Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
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↗
PubMed1982

A study on the in vivo production of thrombosis in rat mesenteric arterioles and action of prostaglandin (PG) I2 on the thrombosis.

We have investigated reproducible and quantitative thrombus formation in rat mesenteric arterioles using electrical stimulation under an inverted microscope. In vivo thrombi were formed in arterioles of 30-40 micrometers diameter by electrical stimulation using a tungsten electrode with a tip of 5 micrometers diameter. A "threshold" response was defined as one in which platelets adhered to the injured site of vascular wall and formed a white body which flowed away intermittently. The thrombus formations were classified into three stages: stage I, thrombi covering up less than 20% of the vessel lumen; stage II, when 20% to 40% of the lumen was covered; or state III, when more than 40% was covered. This preparation was demonstrated to be valuable for testing the potency of anti-thrombotic drugs if we performed the experiment within 2 hr after removing the mesentery from the peritoneal cavity which exposed it to air. PGl2, t a dose of 0.5 micrograms/100 g intravenously administered, inhibited the growth of the thrombus at stage II and III. PGE1, PGD2 and PGE2 had no effect at the same dose on these stages. The threshold response was significantly suppressed by both PGI2 and PGE1 at doses of 5 micrograms/100 g.

Alprostadil↗