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At least 127 records · Page 7Linked to original sources
PubMed1999

Nonfractionated heparin fails to inhibit arterial thrombosis in a human ex vivo thrombosis model.

The effect of nonfractionated heparin on the formation and composition of arterial thrombus is unclear. The purpose of this study in a human ex vivo model was to analyze fibrinoplatelet thrombi and test the inhibitory effect of nonfractionated heparin on arterial thrombus formation. Experiments were carried out in Sakariassen perfusion chambers. Strips coated with either tissue factor (TF) or collagen were exposed to human blood collected from healthy volunteers at an arterial shear stress rate of 2600 s-1 for 1 to 4 min. Platelet deposition was determined using immunoenzymatic techniques to quantify P-selectine, a platelet membrane receptor, in thrombi. Fibrin deposition was determined by quantifying fibrin degradation products released after application of plasmin (D-dimers). Heparin was injected into the blood flow through a blender port system located between the venous puncture site and perfusion chamber. The results of the study showed that in a human ex vivo model, formation of arterial thrombus on two thrombogenic surfaces (tissue factor and collagen) is not inhibited by nonfractionated heparin.

Anticoagulants↗
PubMed2003

Thrombosis in children with acute lymphoblastic leukemia. Part II. Pathogenesis of thrombosis in children with acute lymphoblastic leukemia: effects of the disease and therapy.

At diagnosis, there is evidence of increased thrombin generation in children with acute lymphoblastic leukemia (ALL), the etiology of which is unclear. However, thromboembolism (TE) in children with ALL is most commonly reported after the initiation of antileukemic therapy indicating a possible interaction of the disease and therapy. Antileukemic therapy influences the haemostatic system either by direct effect of the chemotherapeutic agents or indirectly through the effect of supportive care, e.g. central venous line (CVL) or infectious complications secondary to immunosuppression. Asparaginase and steroids are shown to induce hypercoagulable state by suppression of natural anticoagulants, especially AT and plasminogen, and by elevations in F VIII/vWF complex, respectively. In addition, steroid therapy causes hypofibrinolytic state by dose-dependent increase in plasminogen activator inhibitor 1 (PAI-1) levels. Combination of these effects coupled with increased thrombin generation may be responsible for the increased incidence of TE observed with concomitant administration of asparaginase and steroids. Further studies to delineate the mechanism of increased thrombin in generation children with ALL and effects of various chemotherapeutic agents, in isolation and in combination, on haemostatic system are needed.

Adolescent↗
PubMed2003

Thrombosis in children with acute lymphoblastic leukemia: part I. Epidemiology of thrombosis in children with acute lymphoblastic leukemia.

Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy. With the advent of aggressive multimodality therapy, ALL has become a curable disease for majority of pediatric patients. Thromboembolism (TE) is a well-recognized serious complication in association with ALL leading to significant morbidity. It can be potentially fatal in over 50% of the affected patients. Development of TE does interfere with the scheduled treatment plan for ALL and, thus, ultimate outcome from ALL. Recent evidence indicates that concomitant administration of asparaginase and steroids is likely to be associated with higher incidence of TE, especially in children with at least one prothrombotic risk factor. In addition, older children and patients with high risk ALL may be at higher risk for developing TE. However, the epidemiology and the exact pathogenesis of this entity have not yet been clearly defined. To reduce the incidence of TE and its impact on overall outcome as well as on the quality of life in children undergoing treatment for ALL, further studies to define the epidemiology of TE in relation to the biology of ALL and chemotherapy protocols are urgently needed. The purpose of this review is to evaluate the current knowledge of TE in association with ALL in children, especially in relation with the treatment protocols and genetic background. This review will be published in three parts. The first part will review the available information regarding epidemiology of TE in children with ALL.

Child↗