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PubMed1982

A study of the conditions and accuracy of the thrombin time assay of plasma fibrinogen.

The conditions, accuracy, precision and possible error of the thrombin time assay of plasma fibrinogen are determined. Comparison with an estimation of clottable protein by absorbance at 280 nm gave a correlation coefficient of 0.96 and the regression line y = 1.00 x + 0.56 (n = 34). Comparison with a radial immunodiffusion method yielded the correlation coefficient 0.97 and the regression line y = 1.18 x = 2.47 (n = 26). The presence of heparin in clinically applied concentrations produced a slight shortening of the clotting times. The resulting error in the estimated concentrations of fibrinogen was too small to affect the clinical usefulness of the determinations. The influence of fibrin(ogen) degradation products was significant only in excessive amounts in samples containing low levels of fibrinogen.

Animals↗
PubMed1985

Effect of aspirin on serum thrombin time and bleeding time.

The present study describes and utilizes a novel method, the serum thrombin time (STT), as a measure of the time for fibrin clot formation in serum following addition of a supramaximal concentration of fibrinogen. The STT and bleeding time (BT) are selectively prolonged in male subjects 2 hours and 24 hours after ingestion of aspirin. In contrast, the STT is unchanged after aspirin ingestion by female subjects. These data indicate that inhibition of cyclooxygenase product formation by aspirin may alter the third stage of coagulation, specifically, endogenous thrombin activity. Furthermore, the ability of aspirin to prolong the STT appears to be sex-specific. Moreover, the STT may be a clinical reflection of endogenous thrombin activity in vivo as well as in vitro and may be of clinical value as a diagnostic probe in the assessment of medical and surgical disorders.

Adult↗
PubMed2000

Anticoagulation for cardiac surgery in patients receiving preoperative heparin: use of the high-dose thrombin time.

UNLABELLED: Patients receiving heparin infusions have an attenuated activated clotting time (ACT) response to heparin given for cardiopulmonary bypass (CPB). We compared patients receiving preoperative heparin (Group H) to those not receiving heparin (REF group) with respect to ACT, high-dose thrombin time (HiTT), and markers of thrombin generation during CPB. Sixty-five consecutive patients (33 Group H, 32 REF group) undergoing elective CPB were evaluated. ACT and HiTT were measured at multiple time points. Plasma levels of thrombin-antithrombin III complex and fibrin monomer were determined at baseline, during CPB, and after protamine administration. Transfusion requirements and postoperative blood loss were measured and compared. ACT values after heparinization increased less in Group H and were significantly lower than those in the REF group (P < 0.01). HiTT values did not differ significantly between the two groups. Blood loss and transfusion requirements were not significantly different between the two groups. Plasma levels of thrombin-antithrombin III complexes and fibrin monomer also did not differ between groups at any time, despite a lower ACT in Group H after heparinization and during CPB. Our data suggest that thrombin formation and activity are not enhanced in patients receiving heparin therapy, despite a diminished ACT response to heparin. The utility of ACT and the threshold values indicative of adequate anticoagulation for CPB are relatively undefined in patients receiving preoperative heparin. HiTT should be investigated as a safe and accurate monitor of anticoagulation for CPB in patients receiving preoperative heparin therapy. IMPLICATIONS: The diminished activated clotting time response to heparin, in patients receiving preoperative heparin therapy, poses difficulties when attempting to provide adequate anticoagulation for cardiopulmonary bypass. Current data suggest that heparin resistance is not observed when high-dose thrombin time is used to monitor anticoagulation and that a lower activated clotting time value in these patients may be safe.

Anticoagulants↗
PubMed1999

[Increased thrombin time in a patient with multiple myeloma].

We describe a 56-year-old patient with multiple myeloma and very high paraprotein concentration (IgG kappa). Coagulation studies showed unclottable thrombin and reptilase times caused by impaired fibrin polymerization presumably due to the paraproteinemia. There was no obvious bleeding tendency. The differential diagnosis of thrombin time prolongation includes inhibition of the added thrombin by exogenous heparin, hirudin or seldom by endogenous heparin-like anticoagulants or by acquired (bovine) thrombin antibodies, qualitative fibrinogen disorders (congenital and acquired dysfibrinogenemia), quantitative fibrinogen disorders (severe hypo- and afibrinogenemia) and delayed fibrin polymerization due to fibrin/fibrinogen degradation products, paraproteins and antibodies against fibrin(ogen). In multiple myeloma, thrombin time prolongation may seldom be due to endogenous heparin-like anticoagulants or antibodies to thrombin and more frequently to impaired fibrin polymerization by paraproteins. Simultaneous reptilase time prolongation as present in this case hints to this latter possibility.

Diagnosis, Differential↗
PubMed1978

Circulating thrombin time anticoagulant in a procainamide-induced syndrome.

Circulating anticoagulants are unusual in drug-induced syndromes. We evaluated the prolonged thrombin time of plasma from a patient with a procainamide-induced syndrome. This defect was shown to be due to a circulating anticoagulant that was not of fibrin or fibrinogen origin and that prolonged thrombin and reptilase clotting times of plasma. Subclinical doses of heparin sodium induced hemorrhagic manifestations in this patient. Following cessation of heparin therapy, the circulating anticoagulant persisted but the bleeding tendency abated. All clinical and laboratory manifestations of this syndrome abated gradually following cessation of procainamide therapy.

Aged↗
PubMed1993

A quantitative thrombin time for determining levels of hirudin and Hirulog.

The anticoagulant effect of recombinant hirudin (rHir) and Hirulog has been monitored in patients with the activated partial thromboplastin time. Accurate monitoring with this test cannot be achieved if plasmas contain heparin, lupus anticoagulants, low concentrations of fibrinogen or other factors, or elevated fibrinogen-fibrin degradation products (FDP). We have therefore developed a simple, rapid, sensitive clot-based method, the quantitative thrombin time (QTT), to measure levels of rHir and Hirulog in patient plasma (or whole blood). The QTT is performed by mixing a 1:10 dilution of patient plasma (50 microliters) with human fibrinogen (50 microliters, 128 mg/dl) at 37 degrees C; the clotting time is initiated by adding human thrombin (50 microliters, 5-7.5 U/ml). The concentration of Hirulog or rHir in plasma can be determined by comparing the QTT in patient plasma with a standard curve that is generated by adding different concentrations of anticoagulant to pooled normal plasma. Studies with whole blood using the same procedure yield similar results. In the absence of Hirulog or rHir, the baseline QTT is the same in normal and abnormal plasmas (fibrinogen < 150 mg/dl and FDP as high as 1024 micrograms/ml, elevated FDP alone, lupus anticoagulant, or heparin < 0.9 U/ml). When known concentrations of either rHir or Hirulog are added to abnormal plasmas, the mean observed concentrations as determined by the QTT deviate from the expected values by less than 10% (range 0-19%). The data indicate that the QTT is a simple, rapid, and accurate test for the determination of levels of rHir and Hirulog in plasma or whole blood.

Heparin↗
PubMed1984

Hemostasis: the balance concept of procoagulant and inhibitor systems and use of the serial thrombin time (STT).

The balance concept between the procoagulant and inhibitor systems allows a perspective to better diagnose opposite hemostatic mechanisms, especially hemorrhagic tendencies as a result of intravascular consumption coagulopathy from pathologic fibrinolysis. Concepts presented are intended to provide a base for following the ever changing patient therapeutic response in the course of these sometimes fulminant conditions. A concise description of the Serial Thrombin Time test (STT) is presented as a rapid quantitative test for the differentiation of opposing mechanisms affecting hemostasis. Typical patient cases are presented to demonstrate the use of the STT in diagnosis, selection of therapeutic agents, and management of hemorrhagic episodes. Presented are cases of disseminated intravascular coagulation, primary fibrinolysis, coronary thrombosis, and hemophilia.

Blood Coagulation↗
PubMed1994

Comparison of high-dose thrombin time with activated clotting time for monitoring of anticoagulant effects of heparin in cardiac surgical patients.

The activated clotting time (ACT) is routinely used for monitoring of heparin effects during cardiopulmonary bypass (CPB). However, ACT is not a specific assay for heparin and may be influenced by several other factors, which may be misleading with regard to the proper administration of heparin and protamine. In this pilot study, we compared a new test, the high-dose thrombin time (HiTT), with the conventional ACT test for both in vitro and in vivo heparin-induced anticoagulation. Our in vitro results showed that there were heparin dose-dependent increases in ACT and HiTT. Data on 30 adult cardiac patients indicated that HiTT correlated well with heparin concentration both after initial heparin administration and during CPB (r = 0.645 and 0.515). Hypothermia and hemodilution occurring during CPB did not alter HiTT results. ACT also correlated well with both heparin concentration and HiTT before CPB, but the linear relationship was lost during CPB. Our results suggest that HiTT is a useful assay for monitoring heparin effects during cardiac surgery, even during hypothermia and hemodilution.

Adult↗
PubMedDate not supplied

The effect of heparin on three whole blood activated clotting tests and thrombin time.

Whole blood activated clotting time (ACT) can be determined by many different methods that use a variety of clotting cascade activators and end-points. This study compared the results of three whole blood ACT instruments at equivalent concentrations of heparin. Whole blood (9.8 ml) from 10 healthy adult volunteers without coagulation abnormalities was added to 0.2 ml of heparin solution producing heparin concentrations of 0, 0.1, 0.2, 0.4, 0.6, 0.8, and 1.0 U/ml. Coagulation status was determined in duplicate with the Hemochron 400 System (HC), the HemoTec Automated Coagulation Timer (HT), and the TriMed ACTivator (TM). Thrombin times or dilutions (TT) were also determined for each sample. Baseline values did not differ (p greater than 0.05); however, the HT and TM ACT values were significantly longer (p less than 0.05) than the HC ACT values at predicted heparin concentrations greater than 0.2 U/ml. Results from the HT and TM instruments were not significantly different. The HT and TM instruments both provided a greater ACT range over the heparin concentrations tested. Of the tests studied to monitor heparin therapy, mean scaled TTs showed the best correlation with predicted heparin concentrations.

Adult↗
PubMed1976

Evaluation of the role of in vivo proteolysis (fibrinogenolysis) in prolonging the thrombin time of human umbilical cord fibrinogen.

These studies have been directed at evaluating the role played by proteolysis (fibrinogenolysis) in vivo in prolonging the thrombin time of human umbilical cord ("fetal") fibrinogen. The aggregation rate of cord fibrin compared with that from adult plasma is always delayed when the reaction is carried out under conditions of relatively high ionic strength (e.g., 0.29); this difference is not apparent at relatively low ionic strength (e.g., 0.09). In addition, as assessed by turbidimetric techniques, the maximum absorbance attained by cord fibrin is considerably less than that attained by adult fibrin. Coagulable fibrinogen catabolites (i.e., fraction I-5) are present in cord plasma and, like their counterparts from adult plasma, lack various portions of the COOH-terminal region of the A alpha chain. However, their presence in plasma does not explain the behavioral differences between cord and adult fibrin. Moreover, differences revealed by turbidimetric comparison of cord and adult fibrin from plasma fraction I-2 persist in fibrin from fraction I-5; it therefore appears that the COOH-terminal region of the A alpha chain does not contain the structure(s) accounting for the unique behavior of "fetal" fibrinogen.

Female↗