Glanzmann Thrombasthenia Otterhound Type (GT)

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Acronyms: GT
Gene: ITGA2B
Mutation: Point mutation
Mode of inheritance: Autosomal recessive
Breeds: Otterhound

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Product Description

Glanzmann Thrombasthenia Otterhound Type (GT)

Glanzmann Thrombasthenia Otterhound type (GT) is a bleeding disorder in Otterhound dog breed that belongs in group of disorders known as Glanzmann thrombasthenia (GT). Glanzmann thrombasthenia is a disorder occurring in humans and dogs and it was discovered by a Swiss paediatrician in 1918 in a human patient. In dogs, GT was for first time identified in Great Pyrenees and its molecular basis, clinical aspects, platelet function and biochemical data in this fog breed were defined in 1990’s. In Otterhound breed, GT was for first time recognized in 1967, but the same as in Great Pyrenees, its molecular and genetic basis were not known until many years after. Today, Glanzmann thrombasthenia is divided into three categories, type I, type II and variant, and they differ among each other in quantity of expressed glycoproteins αIIb  and b3.

Platelets, or thrombocytes, have a key role in bleeding prevention through clumping of blood vessel injuries. An important component of platelets in the αIIb b3 integrin, also known GPIIb-IIIa complex, which is abundant in healthy thrombocytes. The αIIb b3 integrin mediated the uptake of fibrinogen and like this enables platelet aggregation. Because of this, the complex is also known as fibrinogen receptor. In case of mutation in the genes encoding for these glycoproteins, formation of the αIIb b3 integrin is disabled, which results in a bleeding disorder.

Symptoms and Characteristics

Clinical signs of Glanzmann Thrombasthenia Otterhound type (GT) are primarily mucosal bleeding including epistaxis, gingival bleeding and petechial and ecchymotic hemorrhages. Severity of bleeding can vary, and it is especially problematic in case of trauma or post operation and clotting time is prolonged. When observing blood smears of an affected dog, 30% to 80% of all platelets are seen as bizarre and giant. Platelet aggregation responses in response to all agonists (including ADP, collagen, thrombin, and platelet-activating factor) are minimal or lacking, clot retraction is severely impaired, and intraplatelet fibrinogen content is severely reduced. Protein electrophoresis shows diminished or undetectable amounts of glycoprotein αIIb and b3 on platelet membranes.


Glanzmann Thrombasthenia Otterhound type (GT) is caused by a mutation in the gene encoding for platelet glycoprotein subunit b3. Mutation comprises two changes which result in amino acid substitutions. The GT disorder is inherited in an autosomal recessive manner.  Healthy parents of an affected puppy are obligate heterozygotes, and therefore carry one mutant allele. Heterozygotes have no symptoms. Dogs homozygous for the mutation will display the symptoms of the Glanzmann Thrombasthenia Otterhound type (GT). At conception, each cub has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.


Boudreaux, MK, Catalfamo, JL. (2001): Molecular and genetic basis for thrombasthenic thrombopathia in Otterhounds. Am J Vet Res 2001;62:1797–1804.