Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Desmopressin (DDAVP), a synthetic vasopressin, temporarily corrects bleeding abnormalities associated with mild hemophilia A, von Willebrand disease, and disorders of platelet function. The side effects of DDAVP are considered benign although most of its use has been in adults and older children. We report four children under the age of 2 years who became hyponatremic after intravenous DDAVP administration (0.3 microgram/kg). Three of them developed grand mal seizures. A review of the literature and these cases indicate that associated risk factors for hyponatremia after DDAVP administration include stress, surgery, anesthesia and narcotics (endogenous release of antidiuretic hormone), vomiting (loss of Na+), liver disease (hindered metabolism of DDAVP), renal tubular acidosis (chronically low serum Na+), multiple doses of DDAVP, and overhydration with hyponatremic fluids. DDAVP is not a benign drug in this age group and shows a serious potential for hyponatremia and seizures. Fluid restriction, avoidance of hyponatremic solutions, and close monitoring of serum electrolytes and urine output for at least 15-20 hr after the administration of DDAVP, when used in children under the age of 2 years, is warranted.
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PMID:Hyponatremia and seizures in young children given DDAVP. 250 Aug 51

A new variant of von Willebrand disease (vWD) was identified by a new analytic method which characterizes the ability of plasma von Willebrand Factor (vWF) to bind to purified factor VIII (F.VIII). vWF was isolated from small amounts of plasma by immunoadsorption with a selected monoclonal antibody to vWF previously coated onto wells of microtitration plates. Plasma F.VIII was removed from immobilized vWF by washing with 0.4 mol/L CaCl2; purified F.VIII was then added to the well. The amount of bound F.VIII was estimated directly in the wells by a chromogenic assay and immobilized vWF was estimated by an immunologic a pool of normal plasma, ten control individuals, 13 with hemophilia A and five with type I vWD. In all cases, the dose-response curves were linear and the slopes of the regression lines were essentially the same. The method was then applied to investigate the binding of vWF to F.VIII in two vWD patients (sister and brother) who demonstrated significantly lower activity of F.VIII than of vWF. The first patient, with a long history of epistaxis, bruising, and hematomas, showed a slightly prolonged bleeding time (10 minutes); 15% VIII:C and 39% of vWF:Ag and vWFRCo. Her brother, who has a bleeding syndrome but no hematomas, showed similar data (bleeding time 9 minutes, 20% VIII:C, 53% vWF:Ag and vWFRCo). Similar levels of F.VIII were observed in the two propositi by four different methods (one- and two-stage clotting and chromogenic and immunologic assays). Sodium dodecyl sulfate (SDS) 1.4% agarose gel electrophoresis showed that all multimers of vWF were present in both patients. vWF binding to F.VIII was markedly decreased in the two propositi. The abnormal binding of vWF to F.VIII was not corrected during pregnancy or after infusion of 1-deamino (8-D-arginine) vasopressin despite an increase in vWF levels. The qualitative abnormality of vWF in both patients was associated with a subtle alteration of the multimeric structure by SDS 3% agarose gel electrophoresis in which the two central subbands of the quintuplet of individual oligomers were undetectable or poorly visible. SDS-polyacrylamide gel electrophoresis under reducing conditions demonstrated a single band of 275 Kd in the plasma of both patients, and there was no evidence of a second band corresponding to pro-vWF, the precursor of the mature vWF subunit, suggesting that proteolytic processing of vWF was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New variant of von Willebrand disease with defective binding to factor VIII. 250 47

Derivatives of an antidiuretic hormone raise factor VIII levels in patients with mild or moderate hemophilia A. This case report describes the use of desmo-pressin acetate to raise the factor VIII level in a patient with hemophilia A, before and after extraction of 27 teeth.
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PMID:Desmopressin acetate prophylaxis in a patient with hemophilia A: report of case. 297 70

The effect of the vasopressin analog 1-deamino-8-d-arginine vasopressin (DDAVP) was studied in three normal individuals, 31 subjects with von Willebrand disease, and seven subjects with mild or moderate hemophilia A. None of those with von Willebrand disease had qualitative abnormalities of factor VIII-related antigen (F VIII:RAg). Both intranasal (2 to 4 micrograms/kg) and intravenous (0.2 micrograms/kg) DDAVP were used. All normal subjects, 27 of 31 with von Willebrand disease, and six of seven with hemophilia had a more than 200% increase in F VIII coagulant activity, with lesser but definite increases in F VIII:RAg and ristocetin cofactor activity. Two subjects with severe von Willebrand disease had no increase in F VIII-related activities. In six subjects with von Willebrand disease who had prolonged bleeding times, there was transient correction after DDAVP therapy. None of eight subjects who received DDAVP prior to surgical procedures had any unusual bleeding during or after surgery. None received any blood products. No untoward side effects were noted in any of the 41 subjects. We conclude that DDAVP is a safe and effective alternative to the use of blood products in certain individuals with von Willebrand disease and hemophilia A.
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PMID:DDAVP: a useful alternative to blood components in moderate hemophilia A and von Willebrand disease. 640 6

Desmopressin is a widely used hemostatic drug. It is a synthetic analogue of the natural hormone vasopressin, but, in contrast to vasopressin, it has no pressor activity. The effect is immediate, with two- to sixfold increases in the plasma concentrations of coagulation factor VIII, on Willebrand factor, and tissue plasminogen activator, and increases in platelet adhesiveness of comparable magnitude. Desmopressin is used in patients with mild hemophilia A, von Willebrand's disease, congenital platelet dysfunction, or acquired platelet dysfunction due to uremia or intake of such drugs as aspirin. It may also be used to reduce surgical blood loss in patients without known bleeding diathesis. Optimal hemostatic effect is achieved with a dosage of 0.3 micrograms/kg given intravenously. Other routes of administration are subcutaneous injection or intranasal spray. The latter proved to be efficient for home treatment of patients with bleeding disorders.
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PMID:Desmopressin (DDAVP) and hemostasis. 794 3

A document entitled Guidelines for the Diagnosis and Management of von Willebrand's Disease was produced by the von Willebrand Working Party of the United Kingdom Haemophilia Centre Directors' Organization. Under the chairmanship of Dr Beverley Hunt, an independent board of haematologists and anaesthesiologists reviewed the use of a synthetic vasopressin analogue, desmopressin (DDAVP), in the management of patients with von Willebrand's disease. The Advisory Board considered that production of the guidelines was to be applauded, but that the contraindications for DDAVP were imprecisely defined and may thus be misleading. This paper summarizes the Advisory Board's discussion of the suggestions.
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PMID:The UK guidelines for the use of desmopressin in patients with von Willebrand's disease. Von Willebrand Working Party of the United Kingdom Haemophilia Centre Director's Organization. 908 30

In von Willebrand disease, the main goals of treatment are to correct the dual defect of haemostasis caused by a reduced or abnormal von Willebrand factor (vWF), i.e. the prolonged bleeding time (BT) and the deficiency of factor VIII coagulant activity (FVIII:C). The synthetic vasopressin analogue, desmopressin (DDAVP), has reduced the need for transfusions in most of the mild forms of von Willebrand disease but DDAVP is ineffective in type 3 and in other severe cases of types 1 and 2 von Willebrand disease. For many years cryoprecipitate has been the mainstay of replacement therapy but, after the introduction of virucidal methods, concentrates containing FVIII/vWF have been considered much safer than cryoprecipitate and proposed in von Willebrand disease management. FVIII/vWF concentrates have been produced and tested by many authors but there is only one report describing four virus-inactivated FVIII/vWF concentrates evaluated in a cross-over randomized trial. According to these in vitro and pharmacokinetic data, the following information can be derived: (a) no FVIII/vWF concentrate had an intact multimeric structure similar to that of normal plasma or of cryoprecipitate; (b) all FVIII/vWF concentrates were equally effective in attaining normal and sustained levels of FVIII:C postinfusion, although peak levels were more delayed in the concentrate devoid of FVIII:C; (c) no FVIII/vWF concentrate consistently normalized the BT in a sustained fashion. On the other hand, clinical haemostasis can be achieved in the management of bleeding episodes and of surgery for most of von Willebrand disease cases regardless of whether the BT is corrected; in the few rare cases with mucosal bleeding not controlled by FVIII/vWF concentrates, infusion of DDAVP or platelet concentrates can be administered in addition.
Haemophilia 1998
PMID:Optimizing therapy with factor VIII/von Willebrand factor concentrates in von Willebrand disease. 1002 12

A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.
Haemophilia 2003 Mar
PMID:Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease. 1261 77

Replacement therapy with blood products has long been the only available therapeutic option for patients with bleeding disorders. Plasma-derived cryoprecipitate and factor (F) VIII concentrates, which have been used for hemophilia A patients, involve the risk of transmitting blood-borne diseases. Both plasma-derived and recombinant FVIII concentrates are expensive, and there is a global shortage. The synthetic vasopressin analogue desmopressin acetate (1-deamino-[8-D-arginine]-vasopressin, DDAVP) increases plasma concentrations of coagulation FVIII and von Willebrand factor (vWF) two fold to six fold through endogenous release. The drug is an attractive therapeutic alternative because it carries no risk of transmission of infectious diseases. Desmopressin is today a widely used hemostatic agent not only in patients with mild hemophilia A or von Willebrand disease (vWD) but also in those with congenital or acquired platelet dysfunction. There is a long clinical experience with the drug because it has been used for prevention of bleedings in connection with invasive procedures and for treatment of bleedings since the mid-1970s. Not all hemophilia A patients can be treated. The clinical usefulness depends on the postdesmopressin plasma concentration of FVIII, which in turn depends on the patient's basal FVIII level. Therefore, a test dose is recommended in candidate patients. In general, only the mildest hemophilia A patients respond sufficiently. Optimal hemostatic effect is achieved with a dosage of 0.3 microg/kg given intravenously. An intranasal desmopressin spray is suitable for the home treatment.
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PMID:Desmopressin in mild hemophilia A: indications, limitations, efficacy, and safety. 1264 May 72

The synthetic analog of vasopressin desmopressin (DDAVP) is widely used for the treatment of patients with von Willebrand disease (VWD), hemophilia A, several platelet disorders, and uremic bleeding. DDAVP induces an increase in plasma levels of von Willebrand factor (VWF), coagulation factor VIII (FVIII), and tissue plasminogen activator (t-PA). It also has a vasodilatory action. In spite of its extensive clinical use, its cellular mechanism of action remains incompletely understood. Its effect on VWF and t-PA as well as its vasodilatory effect are likely explained by a direct action on the endothelium, via activation of endothelial vasopressin V2R receptor and cAMP-mediated signaling. This leads to exocytosis from Weibel Palade bodies where both VWF and t-PA are stored, as well as to nitric oxide (NO) production via activation of endothelial NO synthase. The mechanism of action of DDAVP on FVIII plasma levels remains to be elucidated. The hemostatic effect of DDAVP likely involves additional cellular effects that remain to be discovered.
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PMID:Cellular mechanisms of the hemostatic effects of desmopressin (DDAVP). 1287 1


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