and 5 nM APC but remained unchanged with phospholipid and 5 nM APC. Western blotting of plasma factor V confirmed factor V activation in the presence of platelets and APC, but lack of factor V activation with phospholipid and APC. Inclusion of platelets or platelet membrane with phospholipid enhanced rather than inhibited APC catalyzed plasma factor V inactivation. Platelet activation further enhanced factor V activation and inactivation at any given APC concentration.Plasma thrombin generation in the presence of platelets and APC is related to ongoing factor V activation. No inhibition of APC inactivation of FVa occurs in the presence of platelets.

The Reaction of Thiol Compounds with the Vitamin-K Dependent Clotting Factors

1969 ◽  
Vol 21 (03) ◽  
pp. 573-579 ◽  
Author(s):  
P Fantl
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Anaerobic Conditions ◽  
Clotting Factors ◽  
Thiol Compounds ◽  
Aerobic Conditions ◽  
One Stage ◽  
Factor Ii ◽  
Ph Dependent ◽  
The One

SummaryTreatment of human and dog oxalated plasma with 0.2 to 1.0 × 10−1 M 2.3-dithiopropanol (BAL) or dithiothreitol (DTT) at 2–4° C for 30 min results in the reduction of the vitamin-K dependent clotting factors II, VII, IX and X to the respective-SH derivatives. The reaction is pH dependent. Under aerobic conditions the delayed one stage prothrombin time can be partly reversed. Under anaerobic conditions a gradual prolongation of the one stage prothrombin time occurs without reversal.In very diluted plasma treated with the dithiols, prothrombin can be converted into thrombin if serum as source of active factors VII and X is added. In contrast SH factors VII, IX and X are inactive in the specific tests. Reoxidation to active factors II, VII, IX and X takes place during adsorption and elution of the SH derivatives. The experiments have indicated that not only factor II but also factors VII, IX and X have active-S-S-centres.

Two-Stage Procedure for the Quantitative Determination of Autoprothrombin III Concentration and Some Applications

1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers
Keyword(s):  
Prothrombin Time ◽  
Factor Vii ◽  
Two Stage ◽  
Pronounced Increase ◽  
One Stage ◽  
Assay Procedure ◽  
Bovine Plasma ◽  
The One ◽  
Autoprothrombin C

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.

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