Fibrin Degradation Products In Patients Research Articles

Levels of D-dimer, fibrinogen, and fibrinogen degradation product in patients with acute chest pain

To determine the relationship among the levels of D-dimer, fibrinogen (FIB), and fibrin degradation products (FDP) in acute fatal chest pain patients. Methods: We retrospectively analyzed the patients with aortic dissection (AD), pulmonary embolism (PE) or acute myocardial infarction (AMI) from May 1, 2017 to April 30, 2018. All the patients had a chest and/or back pain. Levels of D-dimer, FIB, and FDP were examined at the time of admission, and the patients were further diagnosed by computed tomography angiography (CTA) or percutaneous transluminal coronary intervention (PCI). The levels and negative rates of D-dimer, FIB, and FDP in patients with AD, PE, and AMI were compared. Results: A total of 234 patients were enrolled, including 95 AD, 98 AMI, and 41 PE. In the AD group, the AMI group and the PE group, the negative ratios of D-dimer were 13.68%, 70.41% and 4.88%, respectively; the negative ratios of FDP were 24.21%, 81.63% and 24.39%, respectively. There was no significant difference in negative rates of D-dimer and FDP between the AD group and the PE group (all P>0.05), but negative rates of D-dimer and FDP were significantly higher in the AMI group than those in the AD group and the PE group (all P<0.001). The level of D-dimer in the AMI group was significantly lower than that in the AD group or in the PE group (both P<0.001), while there was no statistically significant difference between the AD group and the PE group (P>0.05). However, there were no significant difference in the FIB levels among 3 groups (all P>0.05). The FDP level in the AMI group was significantly lower than that in the AD group or in the PE group (both P<0.001), while there was no statistically significant difference between the AD group and the PE group (P>0.05). Conclusion: The levels of D-dimer and FDP are increased in AD and PE patients and may be as the useful biomarkers for the high-risk chest pain patients but not for AMI.

Coagulation/fibrinolysis and inflammation markers are associated with disease activity in patients with chronic urticaria

The evaluation of disease severity and activity of chronic urticaria (CU) is essential for the adequate treatment of patients. However, there is no reliable biomarker for such evaluations. Recently, markers of blood coagulation and fibrinolysis have been revealed to be elevated in severe cases of CU. In this article, we studied the coagulation/fibrinolysis and inflammation markers and their relationship to disease activity in patients with CU. Plasma fibrin degradation products (FDP), d-dimer and serum C-reactive protein (CRP) were measured with the assessment of disease severity and skin reaction to autologous serum in 82 patients with CU and 37 patients with acute urticaria, idiopathic angioedema (AE) or inducible types of urticaria (IU). The levels of FDP in patients with CU were significantly higher than those in patients with IU, but no other differences in FDP, d-dimer and CRP were observed among patients with different types of urticaria. These markers of patients with CU were well correlated with each other and significantly associated with disease severity of CU, but not with skin reactions to autologous serum. In 37 patients with CU, levels of all these parameters reduced as their disease condition improved, while they increased when the disease became aggravated. Regarding FDP, this relationship was observed even if FDP concentrations were within normal range throughout the study. The measurement of plasma FDP, d-dimer and serum CRP may be useful for the assessment of disease activity of CU.

Clinical Evaluation of a Monoclonal Antibody-based Enzyme Immunoassay for Fibrin Degradation Products in Patients with Clinically Suspected Pulmonary Embolism

We prospectively evaluated the diagnostic accuracy of the Fibrinostika FbDP assay in 304 consecutive patients with suspected pulmonary embolism and examined potentially useful cut-off points at which the disease can be excluded. The prevalence of pulmonary embolism was 31%. The assay generated an area under the Receiver Operating Characteristic curve of 0.79 (95% CI 0.73-0.84). A cut-off point of 0.05 microg/ml yielded a sensitivity, specificity, negative predictive value and an exclusion efficiency of 100% (95% CI 96-100), 5% (95% CI 2-9), 100% (95% CI 69-100) and 3% (95% CI 2-6), respectively. A clinically useful cut-off point seems to be 0.11 microg/ml which corresponded with a sensitivity, specificity, negative predictive value and an exclusion efficiency of 96% (95% CI 90-99), 27% (95% CI 24-28), 93% (95% CI 84-98) and 20% (95% CI 16-25), respectively. We conclude that the assay has potential clinical utility for the exclusion of pulmonary embolism, but it cannot be used as a sole test.

Characterization of cross-linked fibrin degradation products in patients treated with fibrinolytic agents

Characterization of cross-linked fibrin degradation products in patients treated with fibrinolytic agents

Plasminogen Activator and Its Inhibitor in Cancer Patients Treated With Tumor Necrosis Factor

We noted the presence of plasma fibrin degradation products in patients treated with recombinant human tumor necrosis factor (TNF) in a phase I trial. To further define this observation, we investigated the effects of TNF on the fibrinolytic system in patients entered in the same trial. In the 14 patients studied, fibrinolytic parameters were measured by analyzing blood samples for tissue plasminogen activator and inhibitor at 0, 1, 2, 4, 6, and 18-24 hours after initiation of TNF treatment. We used a chromogenic substrate method to determine activity of plasminogen activator and its inhibitor and an enzyme-linked immunosorbent assay (ELISA) to determine levels of antigen (tissue-type plasminogen activator). Molecular weight was determined by zymographic assay. TNF treatment was associated with tissue-type plasminogen activator induction within 1 hour of TNF initiation. The plasminogen activator produced was consistent with tissue-type plasminogen activator derived from endothelium as evidenced by molecular weight analysis and ELISA. Moreover, induction of plasminogen activator inhibitor occurred following the release of tissue-type plasminogen activator, and our data suggest a dose-response effect for TNF. At high doses (i.e., 200 and 240 micrograms/m2), there was a more rapid and prolonged release of plasminogen activator inhibitor, which had an inverse relationship with the level of antigenic tissue-type plasminogen activator. Zymographic analysis showed urokinase-type plasminogen activator activity in 13 of 14 patients. In three patients, simultaneous measurements of white blood cells and tissue-type plasminogen activator revealed a temporal association between the TNF-associated rapid granulocytopenia at 30 minutes after TNF initiation and release of tissue-type plasminogen activator antigen. The results suggest a positive association between TNF and rapid induction of plasminogen activator activity that is consistent with an endothelial product. It is possible that, at high doses, TNF may interact directly with vascular endothelium, leading to rapid and prolonged production of plasminogen activator inhibitor. There was a dose-response effect between TNF and release of tissue-type plasminogen activator. The release of tissue-type plasminogen activator was preceded by granulocytopenia, which may indicate an association between a proposed TNF-induced granulocyte-endothelial interaction in vivo and release of tissue-type plasminogen activator. These findings demonstrating the effects of TNF on the fibrinolytic system can be analyzed further in experimental systems to determine the implications for use of this agent as a biological response modifier in cancer therapy.

Effect of intraoperative aprotinin administration on postoperative bleeding in patients undergoing cardiopulmonary bypass operation

To study the hemostyptic effect of aprotinin (Trasylol) in patients undergoing extracorporeal circulation for coronary artery bypass operations, we randomized 12 of 24 patients to receive aprotinin in high dosage (about 800 mg) during extracorporeal circulation. From the resulting two groups each, one patient was excluded from the study because of postoperative myocardial infarction (control group) and surgical hemorrhage (aprotinin group) leading to a second operation. Although heparin was used for anticoagulation in all 22 patients, all had a marked increase in plasma levels of thrombin-antithrombin III complexes during extracorporeal circulation, indicating an intravasal activation of coagulation. By monitoring the plasma levels of fibrin degradation products in patients without aprotinin therapy, we recorded a concomitant hyperfibrinolysis significantly less pronounced in patients receiving aprotinin (p less than 0.005). The mean total postoperative blood loss was lower in patients receiving aprotinin (620 ml) than in control patients (1000 ml; p less than 0.03). The results confirm previous reports of a hemostyptic effect of aprotinin in cardiac operations. This effect is probably due to a prevention of hyperfibrinolysis.

Fibrinogen and fibrin degradation products in patients undergoing open-heart surgery

We have determined fibrinogen and fibrin degradation products (FgDP and FbDP respectively) by an ELISA method using specific monoclonal antibodies in 100 patients undergoing cardiopulmonary bypass (CPB) for valvular heart disease and in 60 patients undergoing aorto-coronary bypass surgery. Blood samples were taken pre-operatively and on post-operative days 1 and 5. Post-operative evolution was similar in both patient groups, with a significant increase in FgDP on post-operative days 1 and 5 with respect to baseline value (P less than 0.01). FbDP were also significantly higher on post-operative days 1 and 5 (P less than 0.001), especially the day after surgery in patients with valvular disease as compared with coronary patients (P less than 0.01). Our results indicate that fibrinolysis is more important than fibrinogenolysis after open-heart surgery, which may have pathophysiological implications.

193 Determination of specific plasma fibrin degradation products in patients with pulmonary embolism associated with deep-vein thrombosis treated by fibrinolytic agents

193 Determination of specific plasma fibrin degradation products in patients with pulmonary embolism associated with deep-vein thrombosis treated by fibrinolytic agents

Specific determination and identification of cross-linked fibrin degradation products in patients under thrombolytic therapy for myocardial infarction.

We have demonstrated that the specific determination and identification of plasma FbDP alone is not sufficient to follow the effectiveness of thrombolytic therapy. Some patients who received an intravenous infusion of rt-PA for myocardial infarction had very high plasma FbDP levels, although no recanalization was observed angiographically. Since in many cases the FbDP levels increased after recanalization, it is assumed that rethrombosis may occur during and after t-PA treatment.

Serum fibrin degradation products in acute idiopathic anterior uveitis.

Levels of serum fibrin degradation products were measured by the Staphylococcal clumping test in patients with acute idiopathic anterior uveitis and traumatic anterior uveitis. We found them to be significantly increased (P less than 0.001) in patients with acute idiopathic anterior uveitis (11.0 micrograms/ml). The extent of this increase in the serum levels of fibrin degradation products correlated well with increased severity of the disease. It showed return to normal levels (5.0 micrograms/ml) with the clinical improvement. It increased again with the re-appearance of acute stage of the disease. We found no alteration in the levels of serum fibrin degradation products in patients with traumatic anterior uveitis. We hypothesise that uveal deposition of immune complexes causes secondary platelet damage and intravascular coagulation which results in uveal tissue damage through inflammation.

Rapid detection of cross-linked fibrin degradation products in plasma using monoclonal antibody-coated latex particles.

Conformational and structural changes on conversion of fibrinogen to fibrin and its cross-linking by Factor XIIIa lead to the development of new antigenic determinants that permit differentiation between their plasminolytic cleavage products. A monoclonal antibody (DD-3B6/22) that is specific for cross-linked fibrin derivatives containing the D dimer configuration has been used in developing a latex agglutination procedure that can detect fibrin degradation products in either plasma or serum. Fibrinogen or its degradation products do not cross-react with this antibody. Results were calibrated with an enzyme immunoassay, which used a purified D dimer standard. Plasmas from 40 normal subjects, all having D dimer levels below 250 ng/mL measured by enzyme immunoassay, were all negative by latex assay. In contrast, positive latex agglutination titers were obtained with 87 of 88 patients with demonstrated deep venous thrombosis, pulmonary embolism, or disseminated intravascular coagulation. Compared to enzyme immunoassay, latex agglutination assay is less sensitive, but this latex procedure provides a rapid and less elaborate test for elevated levels of cross-linked fibrin degradation products in patients with thrombosis. Plasma assays for fibrin degradation products are preferable to those using serum.

Detection of fibrin degradation products. A simplified technic.

An agglutination inhibition technic using CrCl3-treated erythrocytes for the quantification of circulating fibrin degradation products in patients with thromboembolic and fibrinolytic states is described.

Characterization of fibrin degradation products in patients on ancrod therapy: comparison with fibrinogen derivatives produced by plasmin.

Summary. The fibrin digestion products which appear in serum of patients having treatment with ancrod have been compared with derivatives of human fibrinogen produced by plasmin by means of immunoelectrophoresis, immunodiffusion and gel filtration techniques. In ancrod‐treated patients the large molecular weight derivatives X and Y, as well as fragments D and E were seen 4 hr after the start of therapy. By 24 hr the main serum component was fragment D with low concentrations of large molecular weight derivatives still present, but fragment E had been cleared from the circulation. The identity of these fragments to the known products of fibrinogen proteolysis by plasmin has been confirmed. It is suggested that the initial degradation of fibrin micro‐clots produced in the circulation during ancrod infusion is mediated by the fibrinolytic enzyme system.