Our First Experience with Magnetic Separation of Platelets for Analyses of Platelet MicroRNA in Patients with Sticky Platelet Syndrome

Introduction: Sticky platelet syndrome (SPS) is referred to as a platelet hyperaggregability triggered by low concentrations of platelet agonists adenosine diphosphate (ADP) and/or epinephrine (EPI). Platelet aggregation with other inducers (collagen, arachidonic acid, ristocetin, and thrombin) remains within a normal range. MicroRNAs (miRNAs) are small, non-coding RNA molecules that play an important role in post-transcriptional regulation of protein expression. More recently, several studies show that the platelets are an abundant source of miRNAs and that the miRNA expression profiles within platelets correlate with the platelet reactivity

Measurement of platelet p-selectin expression by flow cytometry in patients with acute ischemic stroke

Aims: The aim of this study was to asses the platelet activation in the acute phase of ischemic stroke and transient ischemic attack (TIA) by defining p-selectin (CD62) expression by flow cytometry in vivo – without stimulation with agonists. We also studied whether antiplatelet therapy supresses the levels of baseline p-selectin expression and verified if there is a correlation between platelet CD62 expression and the type of ischemic stroke

The Importance and Complications of Sequencing of Von Willebrand Gene in Von Willebrand Disease

Genetic testing in patients with von Willebrand disease completes phenotypic testing with an aim to confirm the von Willebrand factor defect at a molecular level. Structure of the VWF gene was described 30 years ago; since then a large number of mutations leading to VWD have been described in this gene. Thanks to describing these mechanisms it is possible to understand the pathogenesis of the most common congenital bleeding disorder

Genetic variants in the fgb and fgg genes mapping in the beta and gamma nodules of the fibrinogen molecule in congenital quantitative fibrinogen disorders associated with a thrombotic phenotype

Fibrinogen is a hexameric plasmatic glycoprotein composed of pairs of three chains (A\u3b1, B\u3b2, and \u3b3), which play an essential role in hemostasis. Conversion of fibrinogen to insoluble polymer fibrin gives structural stability, strength, and adhesive surfaces for growing blood clots. Equally important, the exposure of its non-substrate thrombin-binding sites after fibrin clot formation promotes antithrombotic properties. Fibrinogen and fibrin have a major role in multiple biological processes in addition to hemostasis and thrombosis, i.e., fibrinolysis (during which the fibrin clot is broken down), matrix physiology (by interacting with factor XIII, plasminogen, vitronectin, and fibronectin), wound healing, inflammation, infection, cell interaction, angiogenesis, tumour growth, and metastasis. Congenital fibrinogen deficiencies are rare bleeding disorders, characterized by extensive genetic heterogeneity in all the three genes: FGA, FGB, and FGG (enconding the A\u3b1, B\u3b2, and \u3b3 chain, respectively). Depending on the type and site of mutations, congenital defects of fibrinogen can result in variable clinical manifestations, which range from asymptomatic conditions to the life-threatening bleeds or even thromboembolic events. In this manuscript, we will briefly review the main pathogenic mechanisms and risk factors leading to thrombosis, and we will specifically focus on molecular mechanisms associated with mutations in the C-terminal end of the beta and gamma chains, which are often responsible for cases of congenital afibrinogenemia and hypofibrinogenemia associated with thrombotic manifestations

On-treatment platelet reactivity in the era of new ADP receptor blockers: data from a real-world clinical practice

Objectives: Several studies have questioned the need for platelet function testing in patients treated with new ADP receptor blockers (ADPRB). The aim of this study was to evaluate the prevalence of high on-treatment platelet reactivity (HTPR) among acute ST-elevation myocardial infarction (STEMI) patients treated with newer ADPRB