CASE REPORT Glanzmann thrombasthenia in a 17-year-old Peruvian Paso mare Macarena G. Sanz 1 , Tamara B. Wills 1 , Peter Christopherson 2 , Melissa T. Hines 1 1 Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA, USA and 2 Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL, USA Key Words Clot retraction, epistaxis, glycoprotein IIb–IIIa, hereditary platelet aggregation, horse, platelets Correspondence Tamara B. Wills, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, PO Box 646610, Pullman, WA 99164, USA E-mail: twills@vetmed.wsu.edu DOI:10.1111/j.1939-165X.2011.00289.x Abstract: A 17-year-old Peruvian Paso mare was evaluated for bilateral epistaxis that had been present for at least 3 years. The mare had mild ane- mia, platelet count within the reference interval, unremarkable coagula- tion times, and a negative Coggins test. On endoscopic examination, structural abnormalities were not observed in the nasal cavities, pharynx, larynx, trachea, or either guttural pouch, but petechiation was noted in the nasal mucosa. Additional tests revealed prolonged cutaneous bleeding time, normal concentration of von Willebrand factor antigen, an abnormal clot retraction test, and failure of plalelet aggregation in response to ago- nists, suggesting a functional disorder of platelets. Genetic analysis indi- cated the horse was homozygous for a 10-base-pair deletion that included the last 3 base pairs of exon 11 and the first 7 base pairs of intron 11 of the gene encoding glycoprotein IIb. The diagnosis was Glanzmann thrombas- thenia (GT) caused by a structural defect in glycoprotein IIb. GT is an au- tosomal recessive disorder caused by a defect in the glycoprotein IIb–IIIa complex on platelet surfaces. Separate genes encode each glycoprotein, and mutations in either gene can result in GT. This case of GT is unique given the age of the mare at the time of diagnosis. We conclude that GT, although an inherited disorder, should be considered in horses with sus- pected dysfunctional platelets, regardless of age. Case Presentation A 17-year-old Peruvian Paso mare was presented to the Washington State University Veterinary Teaching Hospital for evaluation of intermittent bilateral epis- taxis that had been present for 3 years. The exact onset was uncertain because the owner had owned the horse for only 3 years. Hemorrhage in the nasal passages had been confirmed by endoscopic exam, and a persistent mild anemia was noted on a CBC. Biopsy of the nasal mucosa and histologic evaluation revealed moderate lymphoplasmacytic rhinitis suggestive of chronic inflammation. Empirical management, including anti- biotic and corticosteroid treatment and control of po- tential allergens, had been attempted to control the epistaxis with no significant improvement. The owner reported a recent increase in the volume and duration of epistaxis, especially from the right nostril, which worsened in the summer months. On presentation, the mare was in good body con- dition and weighed 380 kg. She had been routinely vaccinated and dewormed, and a recent Coggins test for equine infectious anemia virus was negative. The only abnormality noted on physical examination was moderate right-sided and mild left-sided epistaxis. Oral examination was unremarkable. A CBC revealed ane- mia (hematocrit 21%, reference interval 32–48%) and a platelet count of 148,000 platelets/mL (reference interval 119,000–247,000 platelets/mL). A serum biochemical profile revealed low normal total protein concentration (5.7 g/dL, reference interval 5.6–7.5 g/dL), mild hypo- albuminemia (2.5 g/dL, reference interval 2.8–4.1 g/dL), and normal globulin concentration (3.2 g/dL, reference interval 1.8–4.1 g/dL). The coagulation profile revealed no abnormalities with a one-stage prothrombin time of 10.2 seconds (reference interval 8.7–10.7 seconds) and an activated partial thromboplastin time of 34.9 seconds (reference interval 35.1–44.7 seconds). Endoscopic ex- amination of the upper airway revealed petechiae in the nasal mucosa about 3–4 cm caudal to the nares, which was worse on the right side. Intermittent hemorrhage from the nasal mucosa was apparent in both nostrils. On 48 Vet Clin Pathol 40/1 (2011) 48–51 c 2011 American Society for Veterinary Clinical Pathology Veterinary Clinical Pathology ISSN 0275-6382