Factor VII Deficiency
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US: $45.00 | UK: £40.00
Breeds: Airedale Terrier, Alaskan Klee Kai, American Foxhound, Beagle, German Shorthaired Pointer, German Wirehaired Pointer, Giant Schnauzer, Japanese Spitz, Miniature Schnauzer, Mixed Breed, Papillon, Schnoodle, Scottish Deerhound, Sealyham Terrier, Unspecified, Welsh Springer Spaniel
Factor VII (FVII) Deficiency is a disorder that can cause excessive bleeding. FVII is an autosomal recessive trait. Autosomal recessive traits are traits that can be passed from either parent and require two copies of the gene to show symptoms.
Dogs affected by Factor VII Deficiency do not make enough Factor VII protein. This protein is an essential part of the blood coagulation process (also known as clotting). Under normal circumstances, this factor is designed to clot wounds in order to stop bleeding. This can be exemplified in observing the common scab. Due to a deficiency in this clotting agent, an affected dog may bleed excessively after an injury or surgery.
Affected dogs may not exhibit any symptoms normally; often the condition is not detected until the dog experiences an injury or after a medical procedure. In these circumstances, the dog may require a blood transfusion. However, the condition is typically not fatal as long as there is medical intervention.
Because FVII is a recessive disorder, a dog must have two copies of the mutation in order for the disease to manifest. This means that a dog can have one copy of the mutation and not experience any signs or symptoms of FVII. This dog would be known as a carrier. The carrier can then pass on either the normal gene or the mutated gene to any offspring. If two carriers are bred, there is a 25% per puppy that they will develop symptoms of FVII.
|Affected: Dog has two copies of the Factor VII Deficiency mutation and may develop symptoms. The mutation will be passed to every offspring.
|Carrier: Dog has one copy of the Factor VII Deficiency mutation. The dog may pass the mutation to offspring.
|Clear: Dog is negative for the mutation associated with Factor VII Deficiency.
Callan MB, Aljamali MN, Margaritis P, Griot-Wenk ME, Pollak ES, Werner P, Giger U, High KA. A novel missense mutation responsible for factor VII deficiency in research Beagle colonies. J Thromb Haemost. 2006 Dec; 4(12):2616-22. [PubMed: 16961583]
Carlstrom LP, Jens JK, Dobyns ME, Passage M, Dickson PI, Ellinwood NM. Inadvertent propagation of factor VII deficiency in a canine mucopolysaccharidosis type I research breeding colony. Comp Med. 2009 Aug;59(4):378-82. [PubMed: 19712579]