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Primary Hemostasis (primary + hemostasi)
Selected AbstractsMANAGEMENT OF ANTIPLATELET THERAPY FOR ENDOSCOPIC PROCEDURES: OPTIMAL CESSATION PERIOD OF ANTIPLATELET THERAPY FOR JAPANESEDIGESTIVE ENDOSCOPY, Issue 4 2007Yoshiko Tamai Although antiplatelet agents are widely used for the treatment and prevention of thrombotic diseases, only a few studies have reported the validity of the cessation period prior to endoscopic procedures. In 2002, the American Society for Gastrointestinal Endoscopy (ASGE) published a reference on the management of anticoagulation and antiplatelet therapy for endoscopic procedures, but it should be confirmed as appropriate for use in Asian patients. To evaluate the optimal cessation period of antiplatelet agents prior to endoscopic procedures for Japanese, we have studied: (i) the current clinically adopted cessation period of antiplatelet agents prior to invasive endoscopic procedures in Japan; (ii) the relationship between the cessation period of antiplatelet agents and complications around the invasive endoscopic procedures; (iii) colonic mucosal bleeding time after aspirin ingestion; and (iv) the time course of primary hemostasis after cessation of antiplatelet agents. We conclude that 3 days cessation period for aspirin, 5 days cessation for ticlopidine and 7 days cessation for aspirin + ticlopidine administration should be sufficient for Japanese. [source] The effects of vasoactive agents, platelet agonists and anticoagulation on thrombelastographyACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2007J. Kawasaki Background:, Platelet activation is a critical step in primary hemostasis and clot formation. We tested a hypothesis that platelet stimulating effects of vasoactive agents or platelet agonists could be shown using thrombelastography (TEGŪ) as faster onset or increased clot strength. We further examined if TEGŪ could be modified to evaluate activated platelets as a reversal of anticoagulation in the presence of partial thrombin inhibition. Methods:, Blood samples were obtained from 126 non-cardiac surgical patients. Effects of vasoactive agents on TEGŪ and aggregometry were examined using epinephrine, norepinephrine, vasopressin, desmopressin acetate, milrinone and olprinone (Experiment I). Platelet agonists (epinephrine, ADP and collagen) were separately tested on TEGŪ (Experiment II). Effects of platelet agonists (ADP and collagen) on TEGŪ under anticoagulation in the absence or presence of abciximab were studied (Experiment III). We also tested antiplatelet effects of milrinone and olprinone in the presence of anticoagulants on TEGŪ (Experiment IV). Results:, Neither vasoactive agents nor platelet agonists affected TEGŪ or aggregometry results except for milrinone and olprinone on aggregometry (Experiment I, II). Platelet agonists facilitated clotting in the presence of anticoagulants (Experiment III). Abciximab-treated platelets still exhibited procoagulant effects in the presence of heparin, while not in the presence of argatroban (Experiment III). Platelet inhibition on the modified TEGŪ was more extensive with milrinone than olprinone, and it was dose dependent (Experiment IV). Conclusion:, Modified TEGŪ using heparin or argatroban might delineate the procoagulant effects of platelets by adding platelet specific agonist. [source] Qualitative disorders of platelets and megakaryocytesJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2005A. T. NURDEN Summary., Qualitative disorders of platelet function and production form a large group of rare diseases which cover a multitude of genetic defects that by and large have as a common symptom, excessive mucocutaneous bleeding. Glanzmann thrombasthenia, is enabling us to learn much about the pathophysiology of integrins and of how ,IIb,3 functions. Bernard,Soulier syndrome, an example of macrothrombocytopenia, combines the production of large platelets with a deficit or non-functioning of the major adhesion receptor of platelets, the GPIb-IX-V complex. Amino acid substitutions in GPIb,, may lead to up-regulation and spontaneous binding of von Willebrand factor as in Platelet-type von Willebrand disease. In disorders with defects in the MYH9 gene, macrothrombocytopenias are linked to modifications in kidney, eye or ear, whereas other inherited thrombocytopenias variously link a low platelet count with a propensity to leukemia, skeletal defects, learning impairment, and abnormal red cells. Defects of secretion from platelets include an abnormal , -granule formation as in the gray platelet syndrome (with marrow myelofibrosis), and of organelle biogenesis in the Hermansky,Pudlak and Chediak,Higashi syndromes where platelet dense body defects are linked to abnormalities of other lysosomal-like organelles including melanosomes. Finally, defects involving surface receptors (P2Y12, TP,) for activating stimuli, of proteins essential for signaling pathways (including Wiskott,Aldrich syndrome), and of platelet-derived procoagulant activity (Scott syndrome) show how studies on platelet disorders are helping unravel the pathways of primary hemostasis. [source] Hemostasis and irreducible complexityJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2003W. C. Aird Summary., Coagulation evolved as a means to stem the loss of blood and to defend against pathogens. The complexity of the clotting cascade has been cited as evidence for the existence of divine intervention. The objective of this review is to draw on the debate between creationists and evolutionary biologists to highlight important evolutionary principles that underlie the hemostatic mechanism. I propose the following: (a) as with all biological systems, the hemostatic mechanism displays non-linear complexity; (b) the cellular response represents primary hemostasis owing to its place in the evolutionary time scale and functional importance; and (c) the rapid evolution of the hemostatic mechanism in vertebrates is testimony to the power and versatility of gene duplications and exon shuffling. [source] | ||||||||||