Glanzmann thrombasthenia in an Oldenbourg filly

Authors

  • Susana Macieira,

    1. From the Department of Clinical Sciences (Macieira, Lavoie) and the Department of Pathology and Microbiology (Bédard), Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Québec, Canada; and the Division of Hematology, Hôpital-Sainte-Justine, Montréal, Québec, Canada (Rivard, Champagne). This work was presented in part at the 40th Annual Meeting of the American Society for Veterinary Clinical Pathology, Boston, MA, December 3–7, 2005. Corresponding author: Christian Bédard (christian.bedard@umontreal.ca)
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  • Georges-Étienne Rivard,

    1. From the Department of Clinical Sciences (Macieira, Lavoie) and the Department of Pathology and Microbiology (Bédard), Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Québec, Canada; and the Division of Hematology, Hôpital-Sainte-Justine, Montréal, Québec, Canada (Rivard, Champagne). This work was presented in part at the 40th Annual Meeting of the American Society for Veterinary Clinical Pathology, Boston, MA, December 3–7, 2005. Corresponding author: Christian Bédard (christian.bedard@umontreal.ca)
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  • Josette Champagne,

    1. From the Department of Clinical Sciences (Macieira, Lavoie) and the Department of Pathology and Microbiology (Bédard), Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Québec, Canada; and the Division of Hematology, Hôpital-Sainte-Justine, Montréal, Québec, Canada (Rivard, Champagne). This work was presented in part at the 40th Annual Meeting of the American Society for Veterinary Clinical Pathology, Boston, MA, December 3–7, 2005. Corresponding author: Christian Bédard (christian.bedard@umontreal.ca)
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  • Jean-Pierre Lavoie,

    1. From the Department of Clinical Sciences (Macieira, Lavoie) and the Department of Pathology and Microbiology (Bédard), Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Québec, Canada; and the Division of Hematology, Hôpital-Sainte-Justine, Montréal, Québec, Canada (Rivard, Champagne). This work was presented in part at the 40th Annual Meeting of the American Society for Veterinary Clinical Pathology, Boston, MA, December 3–7, 2005. Corresponding author: Christian Bédard (christian.bedard@umontreal.ca)
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  • Christian Bédard

    1. From the Department of Clinical Sciences (Macieira, Lavoie) and the Department of Pathology and Microbiology (Bédard), Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Québec, Canada; and the Division of Hematology, Hôpital-Sainte-Justine, Montréal, Québec, Canada (Rivard, Champagne). This work was presented in part at the 40th Annual Meeting of the American Society for Veterinary Clinical Pathology, Boston, MA, December 3–7, 2005. Corresponding author: Christian Bédard (christian.bedard@umontreal.ca)
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Abstract

Abstract An 18-month-old Oldenbourg filly was presented with a bleeding diathesis. Laboratory testing included platelet count, gingival bleeding time, prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand factor (vWf) antigen, clottable fibrinogen, clot retraction time, PFA-100 closure time, platelet aggregometry (on platelet-rich plasma), and thrombelastography (TEG). TEG was performed by using kaolin and tissue factor as coagulation activators. Expression of the platelet receptor for fibrinogen was assessed by flow cytometry by using anti-CD41 (αIIb or glycoprotein IIb)/CD61 (βIII or glycoprotein IIIa) and anti-CD41 antibodies. Abnormal laboratory findings included prolonged oral mucosal bleeding time (>12 hours), prolonged closure time with collagen/ADP (>300 seconds), and absence of clot retraction after 60 minutes. TEG reaction times were similar with kaolin and tissue factor in the patient and a control horse. However, maximum amplitudes in the patient were decreased with both kaolin (43.7 mm; control, 63.9 mm) and tissue factor (37.7 mm; control, 57.8 mm). Platelet aggregation responses to ADP and collagen were profoundly reduced in the affected horse compared with a control. Flow cytometry showed an absence of CD41 and decreased expression of CD41/CD61–reacting antigen on the patient's platelets compared with those from a control horse. The laboratory findings supported a diagnosis of Glanzmann thrombasthenia, likely caused by a mutation in the gene encoding the GPIIb subunit.

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