Trade name DDAVP.
A medication used to treat diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease, and high blood urea levels.
Desmopressin stimulates release of von Willebrand factor from blood vessel endothelial cells by acting on the V2 receptor, which leads to decreased breakdown of Factor VIII.
Desmopressin is thus sometimes used directly to treat mild to moderate acquired von Willebrand’s disease and is an effective prophylactic agent for the reduction of bleeding during heart valve replacement surgery.
A synthetic version of vasopressin, the hormone that reduces urine production.
Desmopressin (1-deamino-8-D-arginine vasopressin) is a synthetic form of the normal human hormone arginine vasopressin, a peptide containing nine amino acids.
In hemophilia A and von Willebrand disease, it should only be used for mild to moderate cases.
It may be given nasally, or intravenously, intramuscularally, subcutaneously, by mouth, or under the tongue.
DDAVP (D-amino D-arginine vasopressin)
US: B (No risk in non-human studies)
Safe to use during pregnancy
Bioavailability:
Variable; 0.08–0.16% (by mouth)
Protein binding 50%
Elimination half-life1.5–2.5 hours
Excretion by Kidney and should not be used in people with significant kidney problems or low blood sodium.
It is used to treat nocturnal enuresis, and is usually prescribed in the form of desmopressin acetate, by mouth.
Children with enuresis and taking DDAVP have 2.2 fewer wet nights per week and are 4.5 times more likely to sleep without disruption compared with placebo.
It has some use for adults who have problems with nocturia.
Desmopressin stimulates the release of von Willebrand factor (vWF) from the Weibel–Palade bodies of endothelial cells,.
Desmopressin increases the levels of vWF and coagulant factor VIII 3 to 5-fold.
Promotes the release of von Willebrand factor in patients with coagulation disorders such as von Willebrand disease, mild hemophilia A, factor VIII deficiency, and thrombocytopenia.
It can also be used with uremic induced platelet dysfunction.
It is not effective in the treatment of hemophilia B, factor IX deficiency, or severe hemophilia A.
Its use in hemophilia A depends on whether Factor VIII deficiency is qualitative or quantitative
It is most effective in patients with quantitative deficiencies, because by increasing the release of vWF, the circulating pool of functional factor VIII effectively increases.
With functional defects in factor VIII, the use of desmopressin is not efficacious.
It is used in the treatment of central diabetes insipidus as a replacement for endogenous antidiuretic hormone (ADH).
In diabetes insipidus there is in insufficient quantity due to decreased or non-existent secretion or production of ADH by the posterior pituitary or hypothalamus, respectively.
Desmopressin is not effective at treating nephrogenic diabetes insipidus.
Side effects:
headaches
facial flushing
nausea
hyponatremia
seizures
DDAVP can cause fluid retention, secondary hyponatremia, and seizures.
Fluid intake should be restricted to 1 L for adults in the 24 hours post-DDAVP administration to minimize the risk of dilutional hyponatremia, the rate of which may be higher in adolescents.
Confirmation of normal serum sodium levels is essential prior to any subsequent doses of DDAVP
Nasal spray is no longer approved for use in children in the United States due to potential of hyponatremia.
The drug should be discontinued if patients develop severe vomiting and diarrhea, fever, the flu, or severe cold.
Cautious use during hot weather conditions or following strenuous exercise, as these conditions can place stress on the body’s electrolyte and water balance.
It works by limiting the amount of water that is eliminated in the urine, as it is an antidiuretic.
At the level of the renal collecting duct it binds to V2 receptors, signaling for the translocation of aquaporin channels via cytosolic vesicles to the apical membrane of the collecting duct.
The aquaporin channels in the distal nephron causes increasing water reabsorption from the urine, which becomes passively re-distributed from the nephron to systemic circulation by way of basolateral membrane channels.
It also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor.
Desmopressin is degraded more slowly than recombinant vasopressin, and requires less frequent administration.
While vasopressin may cause arterial hypertension it has little chance of doing so, as it does not does not stimulate ACTH release