Antihaemophilic Factor A Activity, F VIII-Related Antigen and von Willebrand Factor in Hepatic Cirrhosis

Baele, G; Matthijs, E; Barbier, F

doi:10.1159/000207893

Cited by 9 publications

(8 citation statements)

References 20 publications

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“…A similar relationship has been reported in normal subjects in basal condi tions, at least between F VIII:C and F VIIIR:AG [1,3,7,11,18], while there are discordant reports for F VIIIR:RCof [1,5,21], The significant correlations between the F VIII-VWF components found in our cases after VO, notwithstanding their striking and heterogeneous rise, are in agreement with previous observations made using stimuli such as catecholamine administration [7,12] and physical exercise [2,7,17], A highly significant activation of fibrino lysis was recorded following VO, the results of ELT and DBCLT being strictly correlated. This finding supports the belief that the two methods basically measure the same phe nomenon, the release of plasminogen activa tor.…”

Section: Discussionsupporting

confidence: 85%

Correlation between Changes Induced by Venous Occlusion on Factor VIII-von Willebrand Factor Components and Fibrinolytic Activity

Ponari

Pini²,

Poli³

et al. 1984

Pathophysiol Haemos Thromb

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The effects of standardized venous occlusion (VO) on factor VIII-von Willebrand factor (F VIII-VWF) components (F VIIL·C, F VIIIR:AG, F VIIIR:RCof) and on fibrinolytic activity were investigated in 45 healthy subjects, in 28 women on oral contraceptives, and in 78 patients with various chronic diseases (28 with peripheral arterial disease, 19 with liver cirrhosis, 13 with rheumatoid arthritis, and 18 with diabetes). All the three F VIII-VWF components showed highly significant increases, although not of the same magnitude, with consequent variations in the ratios between them. A significant activation of fibrinolysis was also demonstrated with both euglobulin lysis time (ELT) and diluted blood clot lysis time (DBCLT). A strong linear correlation between pre- and post-stasis values was recorded for all the F VIII-VWF components and for the two fibrinolysis tests. No significant relationship was, on the contrary, found between F VIII-VWF and fibrinolytic parameters.

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Section: Discussionsupporting

confidence: 85%

Correlation between Changes Induced by Venous Occlusion on Factor VIII-von Willebrand Factor Components and Fibrinolytic Activity

Ponari

Pini²,

Poli³

et al. 1984

Pathophysiol Haemos Thromb

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“…Liver disease is frequently associated with abnormalities of the blood coagulation system with a reduction in concentration of many of the individual clotting factors (1,2). Several studies have shown, however, that the level of factor VIII is increased in liver disease (3,4,5). Factor VIII circulates as a complex of two proteins (6), the factor VIII procoagulant protein (VIIIC), and the factor VIII related antigen protein (VIIIRAg) which contains von Willebrand factor (VIIIvWF).…”

Section: Introductionmentioning

confidence: 99%

Increased Factor VIII Complex in Fulminant Hepatic Failure

1985

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SummaryIn 30 patients with fulminant hepatic failure (FHF) all three components of the factor VIII complex were significantly increased (VIIIC = 6.43 ± 1.12 u/ml; VIIIRAg = 3.91 ± 0.25 u/ ml; VIIIvWF = 3.89 ± 0.29 u/ml). There was good correlation between all three parameters in control subjects, but only between VIIIRAg and VIIIvWF (r= 0.67; p <0.001) in patients with FHF. VIIIC was significantly higher than VIIIRAg and VIIIvWF. These results suggest that VIIIC and VIIIRAg are increased by different mechanisms in FHF. These processes may include endothelial cell damage, reduced reticuloendothelial system function and lack of production of inactivating substances by the damaged liver.Platelet adhesion to glass beads was increased in FHF (36.4 ± 5.9% compared to 16.6 ± 2.1%, p <0.01). There was no significant correlation between platelet adhesion and any of the parameters of the factor VIII complex. Thus the increase in platelet adhesion cannot be due to the increase in VIIIvWF in FHF.

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“…Therefore because of the necrosis of the liver cells, the hemodynamic changes due to ex panded collaterals in the presence of im paired clearance of activated factors could trigger off disseminated intravascular coagu lation (DIC), inducing bleeding in liver pa tients [21,22,28]. In acute hepatic failure the incidence and magnitude of intravascular co agulation and its relation to the severity of bleeding and prognosis has been assessed [13], Subsequently, in hepatic cirrhosis and in other diseases with liver involvement, evi dence of the relationship between a hypercoagulable state and a significant increase or decrease of most significant parameters in this condition has been reported [1,10,14,18,27], To verify the relationship of bleeding to either a hypercoagulability condition or the severity of hepatic failure, we evaluated fac tor VIII:C (F VIII:C), factor VIIIR:AG (F VIIIR:AG), factor VIII AG/C ratio (F VIII AG/C) and serum fibrin-fibrinogen degrada tion products (FDP) in a group of patients with advanced liver cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

Bleeding in Cirrhotic Patients: A Precipitating Factor due to Intravascular Coagulation or to Hepatic Failure?

Bertaglia¹,

Belmonte²,

Vertolli³

et al. 1983

Pathophysiol Haemos Thromb

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In 24 cirrhotic patients at different stages of hepatic failure, factor VIII: C (F VIIl·C), factor VIΠR:AG (F VIIIR:AG), factor VIII AG/C ratio (F VIII AG/C), and serum fibrin-fibrinogen degradation products (FDP) were investigated. In 11 of the 24 patients, several instances of gastrointestinal bleeding due to esophageal varices rupture were documented and 5 patients died of unarrestable bleeding. In our study, we evaluated whether the cause of bleeding was the development of intravascular coagulation or the severity of hepatic failure. A statistically significant difference between F VIIl·C, F VIIIR:AG/C ratio, and serum FDP was found in bleeding in comparison with non-bleeding patients. An inverse correlation between the F VIII :C plasma level and serum FDP as well as a direct correlation between F VIII AG/C ratio and serum FDP in the group of bleeding patients were also found. These data seem to suggest a hypercoagulable state which was more significant in the 5 patients who died owing to bleeding. Furthermore, only 1 of these patients had severe hepatic failure. From this study it appears that, in cirrhotic patients, bleeding is related more to the appearance of disseminated intravascular coagulation, as a consequence of both hemodynamic and endothelial changes, than to the degree of hepatic failure itself.

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Antihaemophilic Factor A Activity, F VIII-Related Antigen and von Willebrand Factor in Hepatic Cirrhosis

Cited by 9 publications

References 20 publications

Correlation between Changes Induced by Venous Occlusion on Factor VIII-von Willebrand Factor Components and Fibrinolytic Activity

Correlation between Changes Induced by Venous Occlusion on Factor VIII-von Willebrand Factor Components and Fibrinolytic Activity

Increased Factor VIII Complex in Fulminant Hepatic Failure

Bleeding in Cirrhotic Patients: A Precipitating Factor due to Intravascular Coagulation or to Hepatic Failure?

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