Thrombosis research
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Thrombosis research · Jan 2003
Comparative Study Clinical Trial Controlled Clinical TrialImbalances between the levels of tissue factor and tissue factor pathway inhibitor in ARDS patients.
To evaluate the pathogenetic role of tissue factor (TF), tissue factor pathway inhibitor (TFPI), and neutrophil elastase in acute respiratory distress syndrome (ARDS), as well as to test the hypothesis that TFPI levels modified by neutrophil activation are not sufficient to prevent TF-dependent intravascular coagulation, leading to sustained systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), which determine the prognosis of these patients. ⋯ Systemic activation of the TF-dependent pathway not adequately balanced by TFPI is one of the aggravating factors of ARDS. High levels of neutrophil elastase released from activated neutrophils may explain the imbalance of TF and TFPI. Persistent DIC and sustained SIRS contribute to MODS, determining the prognosis of ARDS patients.
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Thrombosis research · Jan 2003
ReviewPrevalence and prevention of venous thromboembolism in patients with acute exacerbations of COPD.
Little information exists on the prevalence and prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients admitted for acute exacerbations of chronic obstructive pulmonary disease (COPD). ⋯ Despite a substantial lack of consistent data, VTE appears as a major threat to patients admitted for acute exacerbation of COPD, and pharmacologic prophylaxis should be considered in all high risk situations. However, methodologically rigorous studies in this setting are still needed.
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Thrombosis research · Jan 2003
Comparative StudyDextran sulfate included in factor Xa assay reagent overestimates heparin activity in patients after heparin reversal by protamine.
A lack of correlation between activated partial thromboplastin time (aPTT), thrombin time (TT) and anti-factor Xa (AXa) activity was observed in patients after cardiac surgery with cardiopulmonary bypass (CBP). Indeed, AXa activity measured by the chromogenic assay, Coamatic Heparin, was higher than expected with regard to results obtained in coagulation assays. To account for this discrepancy, another AXa chromogenic assay was tested. ⋯ We therefore performed in vitro studies consisting in neutralizing unfractionated heparin (UFH) with protamine and measuring AXa activity with the two chromogenic assays. An AXa activity was still measurable with Coamatic Heparin after neutralization, thus strongly suggesting that dextran sulfate dissociates protamine/heparin complexes. We conclude that Coamatic Heparin assays should be avoided when measuring AXa activity in plasma samples immediately after protamine infusion, as inaccurate results may lead to inadequate management of heparin reversal.
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Thrombosis research · Jan 2003
Does the anti-beta2-glycoprotein I antibody provide additional information in patients with thrombosis?
To investigate whether the anti-beta(2)-glycoprotein I (anti-beta(2)GPI) antibody may provide additional information in patients with thrombosis in conjunction with the lupus anticoagulant (LAC) or anticardiolipin (aCL) antibody. ⋯ Single positivity for anti-beta(2)GPI explained 9.2% of thrombotic events in the absence of LAC or aCL. Double or triple positivity for aPLs were associated with a higher rate of thrombosis than single positivity for aPL. Our results suggest that anti-beta(2)GPI provides additional information in patients with thrombosis in conjunction with LAC or aCL.