Comments on Plasma Fibrinogen Levels Measured by Functional Methods

1994 ◽  
Vol 72 (06) ◽  
pp. 985-985 ◽  
Author(s):  
Boguslaw Lipinski ◽  
Scott Federman ◽  
Andrzej S Krolewski
2017 ◽  
Vol 77 (04) ◽  
pp. 396-405
Author(s):  
C Bekos ◽  
C Grimm ◽  
T Brodowicz ◽  
E Petru ◽  
L Hefler ◽  
...  

1973 ◽  
Vol 29 (02) ◽  
pp. 363-374 ◽  
Author(s):  
F. K Beller ◽  
W Theiss

SummaryPlasma fibrinogen, circulating fibrinmonomers (as indicated by a positive ethanol gelation test), fibrinolysis breakdown products and plasma hemoglobin were assayed in 122 rats subjected to endotoxin injection or infusion. The results were correlated with the quantitative measurement of glomerular fibrin deposition. Based on these data four groups were determined : consumption coagulopathy and three stages of increasing severity of disseminated intravascular coagulation (DIG).Consumption coagulopathy was defined by a decrease in plasma fibrinogen and a positive ethanol gelation test in the absence of glomerular fibrin deposition. Plasma hemoglobin and fibrinolysis breakdown products were normal or only slightly increased.DIG as characterized by glomerular fibrin deposition was defined as moderate (1 to 20% glomeruli showing fibrin strands), intermediate (21 to 80%), and severe (81 to 100%). Decrease in plasma fibrinogen and frequence of a positive ethanol gelation test in all stages of DIG were only slightly different from the findings in consumption coagulopathy. However, a sharp increase in plasma hemoglobin levels was noted when glomerular fibrin deposition did occur even in small amounts. At this time only a moderate increase was noted in fibrin(ogen) breakdown products. These two parameters increased only slightly in the group of intermediate DIG. Severe DIG was characterized by a massive increase in fibrin (ogen) breakdown products and high levels of plasma hemoglobin.


1996 ◽  
Vol 76 (02) ◽  
pp. 166-170 ◽  
Author(s):  
Moniek P M de Maat ◽  
Alf E R Arnold ◽  
Stef van Buuren ◽  
J H Paul Wilson ◽  
Cornells Kluft

SummaryElevated plasma fibrinogen levels are associated with an increased risk for cardiac events. Ticlopidine is a drug that inhibits the ADP-induced aggregation of blood platelets and it also has been described that ticlopidine can decrease the plasma fibrinogen level in patients with vascular diseases. The mechanism of this decrease has not yet been elucidated and therefore mechanisms that are known to affect fibrinogen levels were studied, viz. the acute phase reaction, total fibrin plus fibrinogen degradation (TDP) levels and the polymorphisms of the fibrinogen β-gene.The fibrinogen lowering effect of ticlopidine was studied in 26 healthy volunteers, selected on genotype of the BclI polymorphism of the fibrinogen β-gene, and in 26 patients with stable angina pectoris in a double blind, randomized cross-over study. Functional plasma fibrinogen levels were measured with the Clauss assay. Fibrinogen antigen, C-reactive protein (CRP) and TDP levels were measured using an enzyme immuno assay (EIA).In the healthy volunteers the functional fibrinogen levels had decreased by 0.20 g/l (9%, p = 0.005 using the paired Student t-test) after 4 weeks of 250 mg bid ticlopidine administration, whereas fibrinogen antigen, CRP and TDP levels were not significantly changed. In the stable angina pectoris patients the pre-treatment fibrinogen, CRP and TDP levels were significantly higher than in the volunteer group. After four weeks 250 mg bid ticlopidine administration the functional fibrinogen levels had decreased by 0.38 g/l (11%, p < 0.005), whereas the fibrinogen antigen, CRP and TDP levels were not significantly changed. The levels of functional and antigen fibrinogen, CRP and TDP did not change significantly during the placebo period in the volunteers or the patients. Neither in the volunteers nor in the patients was the effect of ticlopidine on the fibrinogen levels associated with the fibrinogen β-gene polymorphisms.Therefore, the fibrinogen lowering effect of ticlopidine is likely to be a modulation of the functionality of the molecule and unlikely to be modulated by the acute phase reaction, TDP-levels or the fibrinogen β-gene polymorphisms.


1977 ◽  
Vol 37 (02) ◽  
pp. 243-252
Author(s):  
Yi-Hsiang Chen ◽  
E. B Reeve

SummaryTo shed some light on the homeostatic regulation of plasma fibrinogen, metabolic studies were made in healthy females, and in normal, thyroidectomized, and thyroxine-treated rabbits. In females, compared with normal males, plasma fibrinogen concentration, plasma and interstitial fibrinogen decreased consequent to an increased fractional catabolic rate and a normal fibrinogen synthesis rate. The interstitial/plasma fibrinogen ratio remained unchanged. In normal rabbits, with increasing body weight fractional catabolic rate and catabolic rate decreased, while fibrinogen concentration and plasma fibrinogen remained constant owing to a simultaneous decrease in fibrinogen synthesis. In addition, fractional transcapillary transfer rate and transcapillary flux also decreased resulting in a shrinkage of interstitial fibrinogen. Thyroidectomy and thyroxine-injection markedly altered fibrinogen metabolism: thyroid hormone accelerated fibrinogen catabolism but also stimulated synthesis. The net result was an increase in plasma fibrinogen and fibrinogen concentration. The interstitial/plasma fibrinogen ratio decreased in thyroxine-treated, and increased in thyroidectomized animals. This study defines the variations of the fibrinogen system parameters in these physiologic and pathologic conditions, and illustrates some patterns of alterations in fibrinogen metabolism.


1976 ◽  
Vol 36 (01) ◽  
pp. 127-132 ◽  
Author(s):  
C. P Warlow ◽  
J. A. N Rennie ◽  
D Ogston ◽  
A. S Douglas

SummaryIn fifteen patients with a cerebro-vascular accident resulting in an acute hemiplegia there was a subsequent rise in the platelet count and plasma fibrinogen level. There were no significant alterations in platelet adhesiveness, plasminogen activator, plasminogen, FR-antigen and haematocrit. Patients diagnosed as developing deep venous thrombosis with the 125I-fibrinogen technique had a significantly lower platelet adhesiveness and plasminogen level than those who were not.


1991 ◽  
Vol 65 (05) ◽  
pp. 487-490 ◽  
Author(s):  
A E Thomas ◽  
F R Green ◽  
C H Kelleher ◽  
H C Wilkes ◽  
P J Brennan ◽  
...  

SummaryWe investigated the association between fibrinogen levels and a HaeIII restriction fragment length polymorphism located at −453 bp from the start of transcription of the β fibrinogen gene. 292 healthy men aged 45 to 69 years, recruited from general practices throughout Britain, were studied. None had a history of ischaemic heart disease. 41.1% (120) were smokers and fibrinogen levels were higher in this group. The frequency of the noncutting allele (designated H2) was 0.19 and was the same in smokers and non-smokers. The H2 allele was associated with elevated levels of fibrinogen in both smokers and non-smokers and the effect of genotype was similar in both groups. After smoking, HaeIII genotype was the strongest predictor of fibrinogen levels and explained 3.1% of the variance in fibrinogen levels. These results confirm earlier studies that variation at the fibrinogen locus contributes to the between-individual differences in plasma fibrinogen level.


1974 ◽  
Vol 31 (03) ◽  
pp. 395-402 ◽  
Author(s):  
V Bocci ◽  
T Conti ◽  
M Muscettola ◽  
A Pacini ◽  
G. P Pessina

SummaryRabbit fibrinogen digest products (FDP) have been separated by Pevikon block electrophoresis yielding fragments D, E and other unidentified FDP.The fragments were injected into rabbits. Surprisingly, as little as 4.3 mg of fragment D elicited a significant increase in plasma fibrinogen concentration 24 hr after injection. The stimulating activity of fragment D is at least 10-fold higher than that of fragment E.


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