scholarly journals Fibrin-fibrinogen degradation products in cerebrospinal fluid.

1976 ◽  
Vol 29 (4) ◽  
pp. 341-344 ◽  
Author(s):  
M J Brueton ◽  
G R Breeze ◽  
J Stuart
Keyword(s):  
Cerebrospinal Fluid ◽  
Degradation Products ◽  
Fibrinogen Degradation Products

Source of fibrin/fibrinogen degradation products in the CSF after subarachnoid hemorrhage

1985 ◽  
Vol 63 (4) ◽  
pp. 573-577 ◽  
Author(s):  
Marinus Vermeulen ◽  
Huub H. D. M. van Vliet ◽  
Kenneth W. Lindsay ◽  
Albert Hijdra ◽  
Jan van Gijn
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Tranexamic Acid ◽  
Degradation Products ◽  
Control Group ◽  
Content Type ◽  
Fibrinogen Degradation Products ◽  
Level Of Consciousness ◽  
Local Fibrinolysis ◽  
Fine Print

✓ In 48 patients with a subarachnoid hemorrhage, levels of fibrin/fibrinogen degradation products (FDP's), total protein, and plasminogen were measured in the cerebrospinal fluid (CSF) between Days 9 and 15 after the bleed. Of these 48 patients, 22 received tranexamic acid. Despite a significant reduction in the incidence of rebleeding in patients taking tranexamic acid, no difference in FDP levels was found between patients receiving tranexamic acid and a control group of patients who were not; nor was any relationship evident between FDP levels and rebleeding. In patients with detectable levels of FDP's, CSF protein and plasminogen values were also increased, and FDP's were found more frequently in the CSF of patients with an impaired level of consciousness or with a neurological deficit. These findings suggest that in the 2nd week after subarachnoid hemorrhage, the presence of FDP's in the CSF reflects a damaged blood-CSF barrier rather than ongoing local fibrinolysis in the subarachnoid space. A finding of FDP's in the CSF is, therefore, an unreliable monitor of antifibrinolytic treatment in subarachnoid hemorrhage and cannot be used for selecting patients at high risk of rebleeding.

Plasma Thrombin Assay using a Chromogenic Substrate in Disseminated Intravascular Coagulation due to Snake Bite Envenomation

1979 ◽  
Vol 41 (03) ◽  
pp. 544-552 ◽  
Author(s):  
R P Herrmann ◽  
P E Bailey
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Snake Bite ◽  
Chromogenic Substrate ◽  
Coagulation Parameters ◽  
Fibrinogen Degradation Products ◽  
Intravascular Coagulation

SummaryUsing the chromogenic substrate, Tos-Gly-Pro-Arg-pNA-HCL (Chromozym TH, Boehringer Mannheim) plasma thrombin was estimated in six cases of envenomation by Australian elapid snakes. All patients manifested findings chracteristic of defibrination due to envenomation by these snakes. Fibrin-fibrinogen degradation products were grossly elevated, as was plasma thrombin in all cases.Following treatment with antivenene, all abnormal coagulation parameters returned rapidly towards normal by 24 hours and plasma thrombin disappeared.

The Measurement of Heparin

1973 ◽  
Vol 30 (03) ◽  
pp. 471-479 ◽  
Author(s):  
K. W. E Denson ◽  
John Bonnar
Keyword(s):  
Degradation Products ◽  
Factor Xa ◽  
Assay Method ◽  
Thrombin Time ◽  
Fibrinogen Degradation Products ◽  
Low Levels

SummaryA method for the measurement of heparin utilising the potentiating effect of heparin on the action of anti-factor Xa is described. The effect on the assay of platelet contamination of plasma, the presence of fibrinogen degradation products and low levels of anti-factor Xa have been studied. The assay method has been compared with the calcium thrombin time method and a group of obstetrical patients have been studied using both methods.

Some Effects of Fibrinogen Degradation Products (FDP) on Blood Platelets

1966 ◽  
Vol 15 (03/04) ◽  
pp. 413-419 ◽  
Author(s):  
Z Jerushalmy ◽  
M. B Zucker
Keyword(s):  
Platelet Aggregation ◽  
Connective Tissue ◽  
Degradation Products ◽  
Blood Platelets ◽  
Adenosine Diphosphate ◽  
Serotonin Release ◽  
Fibrinogen Degradation Products ◽  
Inhibition Of Platelet Aggregation

Summary“Early” fibrinogen degradation products are more potent inhibitors of thrombin-induced clotting than “late” products and also interfere with the ability of thrombin to release serotonin from platelets. “Early” and “intermediate” FDP cause moderate inhibition of platelet aggregation induced by adenosine diphosphate or connective tissue particles. Serotonin release by connective tissue particles is probably not inhibited by FDP.

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.

The Leukocyte Digestion of Fibrinogen Degradation Products (FDP)

1971 ◽  
Vol 26 (03) ◽  
pp. 523-525
Author(s):  
K Gibiński ◽  
B Lipiński ◽  
M Trusz-Gluza
Keyword(s):  
Degradation Products ◽  
Fibrinogen Degradation Products

SummaryWhile the native fibrinogen is not digested by the leucocyte proteases both the early and late FDP are digestible without any denaturating reagent. Thus, this reaction may occur in vivo indicating an unknown role of granulocytes in paracoagulation.

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