Canine Von Willebrand’s Disease is a common bleeding disorder in humans and dogs mostly inherited. Von Willebrand disease prevalence in men is 0.82- 1.6%. It has been diagnosed in over 54 breeds of dogs in the United States of America with high-frequency prevalence in Doberman pinschers. The disease severity varies considerably due to its complicated autosomal incomplete dominant method of transmission (Castaman, Giancarlo, et al., p 95). It is caused due to deficiency of specific protein amount required to assist platelets (the blood cells responsible for clotting), to come together and form clots that heal the injured vessels. The deficient protein that aggravates the problem is known as von Willebrand Factor (vWF). The protein circulates all over them, therefore, should always be present at the region where the blood vessel has been injured to control the excessive bleeding of the vessel.  The paper provides a detailed description of Canine Von Willebrand’s Disease and its method of treatment.

In the treatment or cure of Von Willebrand’s Disease,  administration of the drug known as  1- deamino-8-D- argine vasopressin (DDAVP) has been proved helpful and the best suppressor of the disease globally. This drug increases the von Willebrand Factor level to enhance the clotting process, therefore, fastening the healing of the bruises or injured places in the victims of the disease. It helps to prevent hemorrhage in the compassionate human beings and animals when administered before the time of that bleeding usually occurs (Mannucci & Pier, p 687). DDVAP can also be administered in the dogs to donate blood before blood collection period so that blood samples with high vWF factor activity can be achieved.  DDVAP also known in short as Desmopressin reduces the prolonged partially activated thromboplastin time and the time of bleeding. These effects result from the increase in levels of factor VIII and von Willebrand’s Factor. The drug DDAVP improves platelets adhesion to the wall of the vessel of the injured part.  DDAVP administration causes a rapid and transient release of vWF and factor VIII to form their storage sites, thus allowing the factors to circulate in the bloodstream to prevent bleeding.

The primary source of vWf is endothelium; this was confirmed from research which involved injection of a rat with DDVAP. After the injection, the rat responded in a way that clearly showed the activation of endothelial cells, for example, the expression of P-Selectin. In normal persons, desmopressin injection produces significant changes in the content and vWF localization in vascular cells of endothelial. The change in localization of the vascular endothelial cells makes the protein to move albunically to the cellular basement membrane (Mannucci & Pier, p 691).  The whole process enhances the movement of vWF to the injured blood vessels to help to platelets in clotting. Most of the patients with type 1 Von Willebrand Disease, having vWF that is normally functional but decreased plasma levels, respond to DDVAP with an improved factor of VIII and VFW. Therefore, these are some of the reasons why DDVAP needs to be the first choice in the treatment of Von Willebrand Disease. On the other hand, it is a valuable drug because it avoids blood products exposure and is a cheaper alternative.

The effectiveness of DDVAP in the patients who have Von Willebrand Disease, Hemophilia A and other bleeding disorders, made many countries to employ the drug in treating these kinds of diseases. Because of the drug’s potential in increasing the plasma level of factor VIII and VFW without the calling for blood products, the World Health Organization (WHO) opted to include it in the essential drug list in 1977( Nichols, W. L., et al., 227).  WHO recommended the use of the drug not only in the treatment of hemophilia but also the best drug for the treatment of Von Willebrand’s Disease since the 1970s and remains the most recommended drug up to date. Clinicians in the 1970’s and early 1980’s claimed that desmopressin compound was efficacious not only in bleeding disorders but also in acquired defects of platelets and congenital disorders. DDAVP has also been used in patients undergoing surgery that is characterized by high blood loss showing that the drug can comfortably and efficiently treat the VWD bleeding disorder.

In 1926 Von Willebrand described a family of bleeders in Aland. He carried out studies and tests in these families and found out that the disease was inheritable and was mostly affecting women. During his assessment, he tried through the known drug for treating menorrhagia that is tranexamic acid versus desmopressin (DDAVP). He administered the two drugs subcutaneously and intranasally to the patients who were suffering from VWD and found out that DDAVP was more effective in treating the disease than tranexamic acid (Zhang, Z. P., et al., 7938).  He, therefore, recommended the DDAVP for the treatment of VWD, and after detailed research done by scientists till the 1970s, most of them also considered the drug one of the best. The New Zealand doctors have been using OCTOSTIM solution a drug containing desmopressin acetate, to inject the VWD patients. The patients who have been exposed to the drug have responded very well with reduced bleeding levels even during delivery cases.

In San Bortolo Hospital, Italy, a 32-year-old man was evaluated because of bleeding after extraction of a tooth (Castaman, Marco &Francesco, p 168). The tooth required tranexamic acid administration and suturing. After a detailed diagnosis by the doctors about the family history, it was found that the family only had mild epistaxis. The doctors tried other drugs that could stop bleeding, but to their dismay, bleeding persisted. When they tried desmopressin, the bleeding stopped after some time; therefore they recommended desmopressin for other patients who had VWD. From the study, we can conclude that the most currently effective drug for the treatment of VWD is desmopressin.  The drug presents fewer side effects but works very fast in mobilizing the vWF to help the platelets do quick clotting.

Another case study of San Bortolo Hospital, in Italy a 37-year-old woman was referred to the same hospital having been diagnosed of VWD with iron-deficiency anemia history that resulted from menorrhagia (Castaman, Marco &Francesco, p 169). Both she and one of her daughter 12 years old had reduced VWF: RCO (15 IU/dL). Upon surfing on the internet, she was confused about the many subtypes of VWD bleeding medication to settle on. After the doctor had performed the FVIII: C and platelets aggregation tests, the doctor carried out desmopressin infusion in both the mother and the daughter.  An hour later after the infusion of desmopressin drug, their VWD, and FVIII: C levels were corrected, and after six hours they remained above 50 IU/dL. Therefore, from the two case studies of San Bortolo Hospital, desmopressin (DDAVP) should be the right medication for treatment of all the patients who have the Von Willebrand Disease. In conclusion, Von Willebrand’s Disease is a very dangerous disease on both human beings especially women and dogs such as Doberman pinschers. There exist several drugs claimed to treat the disease, but DDAVP is the most effective medication to quickly and efficiently suppress the disease.  Therefore, the medical facilities should give priority to desmopressin in the treatment of Von Willebrand’s Disease.

 
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