Seminars in thrombosis and hemostasis
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Semin. Thromb. Hemost. · Jan 1997
Randomized Controlled Trial Clinical TrialDosage, anticoagulant, and antithrombotic effects of heparin and low-molecular-weight heparin in the treatment of deep vein thrombosis.
We have performed a prospective, randomized, controlled trial comparing continuous intravenous unfractionated heparin with twice-daily subcutaneous (s.c.) high-dose low-molecular-weight (LMW) heparin in the initial treatment of 50 patients with acute proximal deep vein thrombosis. In this article we analyze the relationship between the dosage of the heparins, the anticoagulant effects on aPTT, and thrombin and factor Xa inhibition to the improvement of the Marder score after a 10-day treatment period. Improvement of the Marder score was observed in about 70% of patients without regard to administration of unfractionated or LMW heparin. ⋯ In contrast to the chromogenic anti-Xa assay, aPTT, thrombin clotting time, and prothrombin time values differed substantially in the two treatment regimens. Treatment of recent deep vein thrombosis with unfractionated heparin profits from laboratory monitoring, whereas monitoring of the anticoagulant effect during the treatment with s.c. LMW heparin does not influence the outcome on thrombus regression.
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In this article, three cases, with antithrombin (AT) abnormality "Toyama" (type IIb), AT abnormality "Aomori" (type IIa), and congenital AT deficiency (type I) with pregnancy and delivery managed with administration of both AT concentrates and low-molecular-weight heparin, are described. Additionally, a case of AT-producing hepatocellular carcinoma, the first case in the world literature, is reported. Following these clinical reports, the development of AT studies on heparin cofactor II, characteristics of the vessel wall related to coagulation-fibrinolysis, and the development of the treatment of thrombosis with low-molecular-weight heparin and herbal drugs are discussed.
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Semin. Thromb. Hemost. · Jan 1997
ReviewMonitoring and management of anticoagulation in children requiring extracorporeal circulation.
Pharmacologic manipulation of hemostasis is a prerequisite for cardiac surgery with cardiopulmonary bypass (CPB) to prevent clot formation in the extracorporeal circuit. Children who require surgical correction of congenital heart defects are at increased risk for prolonged and excessive bleeding after separation from CPB. Heparin remains the anticoagulant of choice for surgery requiring CPB. ⋯ This manuscript reviews the pitfalls in the management of anticoagulation for children undergoing surgery that requires CPB. Pertinent literature related to the use of aprotinin, a serine protease inhibitor that has been shown to improve hemostasis during and after CPB, is discussed. It is hoped that this article will provide a practical guideline for the rational management of anticoagulation in children with congenital heart disease undergoing CPB surgery.
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Semin. Thromb. Hemost. · Jan 1997
Practice Guideline GuidelineProposal for revised diagnostic criteria of essential thrombocythemia and polycythemia vera by the Thrombocythemia Vera Study Group.
The present study revises the criteria of the Polycythemia Vera Group (PVSG) for the diagnoses of essential thrombocythemia (ET) and polycythemia vera (PV) in view of accumulating data on in vitro cultures of hematopoietic progenitors and by adding histopathology from bone marrow biopsies. The majority of ET patients show spontaneous megakaryocyte or erythroid growth or both, but in about 35% the growth pattern is normal. So far none of the patients with reactive thrombocytosis have shown either spontaneous megakaryocyte or erythroid colony growth. ⋯ In reactive thrombocytosis and secondary erythrocytosis the size and morphology of megakaryocytes remain normal and there is no tendency of the megakaryocytes to cluster. Both spontaneous EEC and histopathology of bone marrow biopsies appear to offer specific clues to the diagnosis of overt and latent ET or PV and have the potential to differentiate ET from reactive thrombocytosis and PV from secondary erythrocytosis. Moreover, bone marrow histopathology has the diagnostic power to distinguish and to stage the various MPDs without regard to clinical and laboratory data.
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Semin. Thromb. Hemost. · Jan 1997
Acquired antithrombin deficiency following severe traumatic injury: rationale for study of antithrombin supplementation.
Hemorrhage, head injury, and multiple organ dysfunction are the most frequent causes of mortality in patients who experience severe injury. Acceleration of the coagulation cascade is known to result in hemorrhage secondary to disseminated intravascular coagulation (DIC) and end-organ dysfunction, as manifest by pulmonary and renal failure. Few studies have been conducted to evaluate the effects of injury on the endogenous anticoagulants that inhibit excessive coagulation activation. ⋯ However, patients with adverse outcomes [DIC and adult respiratory distress syndrome (ARDS)] had significant reductions in AT and protein C activities. Decreased levels of AT and protein C 8 hours after admission served as independent predictors of both DIC and ARDS. Prospective, randomized studies should be conducted to evaluate the effect of supplementation of these factors after severe injury has occurred.