Thrombosis research
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Thrombosis research · Jan 2004
Reduced sensitivity of platelets from type 2 diabetic patients to acetylsalicylic acid (aspirin)-its relation to metabolic control.
Aspirin (acetylsalicylic acid, ASA), which is recommended for primary and secondary prevention in diabetes mellitus (DM), has been shown to have a lower antiplatelet activity in diabetic patients. We conducted a crossover designed observational study to evaluate whether there is an association between the parameters relevant to metabolic control of diabetes and platelet sensitivity to aspirin in type 2 diabetic patients. Platelets' ability to adhere and aggregate was monitored with the use of platelet function analyser (PFA-100 collagen/epinephrine closure time, CT(CEPI) or collagen/ADP closure time, CT(CADP)), classical turbidimetric aggregometry and whole blood electrical aggregometry (WBEA), using collagen (WBEA(coll)), ADP (WBEA(ADP)) and arachidonic acid (WBEA(AA)) as platelet agonists, in 48 control healthy volunteers (mean age+/-S. ⋯ Overall, there is evidence that reduced platelets response to aspirin may occur more often in diabetic patients. Poor metabolic control may play a role in the reduced platelet sensitivity to aspirin in DM patients. Thus, our findings strongly support the requirements for an excellent near-normal metabolic control and may suggest a need for alternative ASA dosing schedules in DM patients.
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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.
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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
Comparative Study Clinical TrialQuality assurance program for whole blood prothrombin time-international normalized ratio point-of-care monitors used for patient self-testing to control oral anticoagulation.
Whole blood coagulation monitors are increasingly used for patient self-testing to control oral anticoagulation, but there are no comprehensive quality assurance (QA) programs to check their performance. We report on the experience with one of such programs applied in a field study where patients on prothrombin time (PT)-international normalized ratio (INR) self-testing were asked to bring their monitors to the anticoagulation clinic for checking. PT-INR testing was performed three times over 3 months with 14 patient's monitors and test strips on three recalcified QA plasmas by an experienced laboratory operator. ⋯ Monitors should be recalled periodically to the clinic where they have been prescribed to the patient. During each visit, the clinic may check the monitors and patient self-testing performance as described. Such comprehensive QA system would make monitoring of oral anticoagulant treatment by self-testing safer and more effective.