Soluble fibrin (ethanol gelation test) and fibrin(ogen) degradation products in suspected thrombosis with reference to the 125I-fibrinogen uptake test for detection of thrombus formation

2009 ◽  
Vol 31 (S39) ◽  
pp. 65-74
Author(s):  
T. HAMBORG ◽  
A. SKJENNALD ◽  
H.C. GODAL ◽  
F. BROSSTAD
1987 ◽  
Author(s):  
G Oehler ◽  
H Klaus ◽  
E Spanuth ◽  
K E Stötzer

Hypercoagulability and disseminated intravascularcoagulation (DIC) are characterized by the presenceof circulating fibrin monomer complexes in plasma.In342 patients with possible DIC fibrin monomers, fibrinogen, reptilase time, antithrombin III and othercoagulation parameters were determined at frequent intervals.Testing of soluble fibrin monomer complexeswas performed using a sensitive and reliable haemagglut- ination assay, with red cells sensitized by fibrin monomers (FM-Test) and the ethanol gelation test(EGT). Method comparison regarding the influence offibrinogen levels and fibrin degradation products shows that high fibrinogen levels lead to false positive results with EGT. The same effect is observed forfibrin degradation products and EGT whereas no influence of fibrinogen level and fibrin degradation products on the FM-Test occurs.It could be shown that with normal fibrinogen concentrations (200-400 mg/dl) the positive test results by FMT and EGT are comparable, whereas with fibrinogen concentrations below 200 mg/dl the number of positive results obtained with the EGT amounted to half the number given by FMT. In the case of fibrinogen concentrations above 400 mg/dl, positive results obtained with EGT were 3.3 times higher than FMT. Nearlyidentical results were obtained by comparing the influence of degradation products. In case of high degradation product concentrations, EGT gives 4.5 timesmore positive results than FMT.Further we compared the number of positive test results obtained by the FMT with the level of AT III because it is wellknown that the AT IIIHevel decreases caused by proteolytic activity generated in DIC.In this study it could be shown that fibrin monomer increases in parallel with the decrease of AT III. Thiseffect does not occur with fibrin degradation products.


1972 ◽  
Vol 28 (03) ◽  
pp. 342-350 ◽  
Author(s):  
Y. P Konttinen ◽  
L Kemppainen ◽  
O Turunen

SummaryPerformance and applicability of ethanol-induced gelation and protamine-induced paracoagulation for the demonstration of soluble fibrin monomer complexes and fragment Xo complexes was studied by using 1. fibrin monomer plasma prepared by adding small amounts of thrombin to plasma, 2. clot lysis products, and 3. thrombin -treated mixture of fibrinogen degradation products and plasma. To increase the specificity of the protamine tests only visible fibrin strand formation was recorded as positive. In addition to qualitative tests the amount of paracoagulable material was measured by a spectrophotometric method.The ethanol gelation test proved very simple, reproducible and considerably more sensitive than the protamine tests in demonstrating soluble fibrin monomer complexes, irrespective of whether fibrinogen degradation products were present or not. On the other hand, the protamine tests were clearly superior for demonstration of clot lysis products (fragment Xo complexes). Therefore it seems advisable to perform both types of tests when screening for intravascular coagulation.


Author(s):  
T Hamborg ◽  
A Skjennald ◽  
H C Godal

The study was performed in order to investigate the correlation between EGT, respectively FDP, and a positive FUT (FUT+), confirmed by venography. Control groups: patients 1) with a negative FUT (FOT−) in spite of DVT, 2) without DVT, because a negative venography also implies FUT−. Accordingly, FUT was not accomplished in this group.The material consisted of 41 patients with clinically suspected DVT; 20 with and 21 without DVT. Of the patients with DVT, 9 were definitely FUT+ and 11 definitely FUT−.EGT was applied for detection of soluble fibrin, Thrombo- Wellcotest for FDP and the Chi-squared test for statistical analysis. Blood specimens were analysed 0-1 days before isotope injection in patients with DVT, or 0-2 days before a negative venography.Conclusions: In this material, 1) Concurrently abnormal EGT and FDP was specific for the FUT+ patients. 2) On the other hand, a positive FUT could be excluded when both parameters were normal. 3) In patients with DVT, a positive EGT was found only in the FUT+ patients. (P values in the table refers to comparison with the FUT+ group).


2021 ◽  
Author(s):  
Fumihiro Ogawa ◽  
Yasufumi Oi ◽  
Kento Nakajima ◽  
Reo Matsumura ◽  
Tomoki Nakagawa ◽  
...  

Abstract Background: Coronavirus disease (COVID-19) pneumonitis associated with severe respiratory failure has a high mortality rate. Based on recent reports, the most severely ill patients present with coagulopathy, and disseminated intravascular coagulation (DIC)-like massive intravascular clot formation is frequently observed. Coagulopathy has emerged as a significant contributor to thrombotic complications. Although recommendations have been made for anticoagulant use for COVID-19, no guidelines have been specified.Case presentation: We describe four cases of critical COVID-19 with thrombosis detected by enhanced CT scan. The CT findings of all cases demonstrated typical findings of COVID-19 and pulmonary embolism or deep venous thrombus without critical exacerbation. Two patients died of respiratory failure due to COVID-19.Discussion: Previous reports have suggested coagulopathy with thrombotic signs as the main pathological feature of COVID-19, but no previous reports have focused on coagulopathy evaluated by whole-body enhanced CT scan. Changes in hemostatic biomarkers, represented by an increase in D-dimer and fibrin/fibrinogen degradation products, indicated that the essence of coagulopathy was massive fibrin formation. Although there were no clinical symptoms related to their prognosis, critical COVID-19-induced systemic thrombus formation was observed. Conclusions: Therapeutic dose anticoagulants should be considered for critical COVID-19 because of induced coagulopathy, and aggressive follow-up by whole body enhanced CT scan for systemic venous thromboembolism (VTE) is necessary.


2020 ◽  
Vol 5 (6) ◽  
pp. 1253-1264
Author(s):  
Christopher C Verni ◽  
Antonio Davila ◽  
Carrie A Sims ◽  
Scott L Diamond

Abstract Background Platelet dysfunction often accompanies trauma-induced coagulopathy. Because soluble fibrin impairs platelet glycoprotein VI (GPVI) signaling and platelets of trauma patients can display impaired calcium mobilization, we explored the role of fibrinolysis on platelet dysfunction during trauma. Methods Convulxin-induced GPVI calcium mobilization was investigated in healthy platelet-rich plasma (PRP) pretreated with thrombin and tissue plasminogen activator (tPA). Blood samples from healthy participants (n = 7) and trauma patients (n = 22) were tested for platelet calcium mobilization, plasma D-dimer, platelet D-dimer binding (via flow cytometry), and platelet lumi-aggregometry. Results For healthy platelets, maximal platelet dysfunction was observed when cross-linked soluble fibrin (no tPA) or cross-linked fibrin degradation products (FDPs) were generated in suspension before convulxin stimulation. Lack of fibrin polymerization (inhibited by Gly-Pro-Arg-Pro [GPRP]) or lack of factor XIIIa cross-linking (T101-inhibited) restored GPVI signaling, whereas non–cross-linked FDPs only partially blocked signaling induced by convulxin. In addition, D-dimer added to healthy PRP impaired platelet aggregation and dense granule release induced by various agonists. Plasma D-dimer level was strongly correlated (R = 0.8236) with platelet dysfunction as measured by platelet calcium mobilization induced with various agonists. By 48 to 120 h after trauma, plasma D-dimer levels declined, and platelet function increased significantly but not to healthy levels. Trauma platelets displayed elevated D-dimer binding that was only partially reduced by αIIbβ3-inhibitor GR144053. After 60-minute incubation, washed healthy platelets resuspended in plasma from trauma patients captured approximately 10 000 D-dimer equivalents per platelet. Conclusions During trauma, D-dimer and FDPs inhibit platelets, potentially via GPVI and integrin αIIbβ3 engagement, contributing to a fibrinolysis-dependent platelet loss-of-function phenotype.


1969 ◽  
Vol 25 (9) ◽  
pp. 996-997
Author(s):  
A. Nowak ◽  
S. Niewiarowski ◽  
Z. Czekala ◽  
K. Worowski ◽  
J. Dosiak ◽  
...  

Blood ◽  
2000 ◽  
Vol 96 (8) ◽  
pp. 2793-2802
Author(s):  
Carl-Erik Dempfle ◽  
Sotiria Argiriou ◽  
Klaus Kucher ◽  
H. Müller-Peltzer ◽  
Klaus Rübsamen ◽  
...  

Ancrod is a purified fraction of venom from the Malayan pit viper, Calloselasma rhodostoma, currently under investigation for treatment of acute ischemic stroke. Treatment with ancrod leads to fibrinogen depletion. The present study investigated the mechanisms leading to the reduction of plasma fibrinogen concentration. Twelve healthy volunteers received an intravenous infusion of 0.17 U/kg body weight of ancrod for 6 hours. Blood samples were drawn and analyzed before and at various time points until 72 hours after start of infusion. Ancrod releases fibrinopeptide A from fibrinogen, leading to the formation of desAA-fibrin monomer. In addition, a considerable proportion of desA-profibrin is formed. Production of desA-profibrin is highest at low concentrations of ancrod, whereas desA-profibrin is rapidly converted to desAA-fibrin at higher concentrations of ancrod. Both desA-profibrin and desAA-fibrin monomers form fibrin complexes. A certain proportion of complexes carries exposed fibrin polymerization sites EA, indicating that the terminal component of the protofibril is a desAA-fibrin monomer unit. Soluble fibrin complexes potentiate tissue-type plasminogen activator-induced plasminogen activation. Significant amounts of plasmin are formed when soluble fibrin in plasma reaches a threshold concentration, leading to the proteolytic degradation of fibrinogen and fibrin. In the present setting, high concentrations of soluble fibrin are detected after 1 hour of ancrod infusion, whereas a rise in fibrinogen and fibrin degradation products, and plasmin-α2–plasmin inhibitor complex levels is first detected after 2 hours of ancrod infusion. Ancrod treatment also results in the appearance of cross-inked fibrin degradation productd-dimer in plasma.


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