Plasma Thromboplastin Component (PTC) Deficiency Produced by Prolonged Administration of Prothrombopenic Anticoagulants.

Sise, Herbert S.; Kimball, Delbert M.; Adamis, Dionysios

doi:10.3181/00379727-89-21721

Cited by 33 publications

(6 citation statements)

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“…There is a short period, in other words, early during dicoumarolization when the prothrombin time is lengthened yet Factor V and prothrombin concentration are high, Stuart factor and PTC levels are not significantly reduced, and the thromboplastin generation test is normal. Later during therapy the Stuart factor becomes reduced along with PTC (44)(45)(46) and prothrombin (47).…”

Section: Properties Of Stuart Factormentioning

confidence: 99%

Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Hougie¹,

Barrow²,

Graham³

1957

J. Clin. Invest.

256

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Section: Properties Of Stuart Factormentioning

confidence: 99%

Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Hougie¹,

Barrow²,

Graham³

1957

J. Clin. Invest.

256

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“…Prothrombin, factor VII, and the Christmas factor have many properties in common. They are all adsorbed by inorganic precipitates, are all deficient in coumarin therapy (Naeye, 1956;Sise, Kimball, and Adamis, 1955;Douglas and Mair, 1957), and by this study are shown all to be reduced in concentration in vitamin K deficiency, responding at similar rates to the administration of vitamin K. The possibility is further raised that these three components may be more closely identified than is generally envisaged.…”

Section: Resultsmentioning

confidence: 51%

Some Observations on the Coagulation Defect in Vitamin K Deficiency

Douglas¹

1958

J Clin Pathol

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“…13 it is now known that several factors are affected including those involved in the early stages of the intrinsic mechanism. 23 " 25 Since the intrinsic coagulation mechanism is independent of Factor VII ac-Circulation Research. Volume VIII, November I960 tivity, 13 it is not surprising that the prothrombin time is sometimes a poor index of changes in platelets.…”

Section: Platelet Function and Other Clotting Testsmentioning

confidence: 99%

Dicumarol Therapy

Murphy

Mustard

1960

Circulation Research

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One of the problems of Dicumarol administration has been determination of the adequacy of therapy. A fundamental stage in thrombus formation in the circulation is platelet clumping. Since platelets are involved in both hemostasis and thrombosis, a study of changes in platelet function may prove useful. The effects of Dicumarol on platelet clumping and adhesiveness have, therefore, been studied and related to changes in other clotting mechanisms. Comparison of platelet function in control periods and during Dicumarol administration shows that this drug lowers the adhesive index and prolongs the platelet clumping time to a highly significant degree. The accuracy of estimates of these 2 platelet functions given by 3 other tests, prothrombin time, whole blood clotting time and plasma activity in the thromboplastin generation tests have been compared. By any criterion, degree of correlation, consistency of regression slopes, intercepts or scatter about regression lines, clotting time was the most efficient of the 3 tests for evaluting platelet function. The prothrombin time was the least efficient. Furthermore, hemorrhage from excessive dosage was closely related to the platelet clumping time and clotting time. It should be pointed out, however, that in about one-third of the patients the prothrombin time was as good an index of platelet clumping time as clotting time. While prothrombin times done with 2 different sources of thromboplastin may give congruous results in untreated patients, considerable discrepancies may appear during Dicumarol therapy. If prothrombin time is to be used as a guide to Dicumarol therapy, it is important to establish in each patient separately its reliability as a measure of the behavior of the clotting mechanism as a whole. For those in whom it seems reliable, an individual "therapeutic range" should be determined. For other cases, some other suitable test should be employed. It is emphasized that regulation of Dicumarol dosage is an individual problem and that only those tests shown to be reliable indices of safe effective modifications of clotting mechanism in the individual patient should be used.

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Plasma Thromboplastin Component (PTC) Deficiency Produced by Prolonged Administration of Prothrombopenic Anticoagulants.

Cited by 33 publications

References 0 publications

Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Some Observations on the Coagulation Defect in Vitamin K Deficiency

Dicumarol Therapy

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