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Determination of markers of coagulation activation and reactive fibrinolysis in patients with mechanical heart valve prosthesis at different intensities of oral anticoagulation.

In a group of 60 patients with mechanical heart valve prosthesis prothrombin fragment 1 + 2, thrombin-antithrombin III complexes and D-dimer have been determined in order to assess the residual coagulation activation and the extent of the reactive fibrinolysis. The patients were divided into three subgroups of 20 patients each with different intensities of oral anticoagulation as indicated by International Normalized Ratio (INR) values in the ranges 4.8-3.6, 3.5-2.5 and 2.4-2.1. From the two markers of coagulation activation studied (prothrombin fragment 1 + 2 and thrombin-antithrombin III (TAT)) the prothrombin fragment 1 + 2 was dependent on the INR level in all groups, although the median values were still significantly beneath the lower limit of the reference range. The D-dimer concentrations were unexpectedly high with respect to the low coagulation activation levels, as indicated by the D-dimer/TAT and D-dimer/F 1 + 2 ratios. This demonstrates the enhanced presence of fibrin degradation products as a scarcely described side-effect of oral anticoagulation. The anticoagulant properties of fibrin degradation products might contribute partly to the in vivo haemorrhagic risk in high-intensity oral anticoagulation. These results show, inasmuch as the prothrombin fragment 1 + 2 is concerned, that from the laboratory point of view the residual thrombin activity is low enough to be adequate under the therapeutical regimen followed in this study. However, the question of the efficacy of anticoagulation intensities can only be finally answered by clinical trials.

Administration, Oral

Markers of coagulation and fibrinolysis after fractures of the lower extremities.

The study was performed to detect activation of coagulation and fibrinolysis in terms of prothrombin fragment 1 and 2 (F1 + 2), thrombin-antithrombin III complex (TAT), fibrin degradation products (FbDP), fibrinogen degradation products (FgDP), and soluble fibrin monomers (FM) in plasma from 39 patients with fractures of the lower extremities. We found substantially elevated levels of the molecular markers at admission and on the day after admission (Day 1) compared with control levels. Admission levels of F1 + 2, TAT, FbDP and FgDP were significantly higher compared with levels on day 1, whereas levels of FM were not significantly different between the two days. Generally there were good correlations between all markers of coagulation and fibrinolysis at admission whereas correlations were weaker or absent on day 1. In conclusion we found substantial haemostatic activation as a immediate response to trauma. Increased levels of F1 + 2, TAT, FM, FbDP and FgDP appear to be a normal physiological reaction after fractures of the lower extremities.

Adult

Hypercoagulable state in patients with hypercholesterolemia: effects of pravastatin.

Molecular markers of the coagulation system and the effects of pravastatin on lipid levels and the coagulation markers were studied in 48 patients (mean age, 55 years) with hypercholesterolemia (plasma total cholesterol levels > 280 mg/dl). Each patient received 10 mg of pravastatin daily for 3 months. Plasma total cholesterol and low-density lipoprotein cholesterol levels decreased significantly during treatment and high-density lipoprotein cholesterol levels increased significantly. Above-normal plasma levels of thrombin-antithrombin III complex, fibrinopeptide A, FDP-D-dimer, plasminogen activator inhibitor-I, and thrombomodulin were found in the patients before treatment; each of these was reduced significantly during treatment. The findings suggest the presence of a hypercoagulable state in hypercholesterolemia and that pravastatin might prevent the hypercoagulable state by reducing hypercholesterolemia.

Adult

Gemfibrozil reduces plasma prothrombin fragment F1 + 2 concentration, a marker of coagulability, in patients with coronary heart disease.

The effects of gemfibrozil on several indices of haemostatic activity were explored in male patients with coronary heart disease (CHD). Sixty-three of 71 patients completed a crossover study in which gemfibrozil 1,200 mg/day and matching placebo were each taken in randomised order for 2 months in a double-blind manner, separated by a 2-month washout period. Serum cholesterol decreased by an average (95% confidence interval) of 12 (9 to 15)% and non-fasting triglyceride concentration by 43 (34 to 51)% during active treatment. Plasma prothrombin fragment F1 + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase. Factor VII coagulant activity (VIIc) and antigen concentration, and fibrinopeptide A concentration were not influenced by gemfibrozil in the group overall. However, the VIIc response appeared to be dependent upon the untreated cholesterol level. Hypercholesterolaemic men (cholesterol greater than 6.5 mmol/l) experienced a significant reduction in VIIc averaging 6% of standard during active therapy. Other effects of gemfibrozil were a 5 (2 to 9)% increase in plasma fibrinogen by a gravimetric method, an 11 (8 to 13)% increase in platelet count, and a 6 (2 to 10)% reduction in white cell count. The reduced incidence of CHD following gemfibrozil therapy in hyperlipidaemic patients may arise in part through a reduction in procoagulant activity and thus the risk of an occlusive coronary thrombosis.

Biomarkers

Comparison of markers of coagulation activation in patients under oral anticoagulation at different levels.

Three groups of patients receiving oral anticoagulation treatment were evaluated. The groups consisted of patients with mechanical heart valve prosthesis (n = 60), patients after coronary bypass graft surgery (n = 60) and patients using oral anticoagulation after deep venous thrombosis or pulmonary embolism (n = 60). The patient groups were subdivided into three groups of 20 patients, each group receiving different levels of oral anticoagulation as indicated by the international normalized ratio (INR). Prothrombin fragment 1 + 2, thrombin-antithrombin III complexes and fibrin monomers were determined as coagulation activation makers. The prothrombin fragments 1 + 2 were INR dependent in all groups whereas the thrombin-antithrombin III values were only INR dependent in the group of patients with mechanical heart valve prosthesis. For fibrin monomers no correlation with the INR levels could be found. These results indicate that prothrombin fragment 1 + 2 is the only laboratory quantity of the three, which provides a suitable index of low thrombin activity during anticoagulation therapy.

Administration, Oral

[A clinical study on hemostatic fluctuation during and after cardiopulmonary bypass using hemostatic molecular markers].

Heparin is indispensable anticoagulant for cardiopulmonary bypass, but the dose of heparin is even now under discussion. In this study, hemostatic fluctuation was analyzed during and after the bypass using hemostatic molecular markers. The subjects were 16 adult cases of open heart surgery, 12 males, 4 females. The average age was 55.0 year. Operations were aortocoronary bypass in 12, valvular surgery in 3 and ASD patch closure in one with moderate hypothermic cardiopulmonary bypass. At the beginning of cardiopulmonary bypass, 3 mg/kg heparin was administered and the equivalent amount of protamine sulfate was used for neutralization at the end of the bypass. Platelet count, hematocrit, antithrombin III (ATIII), beta-thromboglobulin, platelet factor 4, fibrinopeptide A, thrombin antithrombin III complex, FDP, D dimer FDP, plasmin alpha 2 plasmin inhibitor complex, tissue plasminogen activator (t-PA), and thrombomodulin (TM) were measured through the operation up to two weeks after surgery. ATIII decreased to 50% of control value all through the bypass. Platelet markers increased immediately, and the activated state continued 3 hours after the bypass. Coagulation markers increased markedly after the aortic declamping, and reached at its peak by three times as control value, immediately after the protamine neutralization and continued for 3 hours. During the bypass, fibrinogenolysis caused by t-PA which was stimulated by non-physiological circulation and stimulating substances, was observed. Fibrinolysis occurred following the hypercoagulability after the neutralization. TM was within normal range before the aortic declamping. But increased gradually after the declamp, and reached twice as much as the base line. It could be concluded that hypercoagulability and high platelet activation might play a role of perioperative thrombosis. Hypercoagulability and increase of serum TM would be related to reperfusion of the lung. The increasing of TM would reflect broad injury of vessel walls after the bypass, because plasma TM increased following the generalized injury of endothelial cells.

Adult

Relationship between perimetric eccentricity and retinal locus in a human eye. Comparison with theoretical calculations.

A blind but grossly normal eye was removed because of severe pain. With the patient's consent, photo-coagulation markers were placed along the horizontal meridian of the retina prior to surgery. The angular coordinates in visual space of the markers were determined by an ophthalmoscopic procedure. The loci of the markers were also determined in a flat preparation following enucleation. The relationship between retinal arc and perimetric eccentricity was found to be approximately linear up to at least 50 degrees. Our findings validate earlier theoretical calculations within this range.

Female

Coagulation activation is associated with genomic-instability-related features in TP53-mutated AML and MDS: routine laboratory patterns beyond classical disseminated intravascular coagulation.

BACKGROUND: Disseminated intravascular coagulation (DIC) is a serious complication of acute myeloid leukemia (AML) associated with poor prognosis. In TP53-mutated AML and myelodysplastic syndrome (MDS), however, the classical ISTH criteria rarely identify overt DIC, although bleeding and thrombotic complications are well documented in acute leukaemia. We hypothesized that these patients exhibit a lower-grade, subclinical coagulation activation that is associated with the underlying genomic-instability-related features of TP53-mutant disease. METHODS: We retrospectively analyzed 107 consecutive patients with TP53-mutated AML (n = 52) or high-risk MDS (MDS, n = 55), median age 65 years, diagnosed and initially evaluated at our centre between 2018 and 2025. Seven routine coagulation markers and 46 co-mutated genes were evaluated for associations with overall survival (OS) using univariate and multivariable Cox regression, continuous dose-response modeling, and unsupervised k-means clustering. Internal validity was assessed by 1000 bootstrap resamples. RESULTS: Overt DIC according to ISTH criteria was rare (15%). Subclinical activation was common: 50% of patients had a D-dimer &#x2265;1&#xa0;&#x3bc;g/mL, 41% a fibrinogen &#x2265;4&#xa0;g/L, and 29% an INR &#x2265;1.2. In univariate analysis, D-dimer, fibrinogen, INR, prothrombin time, and activated partial thromboplastin time were each associated with OS (HR 1.33-1.38 per SD; all p < 0.05). Complex karyotype correlated with higher D-dimer (median 1.39 vs. 0.60&#xa0;&#x3bc;g/mL, p = 0.022) and fibrinogen (3.91 vs. 2.53&#xa0;g/L, p = 0.007), while TP53 variant allele frequency (VAF) showed modest positive correlations with D-dimer (&#x3c1; = 0.21), INR (&#x3c1; = 0.27), and PT (&#x3c1; = 0.27; all p < 0.05). Clustering identified three coagulation phenotypes: Silent (51%), Thrombo-inflammatory (31%), and Consumption-like (18%), showing a graded but statistically non-significant gradient in molecular features and a stepwise decline in median OS (14, 10 and 8 months; log-rank p = 0.041). After adjustment for complex karyotype, TP53 VAF, and favorable co-mutation count, the Consumption-like phenotype was associated with a non-significant increased risk (HR 1.83, 95% CI 0.92-3.65, p = 0.084), whereas favorable co-mutation pathways remained independently protective (HR 0.56, 95% CI 0.35-0.90, p = 0.016). CONCLUSION: In TP53-mutated AML/MDS, coagulation activation intensity is associated with the degree of genomic instability. The three phenotypes may add biological resolution beyond classical DIC and cytogenetic risk groups, but represent laboratory patterns rather than validated bleeding or thrombosis prediction tools. However, after accounting for genomic features, phenotypes were not independent predictors of outcome, with complex karyotype, TP53 VAF, and favorable co-mutation count driving prognosis. Because treatment intensity and other clinical confounders were not available, these survival associations are hypothesis-generating. Coagulation profiling remains inexpensive, widely accessible, and offers a practical window into disease biology that warrants prospective validation.

TP53

L-carnitine and platelet aggregation in uremic patients subjected to hemodialysis.

It has been reported that treatment with L-carnitine at a daily dose of 3 g orally may cause a rise in platelet aggregation and serum triglyceride concentration in hemodialyzed patients. The present double-blind cross-over study has been performed to evaluate the influence of L-carnitine when compared with placebo on platelet aggregation and plasma concentrations of various factors involved in platelet activation. In addition, the concentration of triglycerides, cholesterol and HDL-cholesterol has been evaluated. 18 uremic patients on maintenance hemodialysis for at least 1 year were randomly allocated either to a control group receiving placebo or to a group treated with L-carnitine. Statistical analysis performed by means of ANOVA did not show any significant change in the serum concentration of cholesterol, HDL-cholesterol and triglycerides. Furthermore, platelet aggregation tests (performed with adenosine 5'-diphosphate, epinephrine, thrombin and collagen) and plasma beta-thromboglobulin concentration did not show any statistically significant difference. In addition, the plasma concentration of several coagulation markers, such as factor VIIIc, antithrombin III, alpha 2-antiplasmin, and fibrinopeptide A, did not show any significant variation. The results suggest that under our experimental conditions L-carnitine neither increases the risk of thromboembolism nor alters the serum lipid content in uremic patients on chronic hemodialysis.

Adult

Coagulation and fibrinolysis markers in seminal plasma of patients under evaluation for involuntary childlessness.

Semen specimens from four groups of patients were evaluated for coagulation and fibrinolysis factors: a group of patients with infertile semen and involuntary childlessness (n = 35), a group with fertile semen and involuntary childlessness (n = 39), a group with fertile semen and proven fertility before vasectomy (n = 34) and a group with infertile semen after vasectomy (n = 147). The third patient group with proven fertility before vasectomy was considered as a control group. Only small amounts of fibrinogen, factor VIII:c, plasminogen, antithrombin III, fibrin monomers and plasminogen activator inhibitor-1 were detected in seminal plasma. The thrombin-antithrombin III, D-dimer and tissue plasminogen activator regular concentrations were measured and the D-dimer/thrombin-antithrombin III ratios calculated. The reference ranges were assessed and the quantities were compared in the different patient groups. Significant differences were demonstrated between the prevasectomy group (= control group) and both the postvasectomy and the infertility groups with respect to D-dimer and D-dimer/thrombin-antithrombin III ratio. We conclude that both coagulation and fibrinolysis play a part in coagulum formation and liquefaction of seminal plasma. The balance between coagulation and fibrinolysis (expressed as D-dimer/thrombin-antithrombin III ratio) was significantly different between the control group and the three patient groups. The coagulation/fibrinolysis balance was impaired in the semen from post vasectomy patients and from those with involuntary childlessness and the D-dimer/thrombin-antithrombin III ratios in both these patient groups were very similar.

Antithrombin III

Clinical significance of new coagulation and fibrinolytic markers in ischemic stroke patients.

BACKGROUND AND PURPOSE: We investigated plasma levels of D-dimer products of crosslinked fibrin degradation products, thrombin-antithrombin III complex, and plasmin-alpha 2-antiplasmin complex for detecting coagulation system activation in ischemic stroke patients to determine the possible effect of age on these marker levels. METHODS: We measured plasma levels of these three markers in 54 acute ischemic stroke patients within 5 days of stroke onset, in 44 chronic ischemic stroke patients over 3 months from onset, and in 50 age-matched healthy subjects. We divided the stroke patients into two subgroups, those with visible occlusion and those with nonvisible occlusion having obstruction of the major cerebral artery. RESULTS: The plasma levels of these three markers were significantly (p less than 0.01) higher in the stroke patients than in controls. Significant differences did not exist at any level between the patients and controls in the younger-aged subjects (less than or equal to 64 years of age), but did exist in the older-aged subjects (greater than or equal to 75 years of age). An age-related increase of the marker levels was noted between stroke patients and controls. No significant difference in the three markers was found among any of the stroke patients. CONCLUSIONS: Increased levels of these markers in stroke patients seem to be related mostly to age.

Aged

A comparative evaluation of assays for markers of activated coagulation and/or fibrinolysis: thrombin-antithrombin complex, D-dimer and fibrinogen/fibrin fragment E antigen.

Measurements were made of levels of D-dimer in plasma and serum, thrombin-antithrombin complex (TAT) in plasma and fibrinogen/fibrin fragment E antigen (FgE) in serum in a normal healthy control group and in patients with a range of disorders associated with hypercoagulability. Levels were determined in 31 normal healthy controls, 30 patients with disseminated intravascular coagulation (DIC), 21 patients with deep venous thrombosis (DVT), 27 patients with myocardial infarction (MI), 26 patients with acute leukaemia and 56 patients with liver disease. Considering all subjects, significant correlations were established between the results of all assays. Notably high correlations (r greater than 0.9) were established between plasma and serum levels of D-dimer, between plasma levels of D-dimer and serum levels of FgE, and between serum levels of D-dimer and FgE. All assays showed very high discrimination (sensitivity) between the normal control group and patients with DIC (97-100%), but there were marked differences between the assays in sensitivity for DVT and MI. In general, the FgE assay was more sensitive than the D-dimer assay, whilst both the FgE and D-dimer assays were more sensitive than the TAT assay. The same trends were apparent in the capability of the assays to discriminate between the normal control group and patients with acute leukaemia and liver disease: disorders with an unknown prevalence of activation of coagulation/fibrinolysis. Our results indicated that measurements of fibrinogen/fibrin degradation products (FDPs) in serum were almost unaffected by artefacts. The data further suggested that the broad-spectrum FgE assay was better than the more specific D-dimer assay in detecting clinical hypercoagulability. Our study showed that, in the clinical conditions examined, FDPs were more effective markers of hypercoagulability than TAT.

Acute Disease

Measurement of markers of activated coagulation in antithrombin III deficient subjects.

Functional antithrombin III levels were measured by factor Xa inhibition in 63 members of a large family with type 2 antithrombin III deficiency and individuals were classified as antithrombin III deficient or non-deficient according to the results. F1 + 2 and TAT complexes were measured using an ELISA and FPA levels were measured by radioimmunoassay. Thirty subjects (48%) were classified as antithrombin III deficient and 33 (52%) as antithrombin III non-deficient. The mean level of F1 + 2 was significantly higher in the deficient adults (0.87 +/- 0.26) compared to both the non-deficient adults (0.70 +/- 0.21) (p = 0.03) and the deficient adults receiving warfarin (0.16 +/- 0.01) (p less than 0.001). The differences in the mean values of TAT complexes and FPA between deficient and non-deficient individuals were not statistically significant. These findings suggest that untreated antithrombin III deficient subjects generate more thrombin than their non-deficient family members and that warfarin inhibits this thrombin formation. In this cross-sectional study, it is not possible to correlate the levels of the surrogate makers with future clinical outcome.

Adolescent

Immunohistochemical localization of coagulation, fibrinolytic and antifibrinolytic markers in adenocarcinoma of the lung.

Extravascular coagulation and fibrinolysis are intimately involved in and modulate cancer cell growth, invasion and metastasis. Samples from resection specimens of patients with primary lung cancer (adenocarcinomas) were tested with monoclonal (MAb) and polyclonal (PAb) antibodies against various factors of the coagulation or fibrinolysis systems, or against antigens of inflammatory or proliferating cells. MAb Ki-67 specific to nuclear antigens of proliferating cells showed a distinct but variable staining of cell nuclei throughout the tumor tissue. Nests of tumor tissue stained with cytokeratin-specific antibodies (PKK1), whereas other parts were negative. Fibrin(ogen) and fibronectin were found throughout the tumor tissue stroma and in the alveolar lining, and the most densely stained areas were at the transition zone between normal and tumor tissue. Fibrinolytic system components like tissue plasminogen activators (t-PA), and urokinase (u-PA), and their inhibitors PAI-1 and PAI-2 were all studied. All specimens were negative for t-PA (except endothelial linings), whereas urokinase-specific antibodies stained loosely packed tumor cells and macrophages within the tumor stromal tissue and alveolar septa. Both PAI-1 and PAI-2 were most prominently expressed within interstitial and alveolar macrophages. A weaker staining of tumor tissue cells was demonstrated. Inflammatory cells like macrophages and T lymphocytes were located in aggregates or diffusely spread within tumor stromal tissue. The inflammatory reaction was most intense at the border between normal lung and tumor tissue.

Adenocarcinoma

Significance of hemostatic molecular markers during disseminated intravascular coagulation in patients with liver cirrhosis treated by endoscopic embolization for esophageal varices.

We studied the quantitative changes of hemostatic molecular markers with time during the course of disseminated intravascular coagulation (DIC) induced by endoscopic embolization using thrombin for esophageal varices in nine patients with liver cirrhosis. The plasma levels of D-dimer, a product of plasmin degradation of cross-linked fibrin, and thrombin-antithrombin-III complex (TAT) were significantly higher in patients before treatment when compared with 60 healthy individuals. The plasma levels of TAT, D-dimer, and plasmin alpha 2-plasmin inhibitor complex (PIC) increased significantly 5-15 min after thrombin injection into the varices, earlier than the changes of conventional coagulofibrinolytic factors, reached a maximum level after 180 min, and started to decline after 1 day. Although the plasma PIC level returned to normal after 7 days, both TAT and D-dimer were still above the pretreatment level. Although there was no change in urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA) increased significantly after 5 min. The plasma level of plasminogen activator inhibitor type 1 (PAI-1) showed only a slight elevation after treatment. We propose that the hemostatic molecular markers TAT, D-dimer, and PIC are suitable for the early diagnosis of DIC after endoscopic embolization using thrombin in patients with liver cirrhosis and that the increase of PAI-1 is too small for the regulation of fibrinolysis due to t-PA in DIC occurring in liver cirrhosis.

Adult

Coagulation inhibition and activation in pancreatic cancer. Changes during progress of disease.

BACKGROUND: To elucidate the disturbed hemostatic balance in patients with pancreatic cancer, the levels of plasma coagulation inhibition and coagulation activation were determined. METHODS: Twenty-one patients with adenocarcinoma of the pancreas were followed from time of diagnosis until death, using plasma analyses of coagulation inhibitors and a molecular marker of coagulation activation (thrombin-antithrombin complex, TAT). RESULTS: TAT was increased significantly at the time of diagnosis of pancreatic cancer compared with age-adjusted healthy control subjects (mean, 6.2 +/- 4.6 micrograms/l [standard deviation] versus 2.0 +/- 0.7 micrograms/l). It increased with disease progression (mean in the terminal phase, 14.1 micrograms/l; P < 0.05). Plasma levels of tissue factor pathway inhibitor (TFPI) also were increased significantly at the time of diagnosis compared with the control group (mean, 176 +/- 80% versus 127 +/- 29%; P < 0.05). The TFPI decreased to normal levels (121 +/- 40%) after surgical removal of the pancreatic tumor (n = 4) or relief of the cholestasis using a bypass procedure (n = 6). The TFPI levels increased significantly as the malignant disease progressed (from 1-3 months postoperatively to the terminal phase of disease; mean, 114 +/- 52% versus 154 +/- 60%). There was a significant positive correlation between TFPI levels and bilirubin levels; the correlation coefficient at diagnosis was 0.70 (P < 0.001). The levels of the coagulation inhibitors antithrombin, heparin cofactor II, protein C, and free protein S decreased significantly with disease progression compared with the normal values found at diagnosis. CONCLUSIONS: The mechanism for TFPI increase in cancer is not known. It may be related to the preoperative cholestasis seen in this study, but the increased degree of coagulation activation also may contribute.

Adenocarcinoma

Coagulation disorders and tumor markers in the diagnosis of pancreatic cancer.

Twenty patients (42-80 years old of whom 9 women) affected by instrumentally ascertained pancreatic cancer (7 cases were operated on) were studied. In all of them the following coagulation indices (fibrinopeptide A, FpA; beta-thromboglobulin, BTG; platelet factor IV, PF4; fibrinogen degradation products, XDP) and tumor markers (gastrointestinal cancer associated antigen, GICA; tissue polypeptide antigen, TPA; carcinoembryonic antigen, CEA; alpha-fetoprotein, or AFP) were assessed at the time of diagnosis, and 10 and 30 days after diagnosis, to test whether and which of the above parameters are more sensitive for entertaining the underlying affection. In both operated and nonoperated patients FpA was shown to be the most sensitive index. Lesser sensitivity was shown by XDP, GICA, and BTG. AFP proved to be quite useless as its serum levels constantly fell within the normal range.

Adult