Relationships among tumor burden, tumor size, and the changing concentrations of fibrin degradation products and fibrinolytic factors in the pleural effusions of rabbits with VX2 lung tumors

2006 ◽  
Vol 147 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Mark W.C. Hatton ◽  
Suzanne M.R. Southward ◽  
Bonnie L. Ross ◽  
Bryan J. Clarke ◽  
Gurmit Singh ◽  
...  
Keyword(s):  
Tumor Size ◽  
Degradation Products ◽  
Lung Tumors ◽  
Tumor Burden ◽  
Pleural Effusions ◽  
Fibrin Degradation Products

A Monoclonal Antibody-Based Enzyme Immunoassay for Fibrin Degradation Products in Plasma

1988 ◽  
Vol 59 (02) ◽  
pp. 310-315 ◽  
Author(s):  
P W Koppert ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Enzyme Immunoassay ◽  
Degradation Products ◽  
Blood Clot ◽  
Tissue Type ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator ◽  
Strong Positive Reaction ◽  
Sandwich Type ◽  
Capture Antibody

SummaryWe have developed a sandwich-type enzyme immunoassay (EIA) for the quantitation of fibrin degradation products (FbDP) in plasma with a time-to-result of only 45 minutes.* The assay is based on the combination of the specificities of two monoclonal antibodies (FDP-14 and DD-13), developed in our institute. FDP-14, the capture antibody, binds both fibrinogen degradation products (FbgDP) and FbDP, but does not react with the parent fibrin(ogen) molecules. It has its epitope in the E-domain of the fibrinogen molecule on the Bβ-chain between amino acids 54-118. Antibody DD-13 was raised using D-dimer as antigen and is used as a tagging antibody, conjugated with horse-radish peroxidase. A strong positive reaction is obtained with a whole blood clot lysate (lysis induced by tissue-type plasminogen activator) which is used as a standard. The EIA does virtually not detect FbgDP i. e. purified fragments X, Y, or FbgDP generated in vitro in plasma by streptokinase treatment. This indicates that the assay is specific for fibrin degradation products.We have successfully applied this assay to the plasma of patients with a variety of diseased states. In combination with the assay previously developed by us for FbgDP and for the total amount of FbgDP + FbDP (TDP) in plasma, we are now able to study the composition of TDP in patients plasma in terms of FbgDP and FbDP.

Plasma Thrombospondin as an Indicator of Intravascular Platelet Activation in Patients with Vasculitis

1987 ◽  
Vol 58 (03) ◽  
pp. 850-852 ◽  
Author(s):  
M B McCrohan ◽  
S W Huang ◽  
J W Sleasman ◽  
P A Klein ◽  
K J Kao
Keyword(s):  
Platelet Activation ◽  
Plasma Levels ◽  
Half Life ◽  
Degradation Products ◽  
Plasma Concentrations ◽  
Primary Source ◽  
Positive Correlation ◽  
Activation Marker ◽  
Fibrin Degradation Products ◽  
The Mean

SummaryThe use of plasma thrombospondin (TSP) concentration was investigated as an indicator of intravascular platelet activation. Patients (n = 20) with diseases that have known vasculitis were included in the study. The range and the mean of plasma TSP concentrations of patients with vasculitis were 117 ng/ml to 6500 ng/ml and 791±1412 ng/ml (mean ± SD); the range and the mean of plasma TSP concentrations of control individuals (n = 33) were 13 ng/ml to 137 ng/ml and 59±29 ng/ml. When plasma TSP concentrations were correlated with plasma concentrations of another platelet activation marker, β-thromboglobulin (P-TG), it was found that the TSP concentration inei eased exponentially as the plasma β-TG level rose. A positive correlation between plasma levels of plasma TSP and serum fibrin degradation products was also observed. The results suggest that platelets are the primary source of plasma TSP in patients with various vasculitis and that plasma TSP can be a better indicator than β-TG to assess intravascular platelet activation due to its longer circulation half life.

A Prospective Study of Haemostatic Tests at 28 Weeks Gestation as Predictors of Pre-Eclampsia and Growth Retardation

1989 ◽  
Vol 61 (02) ◽  
pp. 243-245 ◽  
Author(s):  
J G Thornton ◽  
B J Molloy ◽  
P S Vinall ◽  
P R Philips ◽  
R Hughes ◽  
...  
Keyword(s):  
Discriminant Analysis ◽  
Prospective Study ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Degradation Products ◽  
Fetal Growth Retardation ◽  
Fibrin Degradation Products ◽  
A Prospective Study ◽  
Primiparous Women ◽  
Significant Model

SummaryA panel of haemostatic tests was perfomed on 400 primiparous women at 28 weeks to test whether one or more could predict the development of pregnancy complications. Fifteen women subsequently developed pre-eclampsia with significant proteinuria and 13 delivered growth retarded infants. There were no significant differences between mothers in the pre-eclampsia group and 22 randomly selected controls. A stepwise logistic discriminant analysis of the data did not produce a significant model. In the growth retarded group only beta thromboglobulin levels were significantly lower than in the controls (p <0.05), although in the logistic discriminant analysis the inclusion of both beta thromboglobulin and fibrin degradation products led to a borderline significant improvement in fit of the model. We conclude that the haemostatic variables studied are not significantly changed at 28 weeks nor clinically useful predictors of either pre-eclampsia or fetal growth retardation.

Is Quantitative Determination of Fibrin(ogen) Degradation Products and Thrombin-Antithrombin III Complexes Useful to Diagnose Deep Venous Thrombosis in Outpatients?

1989 ◽  
Vol 62 (04) ◽  
pp. 1043-1045 ◽  
Author(s):  
Paul F M M van Bergen ◽  
Eduard A R Knot ◽  
Jan J C Jonker ◽  
Auke C de Boer ◽  
Moniek P M de Maat
Keyword(s):  
Quantitative Determination ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Antithrombin Iii ◽  
Degradation Products ◽  
Family Doctor ◽  
Diagnostic Value ◽  
Impedance Plethysmography ◽  
Fibrin Degradation Products

SummaryWe studied the diagnostic value of recently introduced ELISA’s for the determination of thrombin-antithrombin III (TAT) complexes, fibrin degradation products (FbDP), fibrinogen degradation products (FgDP) and total degradation products (TDP) for deep venous thrombosis (DVT) in plasma of 239 consecutive outpatients, suspected for DVT by their family doctor. DVT was confirmed by impedance plethysmography in 60 patients. Using the 95th percentile range of 42 healthy volunteers the sensitivity for the detection of DVT was: 37% for TAT, 95% for TDP, 92% for FbDP and 90% for FgDP. Specificity was: 88% for TAT, 16% for TDP, 20% for FbDP and 25% for FgDP.We conclude that these assays are of little value in the diagnosis of DVT in outpatients.

A Plasma Clot Lysis Assay Based on the Release of Fibrin Degradation Products: Application to the Diagnosis of Hypofibrinolytic States

1990 ◽  
Vol 63 (01) ◽  
pp. 076-081 ◽  
Author(s):  
Pascale Gaussem ◽  
Sophie Gandrille ◽  
Pascale Molho-Sabatier ◽  
Loïc Capron ◽  
Jean-Noël Fiessinger ◽  
...  
Keyword(s):  
Degradation Products ◽  
Venous Occlusion ◽  
Lower Limbs ◽  
Clot Lysis ◽  
Plasma Clot ◽  
Vein Thrombosis ◽  
Fibrin Degradation Products ◽  
Before And After ◽  
Euglobulin Clot Lysis Time ◽  
Pai 1

SummaryUsing a monoclonal antibody-based assay, we measured the fibrin degradation product release in the supernatant of plasma clots obtained before and after venous occlusion (VO) in 30 patients with definite or suspected vascular thrombosis (19 definite and 2 suspected deep vein thrombosis, 6 recurrent superficial thrombophlebitis, 3 arterial occlusions of lower limbs). tPA and PAI-1 concentrations were determined using ELISA assays; the post-occlusion values were corrected for haemoconcentration. The increase in tPA during VO was correlated with haemoconcentration (r = 0.74), but 3 patients had ineffective VO (<2% increase in proteins). The fibrinolytic response to VO was evaluated using the shortening of the time necessary for the release of 200 μg of fibrin degradation products per mg of fibrinogen (Δ T 200). Two among the 27 patients with effective VO were bad responders with a Δ T 200 <3 h (whereas all the others had Δ T 200 >10 h). These patients had respectively a deficient tPA release (Δ tPA = 1 ng/ml) and an elevated PAI-1 level at rest (33 ng/ml). Several other patients were bad responders in terms of tPA release or of shortening of the euglobulin clot lysis time but they had a normal Δ T 200. This plasma clot test reflects the ability of free tPA to bind to fibrin (the amount of which depends on the level of tPA and PAI-1), and may be useful in the diagnosis of a hypofibrinolytic state.

Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

1993 ◽  
Vol 69 (04) ◽  
pp. 321-327 ◽  
Author(s):  
E Seifried ◽  
M Oethinger ◽  
P Tanswell ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thrombolytic Agent ◽  
Degradation Products ◽  
Maximum Plasma ◽  
Normal Range ◽  
Fibrinogen Degradation Products ◽  
Fibrin Degradation Products ◽  
Rebound Phenomenon ◽  
The Mean

SummaryIn 12 patients treated with 100 mg rt-PA/3 h for acute myocardial infarction (AMI), serial fibrinogen levels were measured with the Clauss clotting rate assay (“functional fibrinogen”) and with a new enzyme immunoassay for immunologically intact fibrinogen (“intact fibrinogen”). Levels of functional and “intact fibrinogen” were strikingly different: functional levels were higher at baseline; showed a more pronounced breakdown during rt-PA therapy; and a rebound phenomenon which was not seen for “intact fibrinogen”. The ratio of functional to “intact fibrinogen” was calculated for each individual patient and each time point. The mean ratio (n = 12) was 1.6 at baseline, 1.0 at 90 min, and increased markedly between 8 and 24 h to a maximum of 2.1 (p <0.01), indicating that functionality of circulating fibrinogen changes during AMI and subsequent thrombolytic therapy. The increased ratio of functional to “intact fibrinogen” seems to reflect a more functional fibrinogen at baseline and following rt-PA infusion. This is in keeping with data that the relative amount of fast clotting “intact HMW fibrinogen” of total fibrinogen is increased in initial phase of AMI. The data suggest that about 20% of HMW fibrinogen are converted to partly degraded fibrinogen during rt-PA infusion. The rebound phenomenon exhibited by functional fibrinogen may result from newly synthesized fibrinogen with a high proportion of HMW fibrinogen with its known higher degree of phosphorylation. Fibrinogen- and fibrin degradation products were within normal range at baseline. Upon infusion of the thrombolytic agent, maximum median levels of 5.88 μg/ml and 5.28 μg/ml, respectively, were measured at 90 min. Maximum plasma fibrinogen degradation products represented only 4% of lost “intact fibrinogen”, but they correlatedstrongly and linearly with the extent of “intact fibrinogen” degradation (r = 0.82, p <0.01). In contrast, no correlation was seen between breakdown of “intact fibrinogen” and corresponding levels of fibrin degradation products. We conclude from our data that the ratio of functional to immunologically “intact fibrinogen” may serve as an important index for functionality of fibrinogen and select patients at high risk for early reocclusion. Only a small proportion of degraded functional and “intact fibrinogen”, respectively, is recovered as fibrinogen degradation products. There seems to be a strong correlation between the degree of elevation of fibrinogen degradation products and the intensity of the systemic lytic state, i.e. fibrinogen degradation.

Hemostatic Disorder of Uremia: The Platelet Defect, Main Determinant of the Prolonged Bleeding Time, Is Correlated with Indices of Activation of Coagulation and Fibrinolysis

1996 ◽  
Vol 76 (03) ◽  
pp. 312-321 ◽  
Author(s):  
Diego Mezzano ◽  
Rodrigo Tagle ◽  
Olga Panes ◽  
Marcos Pérez ◽  
Patricio Downey ◽  
...  
Keyword(s):  
Renal Failure ◽  
Bleeding Time ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Primary Hemostasis ◽  
Prolonged Bleeding Time ◽  
Fibrin Degradation Products ◽  
Von Willebrand ◽  
Pai 1 ◽  
Coagulation And Fibrinolysis

SummarySeveral parameters of primary hemostasis and markers of activation of coagulation and fibrinolysis were measured in 48 patients with severe (creatinine clearance <20 ml/min) chronic renal failure (CRF) without dialysis and diseases or drugs affecting hemostasis. Bleeding time (BT) was prolonged in 25/48 patients, and was correlated with age of patients, severity of renal failure, hematocrit, impairment in platelet aggregation-secretion and decrease in platelet ATP content. Defects in von Willebrand factor played no role in the prolongation of the BT. Multivariate analysis showed that only platelet dysfunction and severity of renal disease were independent predictors of the BT in uremia. The platelet functional disorder was significantly correlated with a reduction in platelet ATP and ADP.High levels of plasma thrombin-antithrombin complexes (TAT), prothrombin fragment F1+2, fibrinogen and factor VIIc were observed in patients with CRF, as described in prethrombotic states. Plasmin-antiplasmin complexes (PAP), fibrinogen and fibrin degradation products (FgDP, FnDP) were significantly increased, and the activity of plasminogen activator inhibitor (PAI-1) was slightly reduced, denoting an activation of fibrinolysis.A negative correlation was found between platelet levels of ATP and ADP with plasma TAT, F1+2 and PAP. Furthermore, plasma PAI-1 activity was negatively correlated with the BT and was lower in patients with prolonged BT as compared with controls and patients with normal BT. These links between primary hemostasis and activation of coagulation and fibrinolysis suggest that increased intravascular generation of thrombin and/or plasmin is an important mediator of the defects in primary hemostasis, prolongation of the BT and, probably, bleeding in CRF.

Exercise-Induced Fibrinolysis – Fact or Fiction?

1982 ◽  
Vol 48 (02) ◽  
pp. 201-203 ◽  
Author(s):  
N A Marsh ◽  
P J Gaffney
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Coagulation Factors ◽  
Vascular Wall ◽  
Strenuous Exercise ◽  
Fibrin Degradation Products ◽  
Real Increase ◽  
Exercise Induced ◽  
Male Subjects

SummaryThe effect of strenuous exercise on the fibrinolytic and coagulation mechanisms was examined in six healthy male subjects. Five min bicycle exercise at a work-rate of 800 to 1200 kpm. min−1 produced an abrupt increase in plasma plasminogen activator levels which disappeared after 90 min. However, there was no change in early or late fibrin degradation products nor was there a change in fibrinopeptide A levels or βthromboglobulin levels after exercise although activated partial thromboplastin times were significantly shortened. It is concluded that strenuous exercise does not produce any real increase in fibrinogen-fibrin conversion nor any real increase in the breakdown of these proteins. The role of exercise-induced release of plasminogen activator remains unclear, but probably helps to maintain plasma levels in a discontinuous manner concurrently with the continuous low-level secretion from the vascular wall. The shortening of partial thromboplastin time may be due to the raised levels of plasminogen activator changing the activation state of other coagulation factors.

Platelet Function in Experimentally Induced Pancreatitis in the Dog

1986 ◽  
Vol 55 (02) ◽  
pp. 197-200 ◽  
Author(s):  
R M Jacobs ◽  
R J Murtaugh ◽  
R H Fertel
Keyword(s):  
Platelet Function ◽  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Plasma Concentrations ◽  
Adenosine Diphosphate ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Functional Defect ◽  
And Function ◽  
Experimentally Induced

SummaryEvidence suggests that changes in prostaglandins and disseminated intravascular coagulation accompany pancreatitis. Both may induce changes in platelet function. We wished to determine if experimentally induced pancreatitis in the dog was associated with altered platelet number and function, and whether there were concomitant changes in prostaglandins. Evidence for disseminated intravascular coagulation in the dogs with pancreatitis were red blood cell fragmentation, increased platelet turnover indicated by macro-platelets and the transient presence of fibrin degradation products in urine. There were no significant changes in platelet count. The platelets from dogs with pancreatitis showed a functional defect characterized by significantly decreased aggregation in response to adenosine diphosphate, arachidonic acid, and collagen. Release of adenosine triphosphate from platelets was reduced in collagen-stimulated aggregation. There were no changes in the plasma concentrations of thromboxane B2, 6-Keto-PGF1a, and PGE2. This defect may have been due to the generation of fibrin degradation products and platelet “exhaustion”.

The Pathogenesis of Thrombotic Thrombocytopenic Purpura

1979 ◽  
Author(s):  
H. C. Kwaan
Keyword(s):  
Plasminogen Activator ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Degradation Products ◽  
Vascular Lesions ◽  
Local Defect ◽  
Laboratory Findings ◽  
Thrombocytopenic Purpura ◽  
Fibrin Degradation Products ◽  
Severity Of The Disease ◽  
Circulating Levels

The vascular lesions with microthrombi were studied in 12 patients with thrombotic thrombocytopenic purpura (TTP), diagnosed by the characteristic clinical and laboratory findings and confirmed histologically in each case. While defibrination was not observed, and with only minimal changes in the circulating levels of fibrinogen, fibrin degradation products and plasminogen activator, the microthrombotic lesion was invariably present. Immunofluorescent and histochemical studies indicated that both platelet and fibrin were present in the microthrombi with the platelet components dominant in many cases. Using the fibrin slide method, plasminogen activator was demonstrated in the uninvolved blood vessels but totally absent in the vessels occluded by microthrombi. in contrast, fibrinolysis is always present in the vessels afflicted with other types of thrombosis, such as the microthrombi in disseminated intravascular coagulation. Since circulating fibrinolytic activity was normal in TTP, the absence of vascular fibrinolysis is a local defect due to either inhibition by the platelet deposits or by local vascular damage. The inability of thrombolysis may explain the absence of systemic defibrination and the severity of the disease.

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