Peer-reviewed veterinary case report
Filly, 18 months old, has bleeding issues - what is Glanzmann
By Macieira, Susana et al.·Published in Veterinary clinical pathology·2007·Department of Clinical Sciences, Canada·View original on PubMed →
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Original publication title: Glanzmann thrombasthenia in an Oldenbourg filly.
- Species:
- horse
Plain-English summary
An 18-month-old Oldenbourg filly was brought in because she was bleeding excessively. Tests showed that her blood wasn't clotting properly, with prolonged bleeding times and poor platelet function. The veterinarians diagnosed her with Glanzmann thrombasthenia, a genetic condition that affects how her platelets work. Unfortunately, this condition means she will always have a risk of bleeding problems, and while there is no cure, managing her environment to prevent injuries is crucial.
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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 (alpha(IIb) or glycoprotein IIb)/CD61 (beta(III) 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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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/17523098/