Beneficial Effect of D.D.A.V.P. On Bleeding-Time in Von Willebrand's Disease

Menon, C.; Berry, Elizabeth W.; Ockelford, Paul

doi:10.1016/s0140-6736(78)92749-6

Cited by 22 publications

(7 citation statements)

References 5 publications

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“…Such an observation is consistent with the view that the involvement of FVIII/VWF in primary haemostasis is not closely reflected by V1IIR:RCo (Mannucci et al, 1976) and suggests that in patients with V W D the component of FVII/VWF involved in the arrest of skin bleeding is not released or made available by DDAVP in sufficient amounts to achieve a satisfactory control of mucosal bleeding. Perhaps the reason for the discrepancy between these and other results with respect to bleeding time changes (Menon et a/, 1978;Theiss &. Schmidt, 1978) is due to the fact that our template method provides a stronger challenge to primary haemostasis, since we find that the bleeding time is often poorly controlled even after cryoprecipitate (Mannucci et al, 1976).…”

Section: Discussioncontrasting

confidence: 79%

“…Schmidt, 1978) is due to the fact that our template method provides a stronger challenge to primary haemostasis, since we find that the bleeding time is often poorly controlled even after cryoprecipitate (Mannucci et al, 1976). Another possibility is that different types of VWD respond differently to DDAVP: this is an interesting hypothesis which deserves further investigation (Menon et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

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Response of Factor VIII/von Willebrand Factor to DDAVP in Healthy Subjects and Patients with Haemophilia A and von Willebrand's Disease

et al. 1981

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These studies were designed with the purpose of providing clinico-pharmacological information relevant to the use of DDAVP in the management of mild haemophilia and von Willebrand's disease (VWD). In healthy subjects, intravenous DDAVP produced its maximal response at a dose of 0.3 micrograms/kg. The extent of the increase in factor VIII coagulant activity (VIII:C) and factor VIII related antigen (VIIIR:Ag) induced by this dose was not significantly different from that observed with the same dose in haemophiliacs and VWD patients. In these, the bleeding time was not shortened. DDAVP given intranasally was followed by a two-fold increase of VIII:C. This route of administration might be adopted to provide an emergency aid in bleeding patients and to yield higher VIII:C levels in blood donors. In healthy subjects, the half-disappearance time of autologous VIII:C after increase induced by i.v. DDAVP is similar to that observed in patients with VWD treated in the same conditions, whereas the response appears to be more prolonged in haemophiliacs. This study shows that the consistency of the VIII:C response tends to decrease when repeated doses are given to healthy subjects. Repeatedly-treated haemophiliacs and VWD patients showed varied patterns, ranging from no change of the response to its early abolishment.

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Section: Discussioncontrasting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Response of Factor VIII/von Willebrand Factor to DDAVP in Healthy Subjects and Patients with Haemophilia A and von Willebrand's Disease

et al. 1981

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“…Shortening of the APTT during infusion of aVP raises the possibility that activation of the intrinsic clotting mechanism occured. The increase in FVIII procoagulant activity (FVIII :C) in response to a VP (2), which also occurs following administration of DDAVP (15,16), was probably responsible. The continuing decrease in APTT after the infusion was probably due to the relatively long half-life of FVIII :C (17).…”

Section: Discussionmentioning

confidence: 99%

Effect of Physiological Concentrations of Vasopressin on Components of the Fibrinolytic System

et al. 1989

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SummaryHigh physiological concentrations of plasma vasopressin (aVP) when achieved by infusion cause an increase in plasma factor VIII coagulant activity and shortening of the euglobulin clot lysis time (ECLT). To investigate the effects of aVP on components of the fibrinolytic pathway and on thrombin generation, t healthy volunteers were infused with saline for 30 min followed by aVP for L hour and blood samples taken every 30 min for measurement of aVR ECtf tissue-type plasminogen activator (t-PA), t-PA inhibition (tPA-I), plasminogen activator inhibitor L (PAI-1 Ag), activated partial thromboplastin time (APTT), fibrinopeptide A (FPA), fibrinopeptide B 15-42 (FPBß 15-42) and crosslinked fibrin breakdown products (XL-FDP). Plasma aVP rose to a median of 75 pg/ml after 90 min and fell to 13.8 pdml 30 min later. The APTT fell from 43.5 to 35 sec (p <0.01) but there was no change in plasma FPA or in XL-FDP. Plasminogen activator activity (106/ECLT2) increased from 25 to 736 units (p <0.01) and t-PA from 200 to 1012 mlU/ml (p <0.01). tPA-I fell from 8.0 to 2.7 IU/ml at 90 min (p <0.05) but PAI-1 Ag remained unchanged. Plasma FPBß 15-42 was 2.4 and 1.2 pmol/ml before infusion with aVP and showed a small rise to 3.5 pmol/ml after 60 min (p <0.05). The results show the effects of aVP on fibrinolysis are mediated by an increase in t-PA. In the absence of thrombin generation the rise in t-PA was not accompanied by changes in XL-FDP.

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“…This drug is used as an alternative to plasma derivatives in the treatment of patients with mild von Willebrand's disease or haemophilia, in the preparation for minor surgery [21]. In some countries, DDAVP is administered to blood donors in order to harvest factor VIII-enriched plasma derivatives [22].…”

Section: Discussionmentioning

confidence: 99%

Availability of endothelial von Willebrand factor and platelet function in diabetic patients infused with a vasopressin analogue

Porta

1982

Diabetologia

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Summary. Acute release of von Willebrand factor and its immunologically detected correspondent, factor VIII-related antigen, from the endothelial ceils into the circulation was induced by an infusion of 1-deamino-8-D-arginine vasopressin in eight normal subjects and eight insulin-dependent diabetic patients. The patients had higher basal levels of von Willebrand factor (140 + 13%) and VIII-related antigen (112 • 18%) than the normal subjects (95 • 5% and 70 • 8%, respectively). 1-deamino-8-D-arginine vasopressin induced a twofold rise of these levels in both groups, yon Willebrand factor/ VIII-related antigen remaining higher in the diabetic patients throughout the experiment. In the normal subjects, platelet retention in glass bead columns increased soon after the infusion but returned to basal values after 2 h. In the patients, it remained high at the end of the infusion. No changes in platelet aggregation occurred. These results suggest that increased plasma yon Willebrand factor/VIII-related antigen in diabetic patients is accompanied by an increased endothelial content of this factor.

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Beneficial Effect of D.D.A.V.P. On Bleeding-Time in Von Willebrand's Disease

Cited by 22 publications

References 5 publications

Response of Factor VIII/von Willebrand Factor to DDAVP in Healthy Subjects and Patients with Haemophilia A and von Willebrand's Disease

Response of Factor VIII/von Willebrand Factor to DDAVP in Healthy Subjects and Patients with Haemophilia A and von Willebrand's Disease

Effect of Physiological Concentrations of Vasopressin on Components of the Fibrinolytic System

Availability of endothelial von Willebrand factor and platelet function in diabetic patients infused with a vasopressin analogue

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