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Latest & greatest articles for Platelet Dysfunction
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Protein kinase C signaling dysfunction in von Willebrand disease (p.V1316M) type 2B platelets von Willebrand disease (VWD) type 2B is characterized by gain-of-function mutations in von Willebrand factor (VWF), enhancing its binding affinity for the platelet receptor glycoprotein (GP)Ibα. VWD type 2B patients display a bleeding tendency associated with loss of high-molecular-weight VWF multimers and variable thrombocytopenia. We recently demonstrated that a marked defect in agonist-induced (...) ) and the adenosine 5'-diphosphate receptor P2Y12. To investigate which Rap1 signaling pathway is affected, we expressed VWF/p.V1316M by hydrodynamic gene transfer in wild-type and Caldaggef1-/- mice. Using αIIbβ3 integrin activation as a read-out, we demonstrate that plateletdysfunction in VWD (p.V1316M) type 2B affects PKC-mediated, but not CDGI-mediated, activation of Rap1. Consistently, we observed decreased PKC substrate phosphorylation and impaired granule release in stimulated VWD type 2B platelets
Severe plateletdysfunction in NHL patients receiving ibrutinib is absent in patients receiving acalabrutinib The Bruton tyrosine kinase (Btk) inhibitor ibrutinib induces plateletdysfunction and causes increased risk of bleeding. Off-target inhibition of Tec is believed to contribute to plateletdysfunction and other side effects of ibrutinib. The second-generation Btk inhibitor acalabrutinib was developed with improved specificity for Btk over Tec. We investigated platelet function (...) in patients with non-Hodgkin lymphoma (NHL) receiving ibrutinib or acalabrutinib by aggregometry and by measuring thrombus formation on collagen under arterial shear. Both patient groups had similarly dysfunctional aggregation responses to collagen and collagen-related peptide, and comparison with mechanistic experiments in which platelets from healthy donors were treated with the Btk inhibitors suggested that both drugs inhibit platelet Btk and Tec at physiological concentrations. Only ibrutinib caused
Brief communication: duration of plateletdysfunction after a 7-day course of Ibuprofen. Despite a paucity of evidence, clinicians routinely advise that patients discontinue using nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, at least 1 week before most surgical procedures.To define the duration of ibuprofen-induced platelet dysfunction.Prospective cohort study.Denver/Aurora, Colorado.11 healthy adult volunteers.Individuals were tested at baseline and serially after (...) completion of a 7-day course of ibuprofen (600 mg orally every 8 hours). The platelet function analyzer (PFA-100, Dade Behring, Newark, Delaware), a test that has replaced the bleeding time in many clinical settings, was used.All participants exhibited normal platelet function before starting ibuprofen. Plateletdysfunction was apparent after completion of the ibuprofen course in 7 of the 11 participants and normalized by 24 hours after the last ibuprofen dose.The sample size in this study was small