Thrombosis research
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Inflammation contributions to the thrombotic response involve both cellular and humoral modulation. Inflammation impacts the initiation, propagation and the inhibitory phases of blood coagulation. Inflammatory mediators like endotoxin and tumor necrosis factor alpha (TNF alpha) elicit the expression of tissue factor on blood cells. ⋯ The procoagulant impact of inflammation can also be seen at the cellular level. Inflammatory mediators like interleukin 6 can increase both platelet count and their responsiveness to agonists like thrombin. All of these events tend to shift the hemostatic balance in favor of clot formation.
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Thrombosis research · Jan 2004
Comparative StudyLow-dose oral vitamin K is safe and effective for outpatient management of patients with an INR>10.
Low-dose oral vitamin K effectively returns an international normalized ratio (INR) between 4.5 and 10.0 to an INR of 2.0-3.0 within 24 h in about 70% of patients. However, the efficacy of oral vitamin K for the treatment of higher INR values has only been studied in one small randomized trial. Treatment of markedly prolonged INR values with low-dose oral vitamin K is attractive because it has the potential to greatly simplify the management of such patients. ⋯ Low-dose (2 mg) oral vitamin K, coupled with temporary warfarin discontinuation, appears to be a safe and effective treatment for severe warfarin associated coagulopathy in non-bleeding patients.
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Thrombosis research · Jan 2004
Evaluation of a novel kallikrein inhibitor on hemostatic activation in vitro.
DX-88 is a potent kallikrein inhibitor that is being studied for the treatment of hereditary angioedema (HAE) and represents a potential alternative to aprotinin in cardiac surgical patients. The current study was designed to evaluate in vitro effects of DX-88 on coagulation in comparison with aprotinin. ⋯ We found that DX-88 delayed contact activator induced coagulation without affecting tissue factor mediated coagulation. For evaluation of coagulation during DX-88 therapy, the use of PT or tissue factor-activated TEG may be preferable.
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Thrombosis research · Jan 2004
Comparison between CoaguChek S- and Owren-type prothrombin time assay for monitoring anticoagulant therapy.
Anticoagulation therapy with warfarin is monitored by the prothrombin time (PT) assay. The PT is standardized using international normalized ratios (INRs). By keeping the INR within specific values, it is possible to reduce potential complications from the treatment. To facilitate the PT monitoring, point-of-care devices suitable for capillary whole blood measurements have been developed. The aims of this study were to compare the INR values obtained by such a device, CoaguChek S, with those obtained from the Owren-type PT assay and to evaluate the differences seen. ⋯ INR analysis of whole blood with CoaguChek S is comparable with INR measured in plasma with Owren chemistry. The activities of factor V and fibrinogen contribute to the deviation seen between the methods. Differences in sensitivity to antiphospholipid antibodies could not be demonstrated.
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Thrombosis research · Jan 2004
The state of platelets preserved in extracorporeal circulation with a glycoprotein IIb/IIIa inhibitor.
Temporary inhibition of platelet function during extracorporeal circulation (platelet anesthesia) can preserve platelet count. We hypothesized that platelet anesthesia with a glycoprotein IIb/IIIa inhibitor could preserve activated platelets. ⋯ In the FK633 group, platelet counts were preserved and beta-thromboglobulin levels remained unchanged, whereas in group C, platelet counts decreased significantly and beta-thromboglobulin increased significantly from 30 and 60 min, respectively. FK633 inhibited platelet aggregation and fibrinogen binding to platelets throughout recirculation. A significant difference between groups with respect to microparticle parameters and thrombin-antithrombin complex levels was evident by 120 min. P-selectin expression increased at 0 min in both groups, and was preserved significantly at 5 min and reduced at 120 min in group F. Platelet counts were preserved by platelet anesthesia during recirculation without platelet activation. These results suggest that FK633 inhibits the amplification loop by reducing the binding of fibrinogen to glycoprotein IIb/IIIa and platelet aggregation.