Disease relevance of Thrombin Time

• Intravenous injection of heparin (200 units/kg) failed to prevent occlusion within 60 minutes in all 10 rabbits, whereas intravenous argatroban infusion at a rate of 100 or 200 micrograms/kg/min for 60 minutes, which prolonged the thrombin time more than fourfold, prevented thrombosis in nine of 13 rabbits (p = 0.002 vs. i.v. heparin) [1].
• To further evaluate the role of sialic acid in the dysfibrinogenemia associated with liver disease, we studied the effect of removal of excess sialic acid residues from the fibrinogen of five patients with liver disease on the thrombin time and fibrin monomer aggregation [2].
• This report describes the clinical course of a patient who at the time of diagnosis of nonmetastatic renal cell carcinoma had dysfibrinogenemia characterized by prolongation of the thrombin and Reptilase times and increased sialic acid content of the purified fibrinogen [3].
• The thrombin time, fibrinogen activity to antigen ratio, and polymerization index failed to differentiate between cirrhosis and HCC [4].
• A syndrome of intracranial hemorrhage with gross prolongation of the prothrombin and partial thromboplastin times, with normal thrombin time, fibrinogen concentrations, and coagulation factor assays is described in four children with homozygous beta-thalassemia [5].

High impact information on Thrombin Time

• Prothrombin times, thrombin times, platelet-function tests and the levels of factors XII, XI, IX, VIII, prekallikrein and high-molecular-weight kininogen were normal [6].
• Circulating thrombin time anticoagulant in a procainamide-induced syndrome [7].
• However, in the presence of amounts of heparin that had only a minor effect upon clot times, SAP (5-40 micrograms/ml) greatly prolonged clot formation, with the thrombin time the most sensitive to SAP [8].
• The inhibited plasma had grossly prolonged prothrombin and activated partial thromboplastin times, but a normal thrombin time [9].
• The thrombin time was corrected by the addition (in vitro) of protamine sulfate or the addition of purified platelet Factor 4 (PF4) to the plasma [10].

Chemical compound and disease context of Thrombin Time

• The dominant findings were: different degrees of thrombocytopenia, abnormal levels of blood fibrinogen, prolonged thrombin time, and positive protamine sulfate test [11].

Biological context of Thrombin Time

• No nitroglycerin-related drug interference with heparin was observed as measured by the activated partial thromboplastin time and the thrombin time [12].
• Platelet count, APTT, throbin time, Reptilase time, Normotest, fibrinogen, Factor-VIII, ethanol gelation test, antithrombin III, fibrinolytic degradation products, alpha1-antitrypsin and alpha2-macroglobulin were studied pre- and postoperatively up to the 10th postoperative day [13].
• Whole blood clotting times (thrombin time, activated partial thromboplastin time), ex vivo platelet aggregation, and template bleeding times were determined [14].
• Platelet aggregation, antithrombin III, reptilase time, fibrinogen, plasminogen, fluid requirements, and hemodynamics were monitored [15].
• Blood-clotting effects are evaluated by activated partial thromboplastin time, thrombin time, and fibrinogen concentration tests [16].

Anatomical context of Thrombin Time

• Prothrombin time, partial thromboplastin time, thrombin time, total serum protein, albumin, globulin, and coagulant protein activity of fibrinogen, prothrombin, and factor VIII were measured before shock, at the end of shock, following resuscitation, and on day 3; thoracic duct lymph values were obtained on day 3 [17].
• Cardiovascular data, together with blood histamine levels and thrombin times, indicated that mast cell degranulation did not occur [18].
• Heparin-binding proteins are involved in thrombin time variability in normal and patient plasmas [19].
• We used thrombin times and a competitive radiometric assay to identify, quantitate and characterize endogenous heparin-like molecules in umbilical cord (n = 58) and normal adult (n = 25) plasma [20].
• Blood samples for monitoring red blood cell (RBC) mass, plasma antithrombin III activity (AT III), activated partial thromboplastin time (APTT), and thrombin time (TT) were taken at 8 hourly intervals during the treatment period and at all of the Control Period Hours [21].

Associations of Thrombin Time with chemical compounds

• A progressive delay in thrombin time was associated with increasing sialic acid content of the patient fibrinogen [22].
• The anticoagulant prolonged the thrombin time but not the reptilase time and was resistant to boiling, proteolytic enzyme digestion, and trichloracetic acid precipitation [10].
• Argatroban given alone increased thrombin time by 454 +/- 18% and aPTT by 160 +/- 3% [23].
• The presence of the high affinity gamma' chain site on fibrinogen molecules did not inhibit fibrinogen conversion to fibrin as assessed by thrombin time measurements, and thrombin exosite binding to fibrin at either site did not inhibit its catalytic activity toward a small thrombin substrate, S-2238 [24].
• Effects of phenformin on blood sugar, serum triglyceride, thrombin time, euglobulin clot lysis time and cardiovascular complications were studied in maturity onset diabetes and in atherosclerotic patients with or without diabetes, for a period of 14-18 months [25].

Gene context of Thrombin Time

• In plasma of IBD patients significantly decreased tissue type plasminogen activator activity (t-PA) (p less than 0.02), increased plasminogen activator inhibition (PAI) (p less than 0.01) and fibrinogen (p less than 0.001), and prolonged thrombin time (p less than 0.001) and prothrombintime (p less than 0.001) were found [26].
• Incubation on ice yielded a decrease to 45% of control, whereas alpha 2-antiplasmin was fully consumed at 37 degrees C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25 degrees C. Thrombin time prolonged to 190% of control [27].
• Activated partial thromboplastin time (APTT), thrombin time (TT), prothrombin time (PT) and tissue factor pathway inhibitor (TFPI) were higher after 8 p.m. injection than after 8 a.m. injection (p < 0.05) while no chrono-pharmacological variation of anti factor Xa (AXa) activity was observed [28].
• Thrombin time dependently phosphorylated HSP27 at Ser-15 and Ser-85 while having no effect on the levels of HSP27 [29].
• Patients exhibited lower ATIII, prolongation of the APTT and TT, but not PT or the reptilase time, which is a consequence of heparinization [30].

Analytical, diagnostic and therapeutic context of Thrombin Time

• The thrombin time (TT), activated partial thromboplastin time (aPTT), and heparin neutralization test were determined at several intervals during the transplantation [31].
• These included determinations of lactate dehydrogenase, creatine kinase, aspartate transaminase, alkaline phosphatase, blood urea nitrogen, total protein, thyroid-stimulating hormone, digoxin, thrombin time, activated partial thromboplastin time, and prothrombin time [32].
• Both zein film and heparin-loaded zein microsphere film were effective in suppressing platelet adhesion, and the heparin-loaded film showed a better anticoagulation as determined with thrombin time (TT) assay [33].
• Therefore, high-dose thromboplastin time and high-dose thrombin time seem to be reliable for monitoring anticoagulation when aprotinin is used during cardiopulmonary bypass [34].
• The patients had significantly higher factor-VIII levels, higher platelet counts, lower factor-V and plasminogen levels, shorter thrombin times and higher serum fibrinogen degradation products (FDP) than the control group [35].

References