Letters to the Editor

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1151-1151
Author(s):  
ARMAND J. QUICK
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Factor Vii ◽  
Factor V ◽  
Letters To The Editor ◽  
Time Determination

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.

Spectrophotometric Assays of Prothrombin in Plasma of Patients Using Oral Anticoagulants

1979 ◽  
Vol 42 (04) ◽  
pp. 1296-1305 ◽  
Author(s):  
R M Bertina ◽  
W van der Marel-van Nieuwkoop ◽  
E A Loeliger
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Oral Anticoagulation ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Factor Xa ◽  
Factor V ◽  
Anticoagulant Treatment ◽  
Factor Ii ◽  
K Deficiency

SummaryTwo spectrophotometric assays for prothrombin have been developed and compared with a one stage coagulant and an immunological assay. One of these assays (called the XAPC assay) uses a combination of factor Xa, phospholipid, Ca2+ and factor V as activator of prothrombin, and measures only normal prothrombin. The second (the ECAR assay) uses Echis carinatus venom as activator. This assay measures both normal prothrombin and PIVKA II (protein induced by vitamin K antagonists/absence). Combination of the results obtained by the XAPC and ECAR assays provides rapid and reliable information on the degree of “subcarboxylation” of prothrombin (oral anticoagulation, vitamin K deficiency).For patients on long term anticoagulant treatment the prothrombin time (Thrombotest) shows better correlation with the ratio prothrombin/prothrombin plus PIVKA II (XAPC/ ECAR) than with the factor II concentration. For patients starting the anticoagulant treatment there is no correlation between the Thrombotest time and the XAPC/ECAR ratio.It seems doubtful that (a) spectrophotometric factor II assay(s) will be as useful as the prothrombin time in the control of oral anticoagulation.

Factor VII Activity and Antigen in Haemophilia B Variants

1980 ◽  
Vol 43 (01) ◽  
pp. 016-019 ◽  
Author(s):  
M G Mazzucconi ◽  
R M Bertina ◽  
D Romoli ◽  
M Orlando ◽  
G Avvisati ◽  
...  
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Normal Values ◽  
Factor Ix ◽  
Factor Vii ◽  
Confidence Limits ◽  
Vitamin K Deficiency ◽  
Haemophilia B ◽  
K Deficiency ◽  
Mild Deficiency

SummaryTwenty three patients belonging to 18 different pedigrees of Haemophilia B were studied with regard to ox-brain prothrombin time and its correlation to factor VII.Eleven among them were B-negative (no detectable factor IX antigen), five were B-reduced (factor IX antigen detectable but below the normal values) and seven were B-positive (normal levels of factor IX antigen).Ox-brain prothrombin time was found prolonged (≥ x̄ + 2.5 SD:99% confidence limits) in nine patients. Factor VII Activity (VII: C) was found reduced in 1/11 B-negative, in 2/5 B-reduced and in 4/7 B-positive patients. Factor VII Antigen (VII: Ag) was found normal in all but one patient.The ratio VII:C/VII:Ag was abnormal in eight patients independently from the variant of Haemophilia B. The underlying defect which causes the prolongation of Ox-brain prothrombin time due to factor VII: C mild deficiency is heterogeneous. Age, a mild Vitamin K deficiency, the presence of an inhibitor of Factor VII activation and other unknown causes, may be responsible for this pattern.

Occult intravascular clotting by means of intravenous injection of thrombin

1959 ◽  
Vol 197 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey ◽  
John Harris ◽  
Kenneth Peters
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Intravenous Injection ◽  
Factor Ix ◽  
Capillary Network ◽  
Factor Vii ◽  
Factor V ◽  
Dilute Solution ◽  
Progressive Decrease ◽  
Stable Factor

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.

Protein Z, a protein seeking a pathology

2008 ◽  
Vol 100 (10) ◽  
pp. 548-556 ◽  
Author(s):  
Marc Vasse
Keyword(s):  
Risk Factor ◽  
Vitamin K ◽  
Factor V Leiden ◽  
Factor Vii ◽  
Factor V ◽  
Factor X ◽  
Protein Z ◽  
Factor V Leiden Mutation ◽  
Thrombotic Risk ◽  
G20210a Mutation

SummaryProtein Z (PZ) is a vitamin K-dependent factor identified in human plasma in 1984 characterized by an homology with other vitamin K-dependent factors (factor VII, IX, X, protein C). In contrast to these factors, PZ does not possess any enzymatic activity but is involved as a cofactor in the down-regulation of coagulation by forming a complex with the protein Z-dependent protease inhibitor (ZPI). ZPI inhibits the activated factor X (FXa) on phospholipid surface. In mice, the disruption of PZ gene is asymptomatic, but the association with the factor V Leiden mutation leads to a quasi complete mortality during the neonatal period with microvascular thrombosis. In humans, PZ is characterized by an unusual wide distribution in plasma, and a major decrease induced by warfarin. Isolated PZ deficiency does not seem to constitute a risk for venous thrombosis, but a severe PZ deficiency could increase the risk of well recognized venous thrombotic risk factors such as factor V Leiden, G20210A mutation or hyperhomocysteinemia. Unexpectedly, a relationship between PZ deficiency and ischemic arterial diseases such as stroke, acute coronary syndromes or peripheral arterial disease was described but not confirmed by all studies. PZ deficiency could be also a risk factor for early fetal losses, and increases the arterial risk in antiphospholipid syndrome. This review analyzes the different studies so far published and discusses the various results obtained in order to understand whether or not protein Z deficiency could be considered as an arterial ischemic risk factor.

Inaccurate therapeutic decisions in patient with lupus anticoagulant as a result of falsely elevated prothrombin time

2015 ◽  
Vol 51 (3) ◽  
pp. 199-202
Author(s):  
Maria Magdalena Jeleńska ◽  
Katarzyna Pawlak ◽  
Monika Budnik ◽  
Hanna Zborowska
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Lupus Anticoagulant ◽  
Reference Range ◽  
Cephalic Vein ◽  
Factor V ◽  
Prolonged Prothrombin Time ◽  
Vein Thrombosis ◽  
Therapeutic Decisions ◽  
Increased Risk

71 year old patient was admitted to the hospital with a suspicion of infective endocarditis. Laboratory investigations using human recombined tromboplastin Innovin showed a considerably prolonged prothrombin time (INR above 4) and APTT. Due this vitamin K was administered (iv). During further investigations using Innovin significantly prolonged prothrombin time persisted, but using thromboplastin Technoplastin HIS was in reference range. Deficiency of vitamin K dependent coagulation factors (VII, X, II), factor V and fibrinogen were not found. Therefore a comparative test using Innovin and three other thromboplastins (Technoplastin HIS Tromborel S, RecombiPlasTin 2G) were performed. These gave prothrombin time in reference range. Prolonged aPTT resulted from presence of lupus anticoagulant. Thrombotic prophylaxis with low molecular weight heparin was applied (2 weeks after admission to the hospital). However, two days later, edema of upper limb has appeared due to cephalic vein thrombosis. There was no central catheter placed in any of central veins. The falsely elevated prothrombin time caused inaccurate therapeutic decisions such as iv supply of vitamin K, and delate antithrombotic treatment of patient with the increased risk of thrombosis (immobilization, inflammations and presence of the lupus anticoagulant). These decision surely contributed to the cephalic vein thrombosis. Our results demonstrated that protothrombin time/INR determined with thromboplastin Innovin can be prolonged also in patients with lupus anticoagulant not submitted to anticoagulation treatment. Therefore, in patients with LA before therapeutic decision, the verification of elevated prothrombin time using other than Innovin thromboplastins is necessary.

Anticoagulants

2006 ◽  
Author(s):  
Richard C. Becker ◽  
Frederick A. Spencer
Keyword(s):  
Clinical Practice ◽  
Prothrombin Time ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Plasma Concentrations ◽  
Therapeutic Index ◽  
Dose Titration ◽  
Direct Thrombin Inhibitors ◽  
Factor V ◽  
High Concentrations

Because of the narrow therapeutic index of warfarin and unfractionated heparin (UFH), monitoring their anticoagulant effects is required. On the other hand, lowmolecular- weight heparin (LMWH) and fibrinolytic agents need to be monitored only under certain circumstances. Although newer anticoagulants will not require routine monitoring for dose titration, a means to determine their systemic effects and individual (patient-specific) response to administration will likely have roles in clinical practice. The prothrombin time is used to monitor vitamin K antagonist therapy. This test is sensitive to the plasma concentrations (activity) of clotting factors II (prothrombin), V, VII, and X. Vitamin K antagonists affect the vitamin K–dependent factors II, VII, IX, and X, as well as proteins C, S, and Z. Thus, the prothrombin time does not reflect the effect of vitamin K antagonists on some factors (IX and proteins C, S, and Z) and is sensitive to others (factor V) (not directly influenced by treatment). The prothrombin time is not an ideal test for monitoring vitamin K antagonists; however, its simplicity and widespread availability have established its place in clinical practice. By convention, prothrombin times are now reported as international normalized ratios (INRs). This is the ratio of the patient’s prothrombin time to a control prothrombin time, raised to a power—the international sensitivity index (ISI). The latter reflects the calibration of the thromboplastin used for the prothrombin time testing to an internationally agreed upon standard. In many laboratories the reagent currently used is a recombinant thromboplastin, which has an ISI of 1.0 There are several cautions related to interpreting the results of prothrombin time tests that are worth monitoring. Since the test is sensitive to the level of factor V in the plasma, improper sample storage or delayed testing may cause loss of factor V (activity) and yield prothrombin time values above the expected range. High concentrations of heparin may also prolong the prothrombin time; this usually occurs when the sample is obtained within a few minutes of administering a bolus dose. Direct thrombin inhibitors, such as hirudin, bivalirudin, argatroban, and ximelagatran, may also prolong the prothrombin time to a variable degree.

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.

SERUM VITAMIN K1 LEVELS AS AN EARLY INDICATOR OF HYPOPROTHROMBINAEMIA ASSOCIATED WITH ANTIBIOTIC THERAPY

1987 ◽  
Author(s):  
S J Machin ◽  
H Cohen ◽  
I J Mackie ◽  
M Shearer ◽  
S D Scott
Keyword(s):  
Antibiotic Therapy ◽  
Prothrombin Time ◽  
Vitamin K ◽  
Serum Vitamin ◽  
Abdominal Sepsis ◽  
Normal Serum ◽  
Factor Vii ◽  
Vitamin K1 ◽  
K Deficiency ◽  
Cefotetan Disodium

The prothrombin time is an insensitive indicator of early vitamin K deficiency and serum vitamin K1 levels may correlate with liver stores. A random non-fasting range of serum vitamin K1 was established in 45 healthy adults of 150-1,530 pg/ml (mean 412 pg/ml). Nine well nourished patients, with normal serum vitamin K1 levels, (mean 546, range 310-1,350 pg/ml), maintained normal prothrombin times and factor VII clotting activity throughout 7 days therapy with cefotetan disodium, an NMTT-containing cephalosporin antibiotic. However, 11 of 20 patients with acute intra-abdominal sepsis and an initially normal prothrombin time who underwent emergency surgery, developed a raised prothrombin time (INR 1.4-3.1) associated with reduction in factor VII activity (0.74 to 0.38 iu/ml) after 3-7 days of antibiotic therapy and the presence of PIVKA II by crossed-immunoelectrophoresis. Nine of these 11 patients had clinical evidence of malnutrition by anthropometric assessment and subnormal serum vitamin K1 (mean 119, range 43-354 pg/ml) levels on admission. Seven received cefotetan but 4 were treated with other non-NMTT containing antibiotics. The 9 patients who maintained normal prothrombin times and factor VII levels had normal nutritional status and normal serum vitamin K1 levels (mean 279, range 103-915 pg/ml) at presentation. A low serum vitamin K1 level was associated with a high incidence of hypopro-thrombinaemia developing following antibiotic therapy and would appear a more sensitive indicator of reduced vitamin K stores than the prothrombin time.

Studies Regarding the Effect of Foreign-Surface Contact on the One-Stage Prothrombin Time Determination

1966 ◽  
Vol 15 (03/04) ◽  
pp. 442-450 ◽  
Author(s):  
J. N Shanberge ◽  
T Matsuoka
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Hemophilia B ◽  
Factor Vii ◽  
One Stage ◽  
Surface Contact ◽  
Time Determination ◽  
Foreign Surface ◽  
The One

SummaryThe shortening of the one-stage prothrombin time of plasma brought about by increased foreign surface contact is dependent upon “activation” of factor VII. This activation of VII is the result of a series of activations involving factors XII, IX and probably XI as well. In this it is similar to the activation of factor VIII. Although the prothrombin time in an individual with hemophilia B or the Hageman trait is ‘‘normal”, no shortening occurs after increased foreign surface contact. Factor VII deficient plasma with normal levels of factors XII and IX is “activated” by “contact” in proportion to the level of VII present. No increase in activity of factors II, V, or X was observed after increased foreign surface contact.

The Effects of Leguminous Seed Extracts on Blood Coagulation

1962 ◽  
Vol 08 (02) ◽  
pp. 256-269
Author(s):  
R. J Speer ◽  
J. L Porter
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Blood Coagulation ◽  
Factor Ix ◽  
Factor Vii ◽  
Clot Lysis ◽  
Factor V ◽  
Leguminous Seed ◽  
Recalcification Time ◽  
Clot Time

SummaryThe saline extracts of one hundred leguminous seed were screened for their effect on blood coagulation by the following tests: thrombin clot time, recalcification time, Quick prothrombin time, clot lysis and clot retraction. Nineteen of these extracts, when reacted with normal plasma, gave a prolonged clot time in at least one of two tests: recalcification time and Quick prothrombin time. The eight which gave a prolonged Quick prothrombin time were tested for inhibition in the following assay systems: Factor V, factor VII-complex, and prothrombin. All nineteen, including the seventeen which prolonged the re-calcification time and the two which did not, were tested for their inhibitory action in the following assay systems: Factor VIII, factor IX, and plasma thromboplastin antecedent.The inhibition of prothrombin, factor V, and factor VII-complex was mild and not specific for any of these factors. Factor V activity was depressed more than the other two. By contrast, the inhibition of factor VIII, factor IX, and plasma thromboplastin antecedent was very strong and demonstrated a relatively high degree of specificity.

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