Coagulation Factor VII and Plasma Triglycerides

1989 ◽  
Vol 19 (3) ◽  
pp. 125-130 ◽  
Author(s):  
J. Carvalho de Sousa ◽  
E. Bruckert ◽  
P. Giral ◽  
C. Soria ◽  
J. Chapman ◽  
...  
Keyword(s):  
Coagulation Factor ◽  
Factor Vii ◽  
Plasma Triglycerides ◽  
Coagulation Factor Vii

Do oxidized fatty acids activate coagulation factor VII during post-prandial lipemia in women?

2003 ◽  
Vol 89 (04) ◽  
pp. 654-659 ◽  
Author(s):  
Robert Wilson ◽  
Karin Lyall ◽  
Margaret Millar ◽  
Louise Smyth ◽  
Claire Pearson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Edible Oils ◽  
Plasma Lipid ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Gas Chromatography Mass Spectrometry ◽  
Walnut Oil ◽  
Plasma Triglycerides ◽  
Coagulation Factor Vii

SummaryFactor VII is activated to VIIa within hours after dietary fat, irrespective of its fatty acid composition. Edible oils contain oxidized material (hydroxy fatty acids, HOFA). Twenty-five fasting women, aged 38 (10) years, consumed 30 g walnut oil containing 26 (6) mg HOFA. Blood was collected 2-hourly to measure plasma triglycerides and plasma lipid HOFA by gas chromatography/mass spectrometry. VII and sTF-dependent VIIa were quantified at 0, 6 and 24 h. Increased plasma triglycerides and HOFA (areas under the-curve 0-8 h, AUC) were related r = 0.83, p <0.001. VIIa increased from 2.6 (1.4) to 4.2 (1.9) ng/mL at 6 h (p <0.001). Plasma VII remained constant. VIIa (6 h) was related to plasma triglycerides- and HOFA-AUC: r = 0.38 and 0.53, respectively (both p <0.05). Plasma VIIa was also related to body weight, fasting triglycerides, HOFA and VII. Only HOFA-AUC and body weight related to VIIa (6 h) in stepwise regression analysis (p = 0.007 and 0.038, respectively). Oxidized, not normal, fat activates VII and could increase coronary risk in humans.

Failure of Thrombolytic Therapy in Patients with Myocardial Infarction Is Associated with High Plasma Levels of Factor VII Antigen

1998 ◽  
Vol 79 (05) ◽  
pp. 928-931 ◽  
Author(s):  
Johan Holm ◽  
Tim Tödt ◽  
Erik Berntorp ◽  
Leif Erhardt
Keyword(s):  
Myocardial Infarction ◽  
Thrombolytic Therapy ◽  
Protein C ◽  
Coagulation Factor ◽  
High Plasma ◽  
Factor Vii ◽  
Plasma Triglycerides ◽  
Coagulation Factor Vii ◽  
Number Of Patients ◽  
On Line

SummaryThrombolytic therapy in acute myocardial infarction fails to re-establish coronary blood flow in a significant number of patients. One reason for this may be haemostatic imbalance. We investigated whether coagulation factor VII antigen (FVIIag), fibrinogen and protein C were related to reperfusion. Plasma from 45 patients was drawn before treatment and reperfusion assessed by means of continuous, on-line, vector-ECG analysis.Amongthe 17 patients with no reperfusion, FVIIag levels were significantly higher than among the 28 with signs of reperfusion (560 vs. 410 μg/l median, p = 0.006). Protein C levels where higher in the group with successful reperfusion (1.10 vs. 1.01 U/ml median, p = 0.03), whereas no difference was seen in fibrinogen levels. The findings were not influenced by plasma-triglycerides, body-mass index, age or time between onset of chest pain and thrombolytic therapy.The results suggest that FVII is of importance for the formation as well as resolution of coronary clots.

Coagulation Factor VII, Dietary Fat and Blood Lipids: A Review

1996 ◽  
Vol 76 (04) ◽  
pp. 492-499 ◽  
Author(s):  
L I Mennen ◽  
E G Schouten ◽  
D E Grobbee ◽  
C Kluft
Keyword(s):  
Dietary Fat ◽  
Blood Lipids ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Coagulation Factor Vii

A Polymorphic Cluster in the 5′ Region of the Human Coagulation Factor VII Gene: Detection, Frequency, and Linkage Disequilibrium

1997 ◽  
Vol 88 (5) ◽  
pp. 445-448 ◽  
Author(s):  
Giorgio Dell'Acqua ◽  
Licia Iacoviello ◽  
Andria D'Orazio ◽  
Rosa Di Bitondo ◽  
Augusto Di Castelnuovo ◽  
...  
Keyword(s):  
Linkage Disequilibrium ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Gene Detection ◽  
Coagulation Factor Vii ◽  
Detection Frequency ◽  
Human Coagulation Factor Vii

A case of an inhibitor autoantibody to coagulation factor VII

Haemophilia ◽  
2003 ◽  
Vol 9 (1) ◽  
pp. 119-120 ◽  
Author(s):  
C. Aguilar ◽  
J. F. Lucía ◽  
P. Hernández
Keyword(s):  
Coagulation Factor ◽  
Factor Vii ◽  
Coagulation Factor Vii

scholarly journals Circulating Tissue Factor Procoagulant Activity and Thrombin Generation in Patients with Type 2 Diabetes: Effects of Insulin and Glucose

2007 ◽  
Vol 92 (11) ◽  
pp. 4352-4358 ◽  
Author(s):  
Guenther Boden ◽  
Vijender R. Vaidyula ◽  
Carol Homko ◽  
Peter Cheung ◽  
A. Koneti Rao
Keyword(s):  
Type 2 Diabetes ◽  
Tissue Factor ◽  
Blood Coagulation ◽  
Coagulation Factor ◽  
Procoagulant Activity ◽  
Factor Vii ◽  
Coagulation Factor Vii ◽  
Glucose Levels ◽  
Study Protocols

Abstract Context: Type 2 diabetes mellitus (T2DM) is a hypercoagulable state. Tissue factor (TF) is the principal initiator of blood coagulation. Objective: Our objective was to examine the effects of hyperglycemia and hyperinsulinemia on the TF pathway of blood coagulation in T2DM. Design: Three study protocols were used: 1) acute correction of hyperglycemia (with iv insulin) followed by 24 h of euglycemia, 2) 24 h of selective hyperinsulinemia, and 3) 24 h of combined hyperinsulinemia and hyperglycemia. Setting: The study took place at a clinical research center. Study Participants: Participants included 18 T2DM patients and 22 nondiabetic controls. Results: Basal TF-procoagulant activity (TF-PCA), monocyte TF mRNA, plasma coagulation factor VII (FVIIc), and thrombin-anti-thrombin complexes were higher in T2DM than in nondiabetic controls, indicating a chronic procoagulant state. Acutely normalizing hyperglycemia over 2–4 h resulted in a small (∼7%) but significant decline in TF-PCA with no further decline over 24 h. Raising insulin levels alone raised TF-PCA by 30%, whereas raising insulin and glucose levels together increased TF-PCA (by 80%), thrombin-anti-thrombin complexes, and prothrombin fragment 1.2. Plasma FVIIa and FVIIc declined with increases in TF-PCA. Conclusion: We conclude that the combination of hyperglycemia and hyperinsulinemia, common in poorly controlled patients with T2DM, contributes to a procoagulant state that may predispose these patients to acute cardiovascular events.

Intracellular readthrough of nonsense mutations by aminoglycosides in coagulation factor VII

2006 ◽  
Vol 4 (6) ◽  
pp. 1308-1314 ◽  
Author(s):  
M. PINOTTI ◽  
L. RIZZOTTO ◽  
P. PINTON ◽  
P. FERRARESI ◽  
A. CHUANSUMRIT ◽  
...  
Keyword(s):  
Coagulation Factor ◽  
Factor Vii ◽  
Nonsense Mutations ◽  
Coagulation Factor Vii
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