Correction of coagulopathy in thrombocytopenia and Glanzmann thrombasthenia models by fibrinogen and factor XIII as assessed by thromboelastometry. Issue 4 (December 2018)

• Record Type: Journal Article
• Authors: Budnik, Ivan; Shenkman, Boris; Morozova, Olga; Andreichyn, Jurii; Einav, Yulia
• Is Part Of: Pathophysiology. Volume 25:Issue 4(2018)
• Page Start: 347
• Page End: 351
• Publication Date: 2018-12
• Subjects: Thrombocytopenia -- Glanzmann thrombasthenia -- Rotation thromboelastometry -- Fibrinogen -- Factor XIII; Physiology, Pathological -- Periodicals; 571.9
• DOI: 10.1016/j.pathophys.2018.05.005
• Languages: English
• ISSNs: 0928-4680

Abstract

Abstract: Thrombocytopenia (TCP) and Glanzmann thrombasthenia (GT) are typical platelet disorders characterized by mild to severe bleeding. This study aims to create in vitro models of TCP and GT and to correct the impaired clot formation by fibrinogen and coagulation factor XIII. The TCP model (mean platelet count, 16 × 10 9 L −1 ) was produced by differential centrifugation of normal blood followed by mixing plasma with packed cells. The GT model was created by treating normal blood with 50 μg/mL eptifibatide, an inhibitor of platelet integrin αIIbβ3. Clot formation was evaluated in whole blood by rotation thromboelastometry. In both models, the extent of clot strength was two-three times lower compared to normal blood. Fibrinogen and, to a lesser extent, factor XIII stimulated the propagation phase of clot formation both in TCP and GT models. Clot strength in TCP was increased by both agents, while in GT by fibrinogen only. Similar results were obtained in blood from patients with primary immune thrombocytopenia and Glanzmann thrombasthenia. In conclusion, the created models may be useful in the development of new ways to correct the impaired coagulation potential in TCP and GT.