Glanzmann thrombasthenia platelets compete with transfused platelets, reducing the haemostatic impact of platelet transfusions
نویسندگان
چکیده
منابع مشابه
Monitoring survival and function of transfused platelets in Glanzmann thrombasthenia by flow cytometry and thrombelastography.
Patients with Glanzmann thrombasthenia (GT) may form isoantibodies which induce refractoriness or inhibition of function of transfused platelets. We monitored the survival and function of transfused platelets by flow cytometry and thrombelastography in a patient with GT. Gating on CD42a+ allowed identification of even a few transfused platelets. Only by gating on these CD41+ CD42a+ cells were w...
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Background—Platelets have been suggested to play a role in the early development of atherosclerosis. As one test of this hypothesis, we assessed whether patients with Glanzmann thrombasthenia who lack platelet glycoprotein IIb 3 (GPIIb/IIIa) complexes or both IIb 3 and the more ubiquitous v 3 cell membrane complexes are protected from development of atherosclerosis. Methods and Results—Seven pa...
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Background: Activated normal platelets undergo many biochemical and morphological changes, some of which are apoptotic. Platelet derived microparticles and shrinked platelets as hallmark of platelet activation and apoptosis disperse surfaces containing procoagulant activity around injured vessels and tissues. This study was conducted to determine microparticles formation and platelet shrinkage ...
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Platelets transfusion is a safe process, but during or after the process, the recipient may experience an adverse reaction and occasionally a serious adverse reaction (SAR). In this review, we focus on the inflammatory potential of platelet components (PCs) and their involvement in SARs. Recent evidence has highlighted a central role for platelets in the host inflammatory and immune responses. ...
متن کاملGlanzmann thrombasthenia
Glanzmann thrombasthenia (GT) is a rare autosomal recessive bleeding syndrome affecting the megakaryocyte lineage and characterized by lack of platelet aggregation. The molecular basis is linked to quantitative and/or qualitative abnormalities of alphaIIb beta3 integrin. This receptor mediates the binding of adhesive proteins that attach aggregating platelets and ensure thrombus formation at si...
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ژورنال
عنوان ژورنال: British Journal of Haematology
سال: 2017
ISSN: 0007-1048
DOI: 10.1111/bjh.14623