scholarly journals Fluctuations in Factor VIII Procoagulant, Antigen and Von Willebrand Factor in Normal Individuals

1977 ◽  
Author(s):  
H.C. Yang ◽  
C. Vaudreuil
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Normal Male ◽  
Normal Individuals ◽  
Factor Viii Antigen ◽  
The Mean ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor ◽  
Ristocetin Cofactor

Fluctuations in the relationship among factor VIII procoagulant (VIIIC), factor VIII antigen (VIIIAG) and von Willebrand factor (vWf, ristocetin cofactor) were studied in two normal females (A&B) and one normal male (C). Biweekly fasting morning plasma samples were obtained over a three week period and assayed on 2 different days. The mean VIIIC/VIIIAG, VIIIC/vWf and VIIIAG/vWf ratios were not significantly different from each other (p>.05) in each of the subjects. However, there were marked day-to-day changes in the three ratios as indicated by the ranges.The results demonstrate that although the ratios among factor VIII procoagulant, factor VIII antigen and von Willebrand factor are relatively fixed, there are significant day-to-day fluctuations.

Comparative Study of Intranasal, Subcutaneous and Intravenous Administration of Desamino-D-Arginine Vasopressin (DDAVP)

1986 ◽  
Vol 55 (01) ◽  
pp. 108-111 ◽  
Author(s):  
M Köhler ◽  
P Hellstern ◽  
C Miyashita ◽  
G von Blohn ◽  
E Wenzel
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Factor Xii ◽  
Additional Advantage ◽  
Mean Values ◽  
Routes Of Administration ◽  
The Mean ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Antigen

SummaryThis study was performed to evaluate the influence of different routes of administration on the efficacy of DDAVP treatment. Ten healthy volunteers received DDAVP intranasally (i.n.), subcutaneously (s.c.) and intravenously (i.v.) in a randomized cross-over trial. Factor XII and high molecular weight (HMW)-kininogen levels increased only slightly after DDAVP administration. The mean increase of factor VIII: C was 3.1 (i. v.), 2.3 (s. c.), and 1.3 (i.n.) - fold over baseline. Ristocetin cofactor (von Willebrand factor antigen) increased 3.1 (2.5), 2.0 (2.3) and 1.2 (1.2) - fold over baseline mean values after i.v., s.c. and i.n. DDAVP, respectively. The half-disappearance time of factor VIII and von Willebrand factor (vWF) after DDAVP ranged from five (factor VIII: C) to eight hours (vWF). The mean increase of fibrinolytic activity was more pronounced after i.v. DDAVP. The antidiuretic effect was moderate with no apparent differences between the routes of application. This study provides further evidence that both i.v. and s.c. DDAVP administration result in an appropriate and reliable stimulation of haemostasis. An additional advantage of s. c. administration is its suitability for home treatment.

scholarly journals Selective absence of large forms of factor VIII/von Willebrand factor in acquired von Willebrand's syndrome. Response to transfusion

Blood ◽  
1979 ◽  
Vol 54 (3) ◽  
pp. 600-606 ◽  
Author(s):  
D Meyer ◽  
D Frommel ◽  
MJ Larrieu ◽  
TS Zimmerman
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Von Willebrand Disease ◽  
Procoagulant Activity ◽  
Factor Viii Related Antigen ◽  
Cofactor Activity ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Ristocetin Cofactor ◽  
Ristocetin Cofactor Activity

Abstract A previously healthy elderly man with mucocutaneous bleeding was found to have a benign monoclonal IgG gammapathy associated with criteria for severe von Willebrand disease (Factor VIII procoagulant activity, Factor-VIII-related antigen, and ristocetin cofactor activity, less than 10% of normal). Associated qualitative abnormalities of factor VIII/von Willebrand factor were demonstrated by radiocrossed immunoelectrophoresis and immunoradiometric assay. The late clinical onset and negative family history are in favor of an acquired form of vWD. The monoclonal gammapathy and abnormalities of factor VIII/von Willebrand factor have been stable over a 10-yr period. No inhibitor to Factor VIII procoagulant activity, ristocetin cofactor activity, or Factor-VIII-related antigen could be demonstrated. Following transfusion of cryoprecipitate (with a normal cross immunoelectrophoretic pattern), there was a rapid removal of the large forms of Factor.-VIII-related antigen, paralleled by a decay of ristocetin cofactor activity. The transfusion study of this patient with acquired von Willebrand disease type II (variant of von Willebrand disease) serves to emphasize the relationship between polydispersity of Factor VIII/von Willebrand Factor and functional heterogeneity.

scholarly journals DDAVP in type IIa von Willebrand's disease

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 465-468 ◽  
Author(s):  
HR Gralnick ◽  
SB Williams ◽  
LP McKeown ◽  
ME Rick ◽  
P Maisonneuve ◽  
...  
Keyword(s):  
Factor Viii ◽  
Protease Inhibitors ◽  
Von Willebrand Factor ◽  
Bleeding Time ◽  
Von Willebrand's Disease ◽  
Von Willebrand’S Disease ◽  
Time Period ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Ristocetin Cofactor

Abstract 1-D-Amino(8-D-arginine)-vasopressin (DDAVP) infusion in three patients with type IIa von Willebrand's disease (vWD) resulted in a normalization of the factor VIII coagulant, factor VIII-related antigen, and von Willebrand factor (vWF) (ristocetin cofactor) activities and the bleeding time. The normalization of these hemostatic parameters persisted for four hours. Over the same time period there was a marked increase in the quantity of the vWF multimers when blood was collected in the presence of protease inhibitors. The vWF multimers present were even larger than the normal. When blood was collected in the absence of protease inhibitors, a smaller increase in the plasma vWF multimers was observed and fewer of the intermediate and larger vWF multimers were seen; multimers larger than those present in normal plasma were not visualized. The platelet vWF multimers and activities did not change with or without inhibitors. These studies suggest that there is a subgroup of patients with type IIa vWD who respond to DDAVP with complete normalization of their hemostatic abnormalities and whose vWF is sensitive to proteolysis.

scholarly journals Quantification of perioperative changes in von Willebrand factor and factor VIII during elective orthopaedic surgery in normal individuals

Haemophilia ◽  
2013 ◽  
Vol 19 (5) ◽  
pp. 758-764 ◽  
Author(s):  
A. Kahlon ◽  
J. Grabell ◽  
A. Tuttle ◽  
D. Engen ◽  
W. Hopman ◽  
...  
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Orthopaedic Surgery ◽  
Normal Individuals ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Factor VIII-von Willebrand factor requires calcium for facilitation of platelet adherence

Blood ◽  
1984 ◽  
Vol 63 (5) ◽  
pp. 996-103 ◽  
Author(s):  
KS Sakariassen ◽  
M Ottenhof-Rovers ◽  
JJ Sixma
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Divalent Cations ◽  
Platelet Adherence ◽  
Human Arteries ◽  
Platelet Spreading ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Ristocetin Cofactor

The role of divalent cations in platelet adherence to deendothelialized human arteries in flowing blood was investigated in an annular perfusion chamber. Spreading of platelets on the subendothelium was impaired below 30 microM of free Ca2+ ions (Ca2+). When Ca2+ was replaced by Mg2+, adherence was unchanged in perfusates without exogenous factor VIII-von Willebrand factor (FVIII-vWF), but the ability of FVIII-vWF to support platelet adherence was lost. Binding of FVIII-vWF to the vessel wall was independent of divalent cations, but bound FVIII-vWF was only able to mediate adherence after exposure to Ca2+. Pretreatment of FVIII-vWF with the calcium chelator EGTA (10 mM) resulted in loss of the ability to facilitate platelet adherence, while the ristocetin cofactor activity remained intact. Full restoration of the ability to mediate platelet adherence could only be obtained by prolonged dialysis against Ca2+ in the millimolar range. These data indicate that divalent cations have at least two separate roles to play in supporting platelet adherence: (1) platelet spreading on the subendothelium requires Ca2+ or Mg2+; (2) FVIII-vWF should be exposed to Ca2+ to obtain its optimal biologic activity in supporting platelet adherence.

scholarly journals High factor VIII antigen levels increase the risk of venous thrombosis but are not associated with polymorphisms in the von Willebrand factor and factor VIII gene

2001 ◽  
Vol 115 (1) ◽  
pp. 156-158 ◽  
Author(s):  
Pieter W. Kamphuisen ◽  
Jeroen C. J. Eikenboom ◽  
Frits R. Rosendaal ◽  
Ted Koster ◽  
Andrew D. Blann ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Factor Viii ◽  
Von Willebrand Factor ◽  
Factor Viii Gene ◽  
Factor Viii Antigen ◽  
Von Willebrand ◽  
Willebrand Factor

Stabilization of the Antihemophilic Factor (VIII :AHF) by the Von Willebrand Factor (VIII :VWF): A Possible Model for Von Willebrand’s Disease

1977 ◽  
Author(s):  
H. J. Weiss ◽  
I. I. Sussman ◽  
L. W. Hoyer
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Von Willebrand's Disease ◽  
Von Willebrand’S Disease ◽  
Crossed Immunoelectrophoresis ◽  
Factor Viii Antigen ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Antihemophilic Factor

When compared with VIII:AHF in normal citrated plasmas, VIII:AHF activity showed increased lability at 37°C in the ‘late’ post-transfusion plasmas (VIII:AHF≫VIII:VWF) of a patient with von Willebrand’s disease, but not in the ‘early’ post-transfusion plasmas in which VIII:AHF~VIII:VWF. VIII:AHF was also labile in the baseline plasmas of 3 patients with von Willebrand’s disease in whom VIII:AHF≫VIII:VWF. In two of these patients the mobility of Factor VIII antigen (on crossed Immunoelectrophoresis) was increased. (VIII:AHF was not excessively labile in 4 other patients in whom VIII :AHF~VIII:VWF). In all of the above cases, VIII:AHF was stabilized by the addition of either purified von Willebrand factor or plasmas of patients with hemophilia, but not by plasmas of patients with severe von Willebrand’s disease. Thus, VIII:VWF may serve to stabilize VIII:AHF and this might explain the post-transfusion findings in von Willebrand’s disease.

Sign in / Sign up

Export Citation Format

Share Document