Relation of Hemorrhage and Thrombosis to Prothrombin during Treatment with Coumarin-Type Anticoagulants

Sise, Herbert S.; Lavelle, S. M.; Adamis, Dionysios; Becker, Robert

doi:10.1056/nejm195808072590603

Cited by 60 publications

(17 citation statements)

References 22 publications

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“…Based on previous findings [5,[11][12][13], the plasma con- centration of native prothrombin may be superior to the INR as a predictor of both hemorrhage and thromboembolism in patients on warfarin. Furie et al [11] conducted a randomized prospective trial comparing the incidence of adverse events when warfarin therapy was regulated within either a prothrombin time index (patient prothrombin time/control prothrombin time) of 1.5-2.0 or a concentration of native prothrombin between 12-24 g/ ml (normal ‫ס‬ 108 ± 19 g/mL).…”

Section: Discussionmentioning

confidence: 99%

“…If the half life of plasma prothrombin is 80 hr [28], it will take 1 week to reach the therapeutic range of 25% native prothrombin assuming: (1) there is instant and total inhibition of gamma carboxylation, (2) no previously formed active prothrombin is released into the circulation, and (3) complete and free exchange exists between the intravascular and extravascular compartments with a similar prothrombin half-life in both compartments. Sise et al [12] measured functional prothrombin concentrations daily after a single dose of 300 mg of intravenous warfarin in five patients who had received no previous anticoagulation.…”

Section: Discussionmentioning

confidence: 99%

“…Overall, the group monitored using the native prothrombin had 85% fewer combined hemorrhagic and thromboembolic complications. Thirty years earlier, Sise et al [12] studied a large group of patients on stable anticoagulation and recommended the regulation of prothrombin concentration between 12-25% using a one-stage factor assay in place of the Quick time. Kornberg et al [13] compared the predictive values of native prothrombin and INR in the monitoring of warfarin prophylaxis following total hip arthroplasty.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of plasma prothrombin and factor VII and urine prothrombin F1 concentrations in patients on long‐term warfarin therapy and those in the initial phase

et al. 1998

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Control of warfarin anticoagulation during the initial phase of therapy is difficult and empirically based. Plasma and urine samples were obtained from normal controls, patients under stable anticoagulation, and patients in the initial phase of anticoagulation. Total plasma prothrombin, des-carboxy (non-adsorbable with barium chloride) prothrombin, and native (total minus non-adsorbable) prothrombin were quantitated using Echis carinatus venom activation. Functional plasma factor VII (VII) was measured using a one-stage clotting assay. Total and des-carboxy urine prothrombin F1 (F1) were measured by ELISA. All urine F1 in normals and both anticoagulated groups was adsorbed by barium chloride. Plasma des-carboxy prothrombin concentration was similar for the two anticoagulated groups and did not correlate with 1/INR. Native prothrombin correlated with 1/INR in both the stable (r = 0.76) and initial phase (r = 0.74) groups. For any given INR, the subjects on stable anticoagulation had lower native prothrombin concentrations than the initial phase patients. Functional factor VII concentration also correlated significantly with 1/INR in both the stable (r = 0.64) and initial phase (r = 0.76) patients. Unlike native prothrombin, VII concentrations did not vary between the two cohorts for any given INR. Previous studies indicate that native prothrombin is a superior predictor of both hemorrhagic and thromboembolic complications during warfarin therapy. Our findings indicate that VII, and not prothrombin, may be the predominant factor monitored by the INR. This further supports the need to reevaluate the usefulness of the INR in the monitoring of warfarin therapy during the initial phase. Am.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Comparison of plasma prothrombin and factor VII and urine prothrombin F1 concentrations in patients on long‐term warfarin therapy and those in the initial phase

et al. 1998

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“…In 1958, Sise et al (2) observed that both hemorrhage and thrombosis in patients receiving a vitamin K antagonist were more closely related to specific plasma prothrombin activity than to the "prothrombin time," a test particularly sensitive to the effect of vitamin K antagonists upon plasma factor VII activity. Reports ofvenous thrombo-embolism in patients with hereditary factor VII deficiency (3,4) also raised uncertainty as to the importance ofdepressed factor VII activity for warfarin's antithrombotic efficacy.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of the anticoagulant effect of warfarin as evaluated in rabbits by selective depression of individual procoagulant vitamin K-dependent clotting factors.

Zivelin¹,

Rao²,

Rapaport³

1993

J. Clin. Invest.

129

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We have evaluated the contribution of depression of individual procoagulant vitamin K-dependent clotting factors to the ability of warfarin to protect rabbits against tissue factor-induced coagulation. Mean activities of individual procoagulant factors were determined, in assays with rabbit substrates, for a group of rabbits achieving a protective degree of anticoagulation with warfarin. Values were: factor VII, 12%; factor IX, 7%; factor X, 14%, and prothrombin, 13%. The effect upon tissue factor-induced coagulation of selective immunodepletion of each factor to a comparable level was then evaluated. Immunodepletion of plasma factor X or prothrombin, but not of factor VII or factor IX, protected otherwise normal rabbits against tissue factorinduced coagulation. Next, we determined the effect upon the protection in warfarin-treated rabbits of selectively restoring factor X or prothrombin before infusing tissue factor. When either factor was selectively restored, warfarin's protective effect was abolished. Moreover, selective restoration of prothrombin sensitized warfarin-treated rabbits to coagulation more severe than observed in nontreated control rabbits. One may extrapolate from these data that depression of both factor X and prothrombin are required for warfarin's clinical antithrombotic efficacy and that depression of plasma prothrombin is particularly important. (J. Clin. Invest. 1993. 92:2131-2140

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“…3 ' 4,15 However, for several days after oral anticoagulant therapy is begun or changed, the INR predominantly reflects changes in the factor VII concentration rather than changes in the prothrombin concentration. [15][16][17][18] Thus, for patients beginning anticoagulant therapy with both heparin and warfarin, supplementing the INR with determinations of functional prothrombin concentration can help decide when to discontinue heparin. Measuring the prothrombin concentration in addition to the INR also may have value when the oral anticoagulant dosage is varied abruptly, eg, before and after emergency surgery.…”

Section: Discussionmentioning

confidence: 99%

A Novel Clotting Assay for Quantitation of Plasma Prothrombin (Factor II) UsingEchis multisquamatusVenom

Petrovan

Rapaport

1999

Am J Clin Pathol

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Relation of Hemorrhage and Thrombosis to Prothrombin during Treatment with Coumarin-Type Anticoagulants

Cited by 60 publications

References 22 publications

Comparison of plasma prothrombin and factor VII and urine prothrombin F1 concentrations in patients on long‐term warfarin therapy and those in the initial phase

Comparison of plasma prothrombin and factor VII and urine prothrombin F1 concentrations in patients on long‐term warfarin therapy and those in the initial phase

Mechanism of the anticoagulant effect of warfarin as evaluated in rabbits by selective depression of individual procoagulant vitamin K-dependent clotting factors.

A Novel Clotting Assay for Quantitation of Plasma Prothrombin (Factor II) UsingEchis multisquamatusVenom

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