Seminars in thrombosis and hemostasis
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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.
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Semin. Thromb. Hemost. · Jan 1996
ReviewManagement of acquired coagulation disorders in emergency and intensive-care medicine.
Coagulation disorders usually confront the emergency physician as bleeding episodes or as abnormalities of laboratory tests. Bleeding has to be treated aggressively, while pathological coagulation tests should be related to a more differentiated diagnosis at first. The most common causes of acquired coagulation disorders are liver disease, vitamin K deficiency, and disseminated intravascular coagulation (DIC). ⋯ Antithrombin III substitution cannot be assumed as established therapy so far. Inhibitors can lead to bleeding, but the most common inhibitor, lupus anticoagulant, rather predisposes to thrombosis. In bleeding patients with inhibitors against single clotting factors, treatment consists of adequate substitution before initiating the diagnostic workup.
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Semin. Thromb. Hemost. · Jan 1996
ReviewCurrent trends in antithrombotic drug and device development.
During the past decade, many significant developments in the clinical management of thrombotic and vascular disorders have occurred. In particular, several newer approaches for the prophylactic and therapeutic management of such disorders as venous thrombosis, acute myocardial infarction, and stroke have been introduced. This has been possible because of the understanding of the molecular mechanisms involved in the thrombogenic process, which plays a key role in the pathophysiology of thrombotic and vascular disorders. ⋯ Thus, an optimal antithrombotic drug approach will include the targeting of all possible sites involved in thrombogenesis. Antithrombotic and anticoagulant drugs will also be useful in the development of such biomedical devices as stents and other vascular support material. Polytherapeutic approaches utilizing combinations of drugs may turn out to be the most effective in the management of thrombotic disorders.
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Semin. Thromb. Hemost. · Jan 1996
Thrombin receptor-related hemostatic defect after cardiopulmonary bypass.
Platelet abnormalities have been blamed for the hemostatic defect that develops after cardiopulmonary bypass (CPB), but investigators have not been able to agree upon an intrinsic platelet abnormality responsible for the observed defect. To better define the blood components responsible for this post-operative hemostatic defect, we compared platelet function in whole blood (WB) to that in platelet-rich plasma (PRP) in 33 patients undergoing coronary artery bypass grafting. We measured platelet aggregation in response to various platelet agonists, including thrombin and TRAP-6 (a 6-amino acid peptide that activates the thrombin "tethered ligand" receptor site). ⋯ In contrast, no corresponding defect in platelet aggregation could be identified in PRP obtained from patients after CPB. These results show that, in post-operative blood samples, blood components present in WB and not in PRP (eg, red blood cells, activated white cells or platelets bound to white cells) diminish the ability of TRAP peptides to activate the thrombin receptor but do not decrease the ability of gamma-thrombin to induce platelet aggregation. This suggests that for circulating platelets after CPB: (1) interactions of platelets with other blood cell elements are the cause of altered postoperative platelet reactivity rather than any intrinsic CPB-induced platelet defect, (2) drugs, such as aprotinin, that limit activation of white cells and the fibrinolytic system may also have beneficial effects on platelet function after CPB, and (3) alternate mechanisms exist that allow thrombin, but not TRAP-6, to activate platelets normally after CPB (perhaps a second, as yet undefined, thrombin receptor).