Why the study?
Qualitative platelet dysfunctions cause thrombocytopathies involving adhesive and procoagulant activation defects, highlighting the need to review procoagulant platelets and traditional defects.
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Design
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Procoagulant platelet modulation remains hypothesis-generating; leaves open targeted therapies for bleeding and thrombosis.
Platelets are active key players in haemostasis. Qualitative platelet dysfunctions result in thrombocytopathies variously characterized by defects of their adhesive and procoagulant activation endpoints. In this review, we summarize the traditional platelet defects in adhesion, secretion, and aggregation. In addition, we review the current knowledge about procoagulant platelets, focusing on their role in bleeding or thrombotic pathologies and their pharmaceutical modulation. Procoagulant activity is an important feature of platelet activation, which should be specifically evaluated during the investigation of a suspected thrombocytopathy.
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Aliotta et al. (2021) studied this question.
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