Boudreaux M K, Kvam K, Dillon A R, Bourne C, Scott M, Schwartz K A, Toivio-Kinnucan M
Department of Pathobiology, Auburn University, AL, USA.
Vet Pathol. 1996 Sep;33(5):503-11. doi: 10.1177/030098589603300504.
An 8-month-old female Great Pyrenees dog with chronic epistaxis and a history of gingival bleeding during shedding of deciduous teeth was evaluated for platelet function. Platelet morphology was normal at both the light and electron microscopic level. Platelet number and mean platelet volume were also normal. Platelet aggregation responses to adenosine diphosphate, collagen, platelet activating factor, and thrombin were markedly reduced, although shape change responses were normal. Clot retraction was markedly impaired. Monoclonal antibody (MoAb) Y2/51, a murine anti-human platelet beta 3 antibody that cross-reacts with canine platelet beta 3, and MoAb 5G11, a murine anti-dog platelet alpha IIb beta 3 antibody, bound minimally to affected dog platelets, as demonstrated by flow cytometry. Binding of MoAb Y2/51 was not detectable by immunoblot. MoAb CAP1, a murine anti-dog fibrinogen receptor-induced binding site antibody, failed to bind to affected dog platelets, as demonstrated by flow cytometry. A reduction in glycoproteins alpha IIb and beta 3 was demonstrated by two-dimensional protein electrophoresis. This is the first reported case of type I Glanzmann's thrombasthenia in the dog that closely resembles the clinical syndrome and the platelet morphology described in type I Glanzmann's thrombasthenia of human beings.
对一只8个月大的雌性大白熊犬进行了血小板功能评估，该犬患有慢性鼻出血，且在乳牙脱落时有牙龈出血史。光镜和电镜下血小板形态均正常。血小板数量和平均血小板体积也正常。尽管形状改变反应正常，但血小板对二磷酸腺苷、胶原、血小板活化因子和凝血酶的聚集反应明显降低。血块回缩明显受损。流式细胞术显示，鼠抗人血小板β3抗体（与犬血小板β3发生交叉反应）单克隆抗体（MoAb）Y2/51和鼠抗犬血小板αIIbβ3抗体MoAb 5G11与患病犬血小板的结合极少。免疫印迹法未检测到MoAb Y2/51的结合。流式细胞术显示，鼠抗犬纤维蛋白原受体诱导结合位点抗体MoAb CAP1未能与患病犬血小板结合。二维蛋白质电泳显示糖蛋白αIIb和β3减少。这是首次报道的犬I型Glanzmann血小板无力症病例，与人类I型Glanzmann血小板无力症所描述的临床综合征和血小板形态极为相似。
