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PubMed2000

Heparin-binding proteins are involved in thrombin time variability in normal and patient plasmas.

The ability of plasma proteins to neutralize the anticoagulant activity of heparin was studied using a thrombin time assay with 20 normal adult and 207 patient plasma samples. The thrombin times of normal adult plasmas spiked with the same amount of heparin were found to vary significantly, and this variability was attributed to differences in heparin-binding proteins among individuals. This possibility was investigated by determining thrombin times for a variety of plasma samples following proteolytic digestion. A study of patient pooled plasma showed that incubation with a protease increased the thrombin time from 23 s to > 300 s, suggesting that the anticoagulant activity of heparin could be neutralized by plasma proteins and released with proteolytic digestion. Incubation of the digested plasma with heparinase I returned the thrombin time almost to control values. In addition, patients who received prior heparin injections had different responses to similar dosages of heparin, as indicated by differences in thrombin times. Thus, the anticoagulant activity of heparin may be affected by the balance between free heparin and protein-bound heparin in plasma.

Adult↗
PubMed1992

Streptokinase induced defibrination assessed by thrombin time: effects on residual coronary stenosis and left ventricular ejection fraction.

OBJECTIVE: To evaluate laboratory markers of defibrination early after thrombolytic therapy and to determine their relation to residual stenosis and left ventricular ejection fraction measured angiographically before discharge from hospital. DESIGN: Prospective analysis of defibrination after streptokinase measured by fibrinogen assay and thrombin time to provide a comparison of these coagulation variables for predicting angiographic responses to treatment in patients with acute myocardial infarction. SETTING: The coronary care unit of a district general hospital. PATIENTS: 44 patients with acute myocardial infarction treated by streptokinase infusion, all of whom underwent paired blood sampling before and one hour after streptokinase and cardiac catheterisation at a median of six (interquartile range 3-9) days later. MAIN OUTCOME MEASURES: Assay of thrombin time and plasma fibrinogen concentrations one hour after streptokinase infusion. Relations between these coagulation variables and residual stenosis in the infarct related coronary artery and left ventricular ejection fraction. Separate analyses are presented for all patients (n = 44) and those with patency of the infarct related artery (n = 35). RESULTS: Streptokinase infusion produced profound defibrination in every patient as shown by changes in thrombin time and circulating fibrinogen. Thrombin time after streptokinase infusion correlated significantly with both residual stenosis (r = -0.43, p < 0.005) and left ventricular ejection fraction (r = 0.38, p < 0.02). The importance of these correlations was emphasised by the interquartile group comparison which showed that a thrombin time > or = 49 seconds predicted a residual stenosis of 74% and an ejection fraction of 65%, compared with 90% and 49% for a thrombin time < or = 31 seconds (p < 0.01). When the analysis was restricted to patients with patency of the infarct related artery, the correlation between thrombin time and residual stenosis remained significant and group comparisons continued to show that patients in the highest quartile range had more widely patent arteries and better preservation of ejection fraction. Analysis of the fibrinogen data, on the other hand, showed insignificant or only marginally significant correlations with these angiographic variables. CONCLUSIONS: Early after streptokinase infusion for acute myocardial infarction, the level of defibrination measured by thrombin time has an important influence on residual coronary stenosis and left ventricular ejection fraction at discharge from hospital, values above 49 seconds being associated with the best angiographic result.

Aged↗
PubMed1989

[Laboratory controls of heparin therapy with thrombin time, partial thromboplastin time and activated recalcification time].

For the laboratory control of a heparin therapy thrombin time, partial thromboplastin time and activated recalcification time are used. On account of distinct differences in the heparin sensitivity of these reactions an indication-related application is necessary. The ability of evidence and the possibility of establishing test-specific therapeutic regions are restricted by differences caused by reagents, individual variability and influence by accompanying haemostasiological changes. The own approach, taking into consideration the so-called heparin resistance, it presented.

Blood Coagulation Tests↗
PubMed1996

A proposed model to monitor heparin therapy using the concentrated thrombin time which allows standardisation of reagents and improved estimation of heparin concentrations.

The concentrated thrombin time (CTT), a thrombin time performed with a high concentration of thrombin, was evaluated as an alternative to the activated partial thromboplastin time (APTT) for monitoring of heparin therapy. Forty-nine plasmas from patients receiving unfractionated heparin therapy were tested. It was first demonstrated that CTTs using three commercial reagents could be standardised against CTTs performed with a reference reagent, MRC reagent 66/305. For comparison, APTTs were performed on the plasmas. As a benchmark of the degree of heparinisation, the heparin concentration of the plasmas was determined by chromogenic anti-IIa heparin assays, therapeutic range being 0.2-0.4 units/ml. The optimal relationships of the CTTs and APTT with the heparin concentration were established. These were used to predict the heparin concentrations of the plasmas from the results of the APTT, CTT performed with the reference reagent, and transformed CTT performed with each of the three commercial reagents. In predicting the assayed plasma heparin concentrations, the accuracy of the APTT was only 53%, while the CTT was from 78 to 82%. The CTT can be standardised and, subject to results of clinical trials, could provide an improved method of monitoring heparin therapy.

Afibrinogenemia↗
PubMed1980

Monitoring of heparin treatment. Comparison of thrombin time, activated partial thromboplastin time, and plasma heparin concentration, and analysis of the behavior of antithrombin III.

Three laboratory methods for monitoring heparin treatment have been compared using 63 plasma samples: the thrombin time, the activated partial thromboplastin time, and the measurement of the heparin concentration using a chromogenic substrate. A good correlation was found between the methods. However, the intensity of anticoagulation was identical in only 27 of the 63 samples (43%) when the thrombin time and the activated partial thromboplastin time were compared. Fully discordant results were recorded for four samples (6%). The thrombin time was found to be more closely related to the plasma heparin concentration than was the activated partial thromboplastin time. Both antithrombin-III activity and immunologic levels were lower in the group with strong heparinization. It is suggested that the thrombin time is a good and safe method for monitoring heparin treatment.

Antithrombin III↗
PubMed1991

Inhibitor of the thrombin time in systemic amyloidosis: a common coagulation abnormality.

Patients with primary systemic amyloidosis (AL) often experience bleeding, and we report a newly recognized coagulation abnormality in AL. Of 103 patients with primary systemic AL studied over 2 years, 41 had prolongation of the thrombin time (range, 25 to 46 seconds; normal, less than 22 seconds) and reptilase time (range, 17 to 39 seconds; normal, 14 to 16 seconds). The fibrinogen from the plasma of 36 patients was precipitated by beta-alanine and diluted to a concentration of approximately 200 mg/dL. The thrombin times of the precipitated fibrinogens were normal in 34 patients, implying that an inhibitor was responsible for the abnormal tests. The addition of patient fibrinogen-free plasma to normal plasma prolonged the thrombin times, and this result confirmed the presence of an inhibitor. The inhibitor is more likely to be present in patients with nephrotic syndrome (20 of our patients) and congestive heart failure (six). A circulating monoclonal protein (24 patients), the presence of amyloid liver involvement (eight), and the presence of amyloid neuropathy (nine) were not predisposing factors. Only one patient had deficiency of factor X. We conclude that inhibition of fibrinogen conversion to a fibrin clot rather than dysfibrinogenemia is the cause of the prolonged thrombin time in primary systemic AL.

Amyloidosis↗
PubMed1976

Effects of source and concentration of thrombin, and divalent cations, on thrombin time of heparinized plasma.

The effects of the source and concentration of thrombin, and those of divalent cations, on the thrombin time (TT) of heparinized plasma were investigated. A correlation between TT and the heparin concentration was obtained only when the thrombin was of human origin and when it was reconstituted in divalent cation solutions. Relatively small variations in thrombin concentration resulted in marked differences in TT of heparinized plasma. Bovine thrombin gave a very prolonged TT of heparinized plasma compared with human thrombin, though the two thrombins gave identical TT's for non-heparinized control plasma. Divalent cation solution, in which thrombin was reconstituted, had a profound influence on TT of heparin plasma. When thrombin was reconstituted in 0.1 M MnCl2 solution, the TT of a plasma containing 0.5 unit heparin per ml. was the same as that of a plasma containing no heparin. The reliability of the thrombin time test as a means of monitoring heparin anticoagulation must be established by individual laboratories via extensive testing of clinical samples.

Animals↗
PubMed1975

An improved method for plasma fibrinogen based on thrombin time measurement.

Methods for plasma fibrinogen based on thrombin time are technically simple, rapid, and sensitive, although "false low" results may occur due to heparin interference. The present modification incorporates Polybrene into buffer to eliminate this heparin interference. The proposed method shown excellent agreement with a reference procedure based on clottable protein, and excellent day-to-day precision (C.V.3.5%). The present method is easily adaptable to semi-automated measurements.

Autoanalysis↗
PubMed1976

Whole-blood thrombin time: a bedside method for determination of heparin activity.

A bedside method of measurement of the whole-blood thrombin time for the determination of heparin activity was used in 300 dialyses. It was easily performed by the whole staff despite the absence of previous training in laboratory work. This test, using a clot timer with an automatic pipette device, gives a minimum risk of exposure to hepatitis virus. An increase of the thrombin time of 50-100 per cent above the starting value (3.7-6.6 sec) was aimed at during the heparin infusion. Bleeding complications, which were minor, were seen only on 18 and fibrin formation only on 26 occasions out of 1500 observations. Within the 50-100 per cent limits bleeding complications were observed on 2 and fibrin formation on only 13 occasions. No protamine was given.

Blood Coagulation Tests↗
PubMed1999

High dose thrombin time versus the activated clotting time during cardiopulmonary bypass.

In this study we compared the High Dose Thrombin Time (HiTT) with the Activated Clotting Time (ACT) during cardiopulmonary bypass (CPB) in non-aprotinin treated patients. On the advice of the HiTT test manufacturer each institution should perform comparative ACT/HiTT assays in the cardiac surgery population. In previous tests our target ACT value of 480 seconds corresponds with a mean HiTT value of 190 seconds. Our results showed that after heparinization (300-400 IU/kg body weight) 8 out of 20 patients did not reach the target ACT of 480 seconds, while the HiTT results in those 8 patients were higher than our target time of 190 seconds. Four heparin pretreated patients who received 400 IU/kg heparin, had relatively low ACT values (467 +/- 14 sec.) and high HiTT values (324 +/- 47 sec.). Before and during CPB there was a poor correlation between the HiTT and ACT (r = 0.38). The results of this study show that for the individual patient the target HiTT of 190 seconds is no guarantee for reaching an adequate ACT of 480 seconds. Although the HiTT may be a very useful assay for monitoring heparin effects during CPB, the determination of the target time can be a point of discussion. In contrast of the advice of the manufacturer we therefore suggest that comparative ACT/HiTT assay should be done in every individual patient to determine a safe target HiTT time, instead of the whole group of patients.

Adult↗
PubMed1995

The prolonged thrombin time of nephrotic syndrome.

PURPOSE: Little information is available that documents the incidence and possible etiology of a prolonged thrombin time (TT) found in children with nephrotic syndrome. We speculated that this prolonged TT might best be explained by an altered fibrinogen similar to that found in the newborn. PATIENTS AND METHODS: We describe 20 children with nephrosis, an unexplained prolonged TT and reptilase time (RT), and an elevated fibrinogen level. Thrombin and/or plasmin effect on plasma fibrinogen was studied by analyzing for soluble monomer, D-dimer, fibrin degradation products, B beta 1-42 peptide, and by polyacrylamide gel electrophoresis (PAGE) and agarose electrophoresis. Structural changes in the fibrinogen molecule were investigated using two-dimensional gel (2D gel) electrophoresis. Fibrinogen was purified via glycine precipitation, and the sialic acid (SA) content was determined. RESULTS: No evidence for in vivo thrombin and/or plasmin effect on fibrinogen could be detected in 13 of 20 children tested. Additionally, no fibrin/fibrinogen degradation products or soluble fibrin complexes were detected using PAGE or agarose electrophoresis in this group of patients. The B beta isoforms of nephrosis fibrinogen were similar in isoelectric point on 2D gel electrophoresis to those of fetal fibrinogen and demonstrated a greater electronegative shift when compared with normal adult fibrinogen. Also, the SA content of nephrosis and fetal fibrinogen were greater than that measured in adult fibrinogen. Both nephrosis and fetal fibrinogen were more resistant to neuraminidase treatment than was normal adult fibrinogen. CONCLUSIONS: These data support the notion that an altered fibrinogen exists in some children with nephrotic syndrome characterized by an increased TT and RT, elevated fibrinogen, and both an increased negative charge and SA content.

Adult↗