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Veterinary clinical pathology2011; 40(1); 48-51; doi: 10.1111/j.1939-165X.2011.00289.x

Glanzmann thrombasthenia in a 17-year-old Peruvian Paso mare.

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 anemia, platelet count within the reference interval, unremarkable coagulation 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 agonists, suggesting a functional disorder of platelets. Genetic analysis indicated 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 thrombasthenia (GT) caused by a structural defect in glycoprotein IIb. GT is an autosomal 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 suspected dysfunctional platelets, regardless of age.
Publication Date: 2011-02-03 PubMed ID: 21291483DOI: 10.1111/j.1939-165X.2011.00289.xGoogle Scholar: Lookup
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Summary

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The scientific research focuses on a case of Glanzmann Thrombasthenia (GT), a blood clotting disorder, detected in a 17-year-old Peruvian Paso Mare with a 3-year history of nosebleeds.

Details of Condition and Investigation

  • The mare was inspected due to a nasal condition, specifically bilateral epistaxis, which had been persisting for at least 3 years.
  • The mare was found to have mild anemia but its platelet count was within the normal range. Coagulation times were also found to be normal, indicating that there were no obvious signs of a systemic clotting disorder. A Coggins test was done which came back negative, ruling out equine infectious anemia.
  • A detailed endoscopic examination was done which did not indicate any structural abnormalities in the nasal cavities, pharynx, larynx, trachea, or guttural pouches, which could have been potential case of the nosebleeds.
  • The examination did, however, find petechiation in the nasal mucosa which are red or purple spots caused by small amounts of bleeding.

Diagnostic Testing and Findings

  • Subsequent diagnostic tests revealed a prolonged cutaneous bleeding time which is a sign of episodic bleeding tendencies.
  • The concentration of von Willebrand factor antigen was found to be normal. This is an important protein required for blood clotting.
  • An abnormal clot retraction test was noted, indicating a problem with clot formation or stability.
  • The failure of platelet aggregation in response to triggers was observed, implying that there was a functional disorder in the platelets of the mare.
  • Genetic analysis was done which indicated the horse to be homozygous for a 10-base-pair deletion in the gene encoding glycoprotein IIb. This is significant as glycoprotein IIb is a key protein in platelets necessary for forming clots.

Conclusion and Implications

  • The combination of these clinical signs and diagnostic results led to the diagnosis of GT which is caused by a structural defect in the glycoprotein IIb-IIIa complex found on platelets.
  • It was concluded that GT should not be ruled out in horses with suspected dysfunctional platelets, regardless of their age. This was a significant finding as GT is a genetic disorder and this case was unique because of the mare’s older age at the time of diagnosis.
  • These findings are important in that they expand our understanding of GT, helping to identify and manage this disorder more effectively in horses in the future.

Cite This Article

APA
Sanz MG, Wills TB, Christopherson P, Hines MT. (2011). Glanzmann thrombasthenia in a 17-year-old Peruvian Paso mare. Vet Clin Pathol, 40(1), 48-51. https://doi.org/10.1111/j.1939-165X.2011.00289.x

Publication

ISSN: 1939-165X
NlmUniqueID: 9880575
Country: United States
Language: English
Volume: 40
Issue: 1
Pages: 48-51

Researcher Affiliations

Sanz, Macarena G
  • Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA, USA.
Wills, Tamara B
    Christopherson, Peter
      Hines, Melissa T

        MeSH Terms

        • Animals
        • Blood Coagulation Tests / veterinary
        • Female
        • Horse Diseases / blood
        • Horse Diseases / diagnosis
        • Horse Diseases / pathology
        • Horses / blood
        • Thrombasthenia / blood
        • Thrombasthenia / diagnosis
        • Thrombasthenia / pathology
        • Thrombasthenia / veterinary

        Citations

        This article has been cited 4 times.
        1. Dahlgren AR, Tablin F, Finno CJ. Genetics of equine bleeding disorders. Equine Vet J 2021 Jan;53(1):30-37.
          doi: 10.1111/evj.13290pubmed: 32463964google scholar: lookup
        2. Satué K, Gardon JC, Muñoz A. Clinical and laboratorial description of the differential diagnoses of hemostatic disorders in the horse. Iran J Vet Res 2020 Winter;21(1):1-8.
          pubmed: 32368218
        3. Leite RO, Ferreira JF, Araújo CET, Delfiol DJZ, Takahira RK, Borges AS, Oliveira-Filho JP. Prevalence of the Mutations Responsible for Glanzmann Thrombasthenia in Horses in Brazil. Animals (Basel) 2019 Nov 13;9(11).
          doi: 10.3390/ani9110960pubmed: 31766112google scholar: lookup
        4. Norris JW, Pombo M, Shirley E, Blevins G, Tablin F. Association of Factor V Secretion with Protein Kinase B Signaling in Platelets from Horses with Atypical Equine Thrombasthenia. J Vet Intern Med 2015 Sep-Oct;29(5):1387-94.
          doi: 10.1111/jvim.13595pubmed: 26290457google scholar: lookup