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[The protraction of the thrombin time under the effect of elastase (does elastase cause heparin liberation?)].
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[On the diagnosis of blood coagulation disorders in obstetrics by means of the thrombin time determination].
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[Importance of thrombine time in the diagnosis of obstetric afibrinogenemia in practice].
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[Blood coagulation studies using capillary blood. II. Thrombin time and fibrinogen].
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[Lengthening of the thrombin time due to an anti-equine antithrombin in a case of hyperthrombocytic myelosis].
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Influence of time and temperature on coagulation analytes in stored plasma.
There is no comprehensive study on the stability of coagulation analytes in plasma. We therefore determined the influence of storage time and temperature on prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, factors V and VIII, antithrombin III, protein C and S in plasma from 20 healthy subjects and 20 patients receiving heparin therapy. The stability in plasma, defined as the period during which there was a change of less than 10% from the initial value, was 8 hours for activated partial thromboplastin time, 24 hours for prothrombin time, 48 hours for factor V and 7 days for thrombin time, fibrinogen, protein C and antithrombin III in healthy subjects at 6 degrees C. Factor VIII and protein S showed 19 and 12 % reduction in activity, respectively, after 8 hours. In volunteers not treated with heparin therapy, activated partial thromboplastin time was stable for 8 hours; prothrombin time for 48 hours; and thrombin time, fibrinogen and antithrombin III for 7 days with sample storage at room temperature. Factor VIII showed a decrease of 18 % after 8 hours. For patients receiving heparin therapy, the stability of the analytes in plasma stored at 6 degrees C was 8 hours for thrombin time, 24 hours for prothrombin time and activated partial thromboplastin time and 7 days for fibrinogen and antithrombin III. Factors V and VIII showed a decrease of 13 % and 20 % respectively after 8 hours. When the plasma of these patients was stored at room temperature, factor V was stable for 8 hours, and prothrombin time for 24 hours, whereas fibrinogen and antithrombin III remained unchanged for 7 days. Activated partial thromboplastin time showed an increase of 13 %, thrombin time a fall of 16 %, and factor VIII a decrease of 18 % after 8 hours.
[Mechanism of erythrocyte sedimentation. XV. Characterization of various bovine fibrinogen fractions using erythrocyte sedimentation rate, thrombin time and immunodiffusion].
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Thrombin time prolongation in cirrhosis in relation to enhanced fibrinogen degradation.
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Evaluation of fibrinolysis in hepatic cirrhosis. Relation of serial thrombin time and euglobulin lysis time.
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The effects of unfractionated heparin, low molecular weight heparin and danaparoid on the thromboelastogram (TEG): an in-vitro comparison of standard and heparinase-modified TEGs with conventional coagulation assays.
To investigate the effects of unfractionated heparin (UFH), low molecular weight heparin (LMWH) and danaparoid (DPD) added to whole blood in vitro on standard and heparinase-modified thromboelastogram (TEG) parameters compared with conventional assays of coagulation. The effects of UFH, LMWH and DPD on standard TEG parameters were compared with the prothrombin time, activated partial thromboplastin time, thrombin time and anti-activated factor X (anti-FXa) activity, at concentrations of these anticoagulants ranging from 0.025 to 1 U/ml. In the second part of the study, the effects of very low concentrations (0.005-0.05 U/ml) of UFH, LMWH and DPD on the difference between standard and heparinase-modified TEG parameters were compared with the prothrombin time, activated partial thromboplastin time, thrombin time and anti-FXa activity. Standard TEG parameters were outside the reference range at lower concentrations of UFH, LMWH and DPD than most conventional coagulation assays were able to detect. Only anti-FXa activity was more sensitive to the presence of these anticoagulants than the standard TEG alone. The lowest concentration of UFH, LMWH and DPD used in this study (0.005 U/ml) caused significant differences between the standard and heparinase-modified alpha-angles of the TEG. In addition, the difference between standard and heparinase-modified TEG parameters distinguished between low concentrations (0.005-0.05 U/ml) of UFH with greater sensitivity than anti-FXa activity, but were less sensitive to LMWH and DPD. The standard TEG is more sensitive to UFH, LMWH and DPD than most conventional coagulation tests, with the exception of anti-FXa activity. Calculation of the difference between standard and heparinase-modified TEG parameters greatly increases the sensitivity of the assay for the effects of these anticoagulants, and is more sensitive to very low quantities of UFH than anti-FXa activity.
Effect of an aortic proteoglycan on platelet aggregation and thrombin time: plasma requirement and active moieties (39898).
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[A heparin-like anticoagulant in a patient with Wegener's granulomatosis].
We identified a circulating, heparin-like anticoagulant in a patient with Wegener's granulomatosis. Routine coagulation studies revealed a significant prolongation of the coagulation time, thrombin time, prothrombin time and activated partial thromboplastin time. Thrombin time and activated partial thromboplastin time failed to improve in a 1:1 mixture with pooled normal plasma. Both test were corrected in vitro by addition of protamine sulfate or toluidine blue and in vivo by intravenous administration of protamine sulfate. Recognition of the existence of this or other similar inhibitors in bleeding patients is of value because of the possibility of treatment with protamine sulfate, which neutralizes the anticoagulant.
[The behavior of Owren's thrombin time in the course of MHV-3 mouse hepatitis].
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Prognostic value of hemostatic parameters after liver transplantation.
The prognostic value of hemostatic parameters after orthotopic liver transplantation was evaluated in 37 consecutive patients. Six simple hemostatic parameters (prothrombin time, activated partial thromboplastin time, thrombin time, thrombin coagulase time, plasma fibrinogen and platelet count) were obtained for each patient pre-transplantation and daily post-transplantation for at least 8 days. Using the results of these tests, the degree of hemostatic impairment was arbitrarily scored from 0 to 6. Starting from the first day post-transplantation, hemostatic parameters improved progressively, reaching plateau values on day 7 post-transplantation. On day 8 there were significant differences in the activated partial thromboplastin time, prothrombin time, and in the overall hemostatic scores between patients who survived at least 6 months and those who died. Comparing these hemostasis parameters with such liver function tests as AST, ALT and serum bilirubin, univariate analysis showed that activated partial thromboplastin time, coagulation score and AST were significant predictors of 6-month survival, but by multivariate analysis (Cox proportional hazard rate model) only the activated partial thromboplastin time was an independent predictor. Hence, a simple coagulation test is useful for predicting the survival of patients undergoing liver transplantation.
Ontogeny of bovine hemostasis.
Ontogeny of selected hemostatic system components was studied in 120 bovine fetuses which had been divided into eight monthly gestational age groups. Fetal blood was subjected to the following tests: platelet count, partial thromboplastin time, prothrombin time, thrombin time, fibrinogen quantitation, and assays for prothrombin and factors V and VIII. Platelet numbers corresponding to adult numbers were in fetal blood at least as early as gestation day 60, and their numbers varied only slightly thereafter. Bovine blood was incapable of in vitro coagulation at gestation day 90, with all samples coagulating by gestation day 150. Fetal coagulation screening test times (partial thromboplastin time, prothrombin time, and thrombin time) shortened during gestation and were near times of adults at birth. Of the four individual coagulation factors tested, only factor VIII reached adult values in the fetus in utero. Amounts of fibrinogen, prothrombin, and factors V and VIII in the neonate exceeded that of normal adult cattle.
Blood clotting disorders during experimental sarcocystiosis in calves.
The effects of experimental infection of calves with Sarcocystis cruzi on the blood coagulation cascade were investigated. Calves were inoculated orally with 1 x 10(5) sporocysts (group S1, n = 6) or with 5 x 10(5) sporocysts of S. cruzi (group S2, n = 3). A group of eight calves served as non-infected controls (group C). The animals were bled once during the first 4 weeks of infection and twice a week thereafter until day 40 p.i. The following parameters were measured: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time, thrombin coagulase time, factors XII, XI, X, IX, VIII:C, VII, V, prekallikrein, fibrinogen, alpha 2-antiplasmin, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin, haematocrit, haemoglobin, numbers of erythrocytes and thrombocytes. The infected calves developed acute sarcocystiosis from 25 (S1) or 29 (S2) days p.i. onwards. During the acute disease, antiproteases tended to elevated values and thrombocyte counts were generally reduced. In group S1 prolonged prothrombin time and reduced activities of factors VII or V were found. In group S2 accelerated prothrombin time and activated partial thromboplastin time, as well as elevated factor X activities, were recorded even before the onset of clinical disease at 19 days p.i. While prothrombin time returned to normal levels thereafter, activated partial thromboplastin time remained short. Activities of factor V, factor VII and factor X were significantly reduced in group S2 at the onset of acute sarcocystiosis, and one of the three calves died at 29 days p.i. The other parameters were not significantly affected by either dose of infection. No evidence for a classical disseminated intravascular coagulation syndrome could be found; however, it was demonstrated that S. cruzi alters plasma coagulation in a dose-dependent way.
Bleeding diathesis in multiple myeloma.
Patients with multiple myeloma having a higher titer of serum paraproteins can manifest hemostatic abnormalities. Most of these abnormalities predispose the patient to hemorrhage. Less commonly, thrombotic complications may occur in association with paraprotein disorders. We investigated a 56-year-old female diagnosed with multiple myeloma (type IgG kappa, 59 g/L) whose coagulation profile showed an increase in thrombin time and prothrombin time. To investigate the etiology of the abnormal coagulopathy, further diagnostic studies including coagulation factor assays, platelet aggregation studies, replitase time, mixing studies using pooled normal plasma, and protamine were performed. Mixing studies demonstrated correction of the prothrombin time. Thrombin time was near-corrected but the replitase-time was not corrected by these mixing studies. After chemotherapy, the paraprotein concentration decreased (12g/L) and the coagulation results returned to normal. Patients with multiple myeloma may develop bleeding diathesis secondary to a variety of mechanisms. One such mechanism is direct inhibition of fibrin monomer aggregation due to the paraprotein, resulting in prolongation of the thrombin time and the replitase time. The failure to correct the former by the addition of protamine further augments the direct role of FAB portion of the paraprotein molecule on inhibition of fibrin monomers.