Congenital Type III von Willebrand's disease unmasked by hypothyroidism in a Shetland sheepdog.

A 7-year-old, spayed female Shetland sheepdog had sudden onset of right-sided epistaxis. Diagnostic tests revealed Type III von Willebrand's disease and primary hypothyroidism leading to an acute hypothyroid crisis and acquired factor VIII (FVIII) deficiency. Levothyroxine therapy normalized the serum thyroxine and FVIII concentrations. The delayed onset of disease and the reversible FVIII deficiency that was corrected with levothyroxine therapy, support a role for hypothyroidism in the pathogenesis of this dog's sudden bleeding tendency as has been seen with hypothyroidism in humans.

Maladie de Willebrand congénitale de type III mise au jour par l'hypothyroïdisme chez une chienne berger Shetland. Une chienne Shetland stérilisée âgée de 7 ans a manifesté l'apparition soudaine d'épistaxis du côté droit. Des tests diagnostiques ont révélé la maladie de von Willebrand de type III et l'hypothyroïdisme primaire provoquant une crise d'hypothyroïdisme aiguë et une déficience du facteur acquis VIII (FVIII). Une thérapie à la lévothyroxine a normalisé la thyroxine sérique et les concentrations de FVIII. L'apparition tardive de la maladie et la déficience réversible de FVIII, qui a été corrigée à l'aide de thérapie à la lévothyroxine, militent en faveur du rôle de l'hypothyroïdisme dans la pathogénèse de la tendance soudaine aux saignements de la chienne, comme nous l'observons dans l'hypothyroïdisme chez les humains.(Traduit par Isabelle Vallières).

Recurrent hemorrhage caused by type 3 von Willebrand disease in a domestic long-haired cat.

OBJECTIVE: To describe a case of spontaneous epistaxis in a cat with type 3 von Willebrand disease (VWD) and detail the successful management of hemorrhagic episodes on 2 occasions. CASE SUMMARY: A 3.6 kg, 1-year-old, female mixed-breed domestic long-haired cat presented for spontaneous epistaxis. Hemostasis testing at presentation revealed normal prothrombin and activated partial thromboplastin times, a slightly decreased platelet count of 168 × 10(9) /L [168 × 10(3) /µL] (reference interval 200-500 × 10(9) /L [200-500 × 10(3) /µL]) and prolonged buccal mucosal bleeding time of 168 seconds (reference interval <150 s). Specific activities of coagulation factors VIII, IX, XI, and XII were all within reference intervals. Plasma von Willebrand factor concentration, however, was markedly reduced at <0.1% of normal. These findings are compatible with a diagnosis of severe type 3 VWD. The initial occurrence of epistaxis resolved spontaneously soon after admission; however, the cat required a packed RBC transfusion for blood loss anemia. Desmopressin acetate was administered, but failed to arrest hemorrhage during a second episode of epistaxis 12 months later. The second episode was successfully controlled by transfusion of 6.7 mL/kg feline fresh frozen plasma. NEW AND UNIQUE INFORMATION: This is the first description of severe type 3 VWD in a domestic cat and only the second report of VWD in this species. Unlike human beings and primates with type 3 VWD, the affected cat did not have a concomitant deficiency of coagulation factor VIII or consistent prolongation of activated partial thromboplastin time. Clinicians should therefore include VWD in the list of differentials for cats with signs of abnormal hemorrhage and confirm the diagnosis with specific measurement of plasma von Willebrand factor concentration.