Abstract
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.
Highlights
Platelets or thrombocytes are small (2–5 μm) discoid anucleated cells produced by megakaryocytes
In addition to the traditional platelet aggregation assays, flow cytometry has the advantage of rapidly acquiring intrinsic properties from thousands of single platelets, of requiring small blood volumes enabling the analysis of samples from thrombocytopenic patients, and the exploration of more than only one endpoint of the heterogeneous profiles, as performed with traditional aggregation assays
Flow cytometry is able to point out surface membrane receptor deficiencies, such as Bernard Soulier Syndrome (BSS) or Glanzmann thrombasthenia (GT), as well as secretion endpoint defects
Summary
Platelets or thrombocytes are small (2–5 μm) discoid anucleated cells produced by megakaryocytes. They are released in the blood stream where they circulate for 7–10 days to be eventually cleared by the spleen and the liver [1]. Platelet disorders cause defective clot formation that may induce a bleeding or thrombotic diathesis. Platelet disorders can be either inherited or acquired and are characterized by (i) quantitative defects, with an abnormal number of circulating platelets, either high (thrombocytosis) or low (thrombocytopenia); and/or (ii) qualitative platelet dysfunctions (thrombocytopathies) [2]. We summarize intrinsic platelet anomalies resulting in defects of the various traditional activation endpoints, such as adhesion and aggregation (See Section 2), and we offer an in-depth and complete overview of the accumulating evidence for the physiological and clinical role of procoagulant platelets as an alternative, increasingly recognized critical endpoint of platelet function (see Sections 3 and 4)
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