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Platelet Dysfunction

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81. Use of platelet transfusions

risk factors for bleeding are corrected: anaemia (iron and erythropoietin), uraemia (dialysis) (1B). If renal biopsy is urgent consider desmopressin (DDAVP) pre- procedure (1B) or oestrogen if time allows (2B) ? Avoid platelet transfusion in renal failure since infused platelets will acquire a dysfunction similar to the patients’ own platelets and platelet transfusion may result in alloimmunisation (1B) Recommendations for Therapeutic Platelet Transfusions ? In severe bleeding, maintain (...) if time allows (2B) ? In renal failure platelet transfusion should be avoided as infused platelets will acquire a dysfunction similar to the patient’s own platelets and may result in alloimmunisation (1B) THERAPEUTIC PLATELET TRANSFUSIONS There is little evidence for the effectiveness of platelet transfusions or the optimal dose when a patient with thrombocytopenia is actively bleeding i.e. WHO grade 2 or above (Estcourt, et al 2013). This may reflect the challenges involved in conducting trials

2016 British Committee for Standards in Haematology

82. Platelets and vascular integrity: how platelets prevent bleeding in inflammation. Full Text available with Trip Pro

in concert as building blocks of the hemostatic plug but also act individually as gatekeepers of the vascular wall to help preserve vascular integrity while coordinating host defense. Variants of this recently appreciated hemostatic function of platelets that we refer to as "inflammation-associated hemostasis" are engaged in different contexts in which the endothelium is challenged or dysfunctional. Although the distinguishing characteristics of these variants and the underlying mechanisms (...) Platelets and vascular integrity: how platelets prevent bleeding in inflammation. Platelets play a central role in primary hemostasis by forming aggregates that plug holes in injured vessels. Half a century ago, detailed studies of the microvasculature by electron microscopy revealed that under inflammatory conditions that do not induce major disruption to vascular structure, individual platelets are mobilized to the vessel wall, where they interact with leukocytes and appear to seal gaps

2017 Blood

83. Mechanisms of platelet activation by the pneumococcus and the role of platelets in community-acquired pneumonia. Full Text available with Trip Pro

Mechanisms of platelet activation by the pneumococcus and the role of platelets in community-acquired pneumonia. There is increasing recognition of the involvement of platelets in orchestrating inflammatory responses, driving the activation of neutrophils, monocytes and vascular endothelium, which, if poorly controlled, may lead to microvascular dysfunction. Importantly, hyperreactivity of platelets has been implicated in the pathogenesis of myocardial injury and the associated particularly (...) high prevalence of acute cardiovascular events in patients with severe community-acquired pneumonia (CAP), of which Streptococcus pneumoniae (pneumococcus) is the most commonly encountered aetiologic agent. In this context, it is noteworthy that a number of studies have documented various mechanisms by which the pneumococcus may directly promote platelet aggregation and activation. The major contributors to platelet activation include several different types of pneumococcal adhesin, the pore

2017 Journal of Infection

84. Changes in platelet Bax levels contribute to impaired platelet response to thrombin after cardiopulmonary bypass: prospective observational clinical and laboratory investigations. Full Text available with Trip Pro

Changes in platelet Bax levels contribute to impaired platelet response to thrombin after cardiopulmonary bypass: prospective observational clinical and laboratory investigations. Anucleate platelets can undergo apoptosis in response to various stimuli, as do nucleated cells. Cardiopulmonary bypass (CPB) causes platelet dysfunction and can also activate platelet apoptotic pathways. We therefore evaluated time-dependent changes in blood platelet Bax (a pro-apoptotic molecule) levels and platelet (...) dysfunction after cardiac surgery.We assessed blood samples obtained from subjects having on-pump or off-pump coronary artery bypass graft surgery ( n =20 each). We also evaluated the in vitro effects of platelet Bax increase in eight healthy volunteers.Thrombin-induced platelet calcium mobilisation and platelet-surface glycoprotein Ib (GPIb) expression were lowest at weaning from CPB and did not recover on postoperative day one. On-pump surgery increased platelet expression of Bax, especially

2017 British Journal of Anaesthesia

85. Flow Devices to Assess Platelet Function: Historical Evolution and Current Choices. (Abstract)

Flow Devices to Assess Platelet Function: Historical Evolution and Current Choices. Platelet function testing, which began more than a hundred years ago, is a time-consuming and uncertain process. Simulating hemostasis and the blood vessel microenvironment in vitro is challenging, which poses a difficulty for diagnosing platelet dysfunction and mild von Willebrand disease (VWD). In an effort to simulate the rheological microenvironment within blood vessels, several blood flow devices have been (...) introduced since the 1980s. These devices are capable of reproducing the shear rates found in arterioles and venules, and of incorporating endothelial cell monolayers and surfaces with adsorbed platelet-adhesive proteins. The authors will describe and review here the presently most well-known blood flow devices. The technologies inherent in these devices offer a combination of physiologic accuracy and small blood volume requirements in the evaluation of platelet disorders and mild VWD (or "symptomatic

2019 Seminars In Thrombosis And Hemostasis

86. Frequency and Clinical Impact of Platelet Factor 4-Specific Antibodies in Patients Undergoing Extracorporeal Membrane Oxygenation. (Abstract)

immunized within 10 days. PF4-specific IgG Abs did not affect the clinical or biological course of most patients. HIT was suspected in only two patients with ECMO circuit dysfunction and unexpected platelet count decrease after day 5. High levels of PF4-specific IgG were detected in both patients, and HIT was confirmed by a serotonin release assay, which was also more sensitive when exogenous PF4 was present. PF4-specific Abs are common during ECMO but are mostly non-pathogenic and not associated (...) with a less favorable prognosis. However, an abnormal platelet count evolution, in particular if associated with ECMO circuit dysfunction, should prompt the search for pathogenic PF4-specific IgG.Georg Thieme Verlag KG Stuttgart · New York.

2019 Thrombosis and haemostasis

87. Platelets as Potent Signaling Entities in Type 2 Diabetes Mellitus. (Abstract)

Platelets as Potent Signaling Entities in Type 2 Diabetes Mellitus. Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a dysregulated circulating inflammatory molecule tendency. T2DM is closely associated with systemic inflammation, endothelial dysfunction, cardiovascular risk, and increased clotting susceptibility. Platelets have fundamental roles in the development and propagation of inflammation and cardiovascular risk. They signal through membrane receptors, resulting (...) in (hyper)activation and release of inflammatory molecules from platelet compartments. This review highlights how circulating inflammatory molecules, acting as platelet receptor ligands, interact with platelets, causing platelets to be potent drivers of systemic inflammation. We conclude by suggesting that focused platelet research in T2DM is an important avenue to pursue to identify novel therapeutic targets, and that platelets could be used as cellular activity sensors themselves.Copyright © 2019

2019 Trends in Endocrinology and Metabolism

88. Epithelial (E)-Cadherin is a Novel Mediator of Platelet Aggregation and Clot Stability. Full Text available with Trip Pro

utilized a megakaryocyte-specific E-cadherin knockout mouse model. Loss of E-cadherin in megakaryocytes does not affect megakaryocyte maturation, platelet number or size. However, platelet dysfunction in the absence of E-cadherin is revealed when conditional knockout mice are challenged with acute antibody-mediated platelet depletion. Unlike wild-type mice that recover fully, knockout mice die within 72 hours post-antibody administration, likely from haemorrhage. Furthermore, conditional knockout mice (...) Epithelial (E)-Cadherin is a Novel Mediator of Platelet Aggregation and Clot Stability. Cadherins play a major role in mediating cell-cell adhesion, which shares many parallels with platelet-platelet interactions during aggregate formation and clot stabilization. Platelets express epithelial (E)-cadherin, but its contribution to platelet function and/or platelet production is currently unknown. To assess the role of E-cadherin in platelet production and function in vitro and in vivo, we

2019 Thrombosis and haemostasis

89. Dynamin 2 is required for GPVI signaling and platelet hemostatic function in mice. (Abstract)

by dynasore treatment. Dynasore-treated platelets had attenuated function when stimulated via GPVI, as evidenced by reduced GPIbα down-regulation, α-granule release, integrin αIIbβ3 activation, and spreading onto immobilized fibrinogen. By contrast, responses to the G-protein coupled receptor agonist thrombin were minimally affected by dynasore treatment. GPVI expression was severely reduced in Dnm2Plt-/- platelets, which were dysfunctional in response to stimulation via GPVI, and to a lesser extent (...) Dynamin 2 is required for GPVI signaling and platelet hemostatic function in mice. Receptor-mediated endocytosis, which contributes to a wide range of cellular functions, including receptor signaling, cell adhesion, and migration, requires endocytic vesicle release by the large GTPase dynamin 2. Here, the role of dynamin 2 was investigated in platelet hemostatic function using both pharmacological and genetic approaches. Dnm2fl/f PF4-Cre (Dnm2Plt-/-) mice specifically lacking dynamin 2 within

2019 Haematologica

90. Recent advances in inherited platelet disorders. (Abstract)

platelet defects, and highlights how these studies have provided insights into platelet development and function.Novel genes recently implicated in human platelet dysfunction include the galactose metabolism enzyme UDP-galactose-4-epimerase in macrothrombocytopenia, and erythropoietin-producing hepatoma-amplified sequence receptor transmembrane tyrosine kinase EPHB2 in a severe bleeding disorder with deficiencies in platelet agonist response and granule secretion. Recent studies of disease-associated (...) Recent advances in inherited platelet disorders. The increasing use of high throughput sequencing and genomic analysis has facilitated the discovery of new causes of inherited platelet disorders. Studies of these disorders and their respective mouse models have been central to understanding their biology, and also in revealing new aspects of platelet function and production. This review covers recent contributions to the identification of genes, proteins and variants associated with inherited

2019 Current Opinion in Hematology

91. Propensity and impact of autologous platelet rich plasma use in acute type A dissection. (Abstract)

. The purpose of this study is to evaluate the effectiveness of autologous platelet rich plasma as a blood conservation technique during open surgical repair of acute type A aortic dissection.We reviewed all acute type A aortic dissection cases using hypothermic circulatory arrest, excluding patients presenting in extremis. Perioperative transfusion requirements and clinical outcomes were analyzed. The end points analyzed included early mortality, postoperative stroke, renal dysfunction, prolonged (...) Propensity and impact of autologous platelet rich plasma use in acute type A dissection. Coagulopathy in patients undergoing open repair of acute type A aortic dissection using cardiopulmonary bypass and hypothermic circulatory arrest is a common complication. Autologous platelet rich plasma is an intraoperative blood conservation technique, which has been shown in previous studies to promote hemostasis, leading to a reduction of blood product transfusions during elective aortic surgery

2019 Journal of Thoracic and Cardiovascular Surgery

92. Association Between Hypertension, Platelet Reactivity, and the Risk of Adverse Events After Percutaneous Coronary Intervention (From the ADAPT-DES Study). (Abstract)

Association Between Hypertension, Platelet Reactivity, and the Risk of Adverse Events After Percutaneous Coronary Intervention (From the ADAPT-DES Study). Hypertension is associated with vascular and endothelial dysfunction that may result in a greater propensity for reactive platelets to cause thrombosis. We sought to assess whether the risk of major adverse cardiac events (MACE) after percutaneous coronary intervention (PCI) in patients with on-clopidogrel residual high platelet reactivity

2019 American Journal of Cardiology

93. Vascular PAR4 upregulation, increased platelet aggregation, and coronary lipid deposits induced by long-term dabigatran administration-results from a diabetes animal model. (Abstract)

atherosclerotic and atherothrombotic risk. SUMMARY: Background Besides its role in the coagulation cascade, thrombin contributes to platelet aggregation and to a plethora of non-hemostatic functions. Objectives To assess the impact of long-term thrombin inhibition with dabigatran etexilate (DE) on platelet aggregation and on extrahemostatic thrombin-related functions in diabetic and control rats. Methods Markers of inflammation, endothelial dysfunction, oxidative stress, angiogenesis and cell adhesion (...) Vascular PAR4 upregulation, increased platelet aggregation, and coronary lipid deposits induced by long-term dabigatran administration-results from a diabetes animal model. Essentials The impact of long-term thrombin inhibition outside the coagulation cascade is far from clear. We aimed to assess the impact of dabigatran etexilate (DE) in diabetic and control rats. In diabetic rats, DE increased platelet aggregation and lead to coronary lipid deposits. Long-term thrombin inhibition may increase

2019 Journal of Thrombosis and Haemostasis

94. Human Low-Affinity IgG Receptor FcγRIIA Polymorphism H131R Associates with Subclinical Atherosclerosis and Increased Platelet Activity in Systemic Lupus Erythematosus. Full Text available with Trip Pro

Human Low-Affinity IgG Receptor FcγRIIA Polymorphism H131R Associates with Subclinical Atherosclerosis and Increased Platelet Activity in Systemic Lupus Erythematosus. Essentials Systemic lupus erythematosus (SLE) patients are at increased risk for premature CVD. Platelet activity, vascular dysfunction and carotid artery plaque are associated with FcγRIIA genotype in SLE. FcγRIIA genotype was not associated with platelet activity or carotid plaque in healthy controls. FcγRIIA represents a link (...) that connects platelet activity, vascular health and CVD in SLE. SUMMARY: Background Systemic lupus erythematosus (SLE) is a complex autoimmune disease associated with an elevated risk of premature cardiovascular disease. Platelets express receptors contributing to inflammation and immunity, including FcγRIIA, the low affinity receptor of the Fc portion of IgG antibodies. The variation at a single amino acid substitution, H131R, in the extracellular binding domain alters the affinity for IgG, which may

2019 Journal of Thrombosis and Haemostasis

95. Targeting CD39 Toward Activated Platelets Reduces Systemic Inflammation and Improves Survival in Sepsis: A Preclinical Pilot Study. (Abstract)

Targeting CD39 Toward Activated Platelets Reduces Systemic Inflammation and Improves Survival in Sepsis: A Preclinical Pilot Study. Sepsis is associated with a systemic inflammatory reaction, which can result in a life-endangering organ dysfunction. Pro-inflammatory responses during sepsis are characterized by increased activation of leukocytes and platelets, formation of platelet-neutrophil aggregates, and cytokine production. Sequestration of platelet-neutrophil aggregates (...) in the microvasculature contributes to tissue damage during sepsis. At present no effective therapeutic strategy to ameliorate these events is available. In this preclinical pilot study, a novel anti-inflammatory approach was evaluated, which targets nucleoside triphosphate hydrolase activity toward activated platelets via a recombinant fusion protein combining a single-chain antibody against activated glycoprotein IIb/IIIa and the extracellular domain of CD39 (targ-CD39).Experimental animal study and cell culture

2019 Critical Care Medicine

96. Rationale and Design of the High Platelet Inhibition with Ticagrelor to Improve Left Ventricular Remodeling in Patients with ST-Segment Elevation Myocardial Infarction (HEALING-AMI) Trial. Full Text available with Trip Pro

Rationale and Design of the High Platelet Inhibition with Ticagrelor to Improve Left Ventricular Remodeling in Patients with ST-Segment Elevation Myocardial Infarction (HEALING-AMI) Trial. Impaired recovery from left ventricular (LV) dysfunction is a major prognostic factor after myocardial infarction (MI). Because P2Y₁₂ receptor blockade inhibits myocardial injury, ticagrelor with off-target properties may have myocardial protection over clopidogrel. In animal models, ticagrelor vs (...) (NT-proBNP) at 6 months representing post-MI remodeling processes. Changes of LV end-systolic/diastolic volume indices and LV ejection fraction between baseline and 6-month follow-up will be also evaluated. Analysis is per protocol.HEALING-AMI is testing the effect of ticagrelor in reducing adverse LV remodeling following STEMI. Our trial would show the benefit of ticagrelor vs. clopidogrel related to the recovery of post-MI LV dysfunction beyond potent platelet inhibition.ClinicalTrials.gov

2019 Korean circulation journal Controlled trial quality: uncertain

97. The contribution of oxidative stress to platelet senescence during storage. (Abstract)

The contribution of oxidative stress to platelet senescence during storage. Platelets for transfusion become senescent and dysfunctional during storage, resulting in a markedly short shelf life (5 days). We hypothesized that oxidative stress might account for this decline.Human platelets were treated with or without antioxidants before storage, and samples were collected and analyzed at different time points. Platelet senescence was determined by senescence-associated β-galactosidase assay (...) with antioxidants successfully prevented this increase and also mitigated senescence levels of stored platelets. Finally, resveratrol, a natural antioxidant, was utilized as a novel storage additive to safely extend platelet shelf time. We showed that the addition of resveratrol efficiently postponed platelet senescence and ameliorated platelet storage lesion.Platelets during storage became senescent and dysfunctional over time, and we found that oxidative stress might account for this decline. The addition

2019 Transfusion

98. Increased concentrations of platelet- and endothelial-derived microparticles in patients with myocardial infarction and reduced renal function- a descriptive study. Full Text available with Trip Pro

Increased concentrations of platelet- and endothelial-derived microparticles in patients with myocardial infarction and reduced renal function- a descriptive study. Patients with chronic kidney disease (CKD) have a high risk of recurring thrombotic events following acute myocardial infarction (AMI). Microparticles (MPs) are circulating small vesicles shed from various cells. Platelet microparticles (PMPs) reflect platelet activation and endothelial microparticles (EMPs) reflect endothelial (...) activation or dysfunction. Both increase following AMI, and may mediate important biological effects. We hypothesized that AMI patients with CKD have further elevated PMPs and EMPs compared with non-CKD patients, despite concurrent antithrombotic treatment.We performed a descriptive study of patients with AMI. Fasting blood samples were acquired from 47 patients on dual antiplatelet treatment. Patients were stratified by renal function: normal (H; n = 19) mean eGFR 88; moderate CKD (CKD3; n = 15) mean

2019 BMC Nephrology

99. Medical therapies to reduce chronic kidney disease progression and cardiovascular risk: anti-platelet therapy

Medical therapies to reduce chronic kidney disease progression and cardiovascular risk: anti-platelet therapy ____________________________________________________________________________________________________________ Early Chronic Kidney Disease July 2012 Page 1 of 9 Medical therapies to reduce chronic kidney disease progression and cardiovascular risk: anti- platelet therapy Date written: July 2012 Author: Richard Phoon, David Johnson GUIDELINES a. We suggest that aspirin therapy should (...) disease were combined with MeSH terms and text words for aspirin, clopidogrel and anti-platelet therapy. The search was carried out in Medline (1994 – October 2009) and the Cochrane library. No language restrictions were placed on the search. The conference proceedings of the American Society of Nephrology from 1994 - 2008 were also searched for trials. A search update was conducted in Medline (2009 – May 2012) using the same MeSH terms and text words. Date of search/es: November 2009 and May 2012

2013 KHA-CARI Guidelines

100. Antiplatelet (aspirin) therapy as a new option in the treatment of vasculogenic erectile dysfunction: a prospective randomized double-blind placebo-controlled study. (Abstract)

Antiplatelet (aspirin) therapy as a new option in the treatment of vasculogenic erectile dysfunction: a prospective randomized double-blind placebo-controlled study. To investigate the efficiency of antiplatelet (aspirin) therapy in vasculogenic erectile dysfunction (VED) patients with a high mean platelet volume.A total of 184 patients diagnosed with VED between the ages of 18 and 76 were randomly divided into two groups and treated for 6 weeks [group 1: 120 patients (mean age 48.3), aspirin

2018 International urology and nephrology Controlled trial quality: uncertain

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