Thrombotic stroke associated with elevated plasma factor VIII

1980 ◽  
Vol 8 (4) ◽  
pp. 435-437 ◽  
Author(s):  
Kenneth S. Kosik ◽  
Bruce Furie
Keyword(s):  
Factor Viii ◽  
Elevated Plasma ◽  
Plasma Factor

Factor VIII expression in liver disease

2004 ◽  
Vol 91 (02) ◽  
pp. 267-275 ◽  
Author(s):  
Martine Hollestelle ◽  
Hendrika Geertzen ◽  
Irene Straatsburg ◽  
Thomas van Gulik ◽  
Jan van Mourik
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Factor Viii ◽  
Rna Extraction ◽  
Control Group ◽  
Mrna Levels ◽  
Protein Distribution ◽  
Elevated Plasma ◽  
Cirrhotic Tissue ◽  
Plasma Factor

SummaryLiver disease is associated with markedly elevated plasma factor VIII (FVIII) levels, whereas the synthesis of many other coagulation factors and proteins is reduced. In order to define the mechanism of FVIII increase, we have determined the expression levels of FVIII, both at mRNA and protein level, in patients with liver disease who underwent partial liver resection. In addition, the expression of von Willebrand factor (VWF) and low density lipoprotein receptor-related protein (LRP), proteins known for their ability to modulate FVIII plasma levels, were examined. Tissue samples for RNA extraction were obtained from 4 patients with cirrhosis, 9 patients with liver failure without cirrhosis and 6 patients with liver metastasis of a colon or rectum carcinoma (control group). In patients with liver cirrhosis hepatic FVIII and LRP mRNA levels were significantly lower than controls (p ≤ 0.010), while VWF mRNA was significantly higher (p ≤ 0.050). Immunohistochemical analysis revealed that cellular VWF protein distribution was also increased in cirrhotic livers compared to liver tissue from patients with non-cirrhotic liver disease. In cirrhotic tissue enlarged portal veins appeared to overgrow FVIII producing sinusoidal endothelial cells. Similarly, the number of LRP-producing cells appeared to be lower in cirrhotic tissue than in controls. The plasma concentration of both FVIII and VWF was significantly higher in patients with cirrhosis than control subjects (p = 0.038 and 0.010 respectively). These results demonstrate that elevated plasma FVIII levels in liver cirrhosis are associated with increased hepatic biosynthesis of VWF and decreased expression of LRP, rather than increased FVIII synthesis.

Elevated Plasma Factor VIII and D-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children

2004 ◽  
Vol 351 (11) ◽  
pp. 1081-1088 ◽  
Author(s):  
Neil A. Goldenberg ◽  
R. Knapp-Clevenger ◽  
Marilyn J. Manco-Johnson
Keyword(s):  
Factor Viii ◽  
Elevated Plasma ◽  
Plasma Factor ◽  
Poor Outcomes ◽  
D Dimer

Venous thrombosis in a family with defective release of vascular plasminogen activator and elevated plasma factor VIII/von Willebrand's factor

1983 ◽  
Vol 74 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Nancy W. Stead ◽  
Kenneth A. Bauer ◽  
Thomas R. Kinney ◽  
James G. Lewis ◽  
Elizabeth E. Campbell ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Factor Viii ◽  
Plasminogen Activator ◽  
Elevated Plasma ◽  
Plasma Factor ◽  
Von Willebrand’S Factor

scholarly journals Elevated plasma factor VIII and d-dimer levels as predictors of poor outcome of thrombosis in children

2005 ◽  
Vol 41 (1) ◽  
pp. 176 ◽  
Author(s):  
NA Goldenberg ◽  
R Knapp-Clevenger ◽  
MJ Manco-Johnson
Keyword(s):  
Factor Viii ◽  
Elevated Plasma ◽  
Poor Outcome ◽  
Plasma Factor ◽  
D Dimer

scholarly journals Procoagulant activity induced by vascular injury determines contribution of elevated factor VIII to thrombosis and thrombus stability in mice

Blood ◽  
2011 ◽  
Vol 118 (14) ◽  
pp. 3960-3968 ◽  
Author(s):  
Kellie R. Machlus ◽  
Feng-Chang Lin ◽  
Alisa S. Wolberg
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Tissue Factor ◽  
Vascular Injury ◽  
Thrombin Generation ◽  
Elevated Plasma ◽  
Vessel Occlusion ◽  
Short Treatment ◽  
Plasma Factor

Abstract Studies have correlated elevated plasma factor VIII (FVIII) with thrombosis; however, it is unclear whether elevated FVIII is a proinflammatory biomarker, causative agent, or both. We raised FVIII levels in mice and measured the time to vessel occlusion (TTO) after ferric chloride–induced injury. Compared with control (saline-infused) mice, elevated FVIII had no effect after longer (3-minute) carotid artery injury, but it shortened the TTO after shorter (2-minute) injury (P < .008). After injury, circulating thrombin-antithrombin (TAT) complexes were lower after short versus long injury (P < .04), suggesting short treatment produced less coagulation activation. TAT levels in FVIII-infused mice were higher than in controls after short, but not longer, injury. Accordingly, elevated FVIII had no effect on in vitro thrombin generation or platelet aggregation triggered by high tissue factor, but it increased thrombin generation rate and peak (2.4- and 1.5-fold, respectively), and it accelerated platelet aggregation (up to 1.6-fold) when initiated by low tissue factor. Compared with control mice, elevated FVIII stabilized thrombi (fewer emboli) after short injury, but it had no effect after longer injury. TTO and emboli correlated with TATs. These results demonstrate dependence of FVIII activity on extent of vascular injury. We propose elevated plasma FVIII is an etiologic, prothrombotic agent after moderate but not extensive vascular damage.

Sign in / Sign up

Export Citation Format

Share Document