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Sökning: WFRF:(Greinacher A)

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31.
  • Greinacher, A., et al. (författare)
  • Predonation finger lancet punctures : a potential risk factor for interdonor pathogen transmission in the blood donor clinic
  • 2016
  • Ingår i: Vox Sanguinis. - : Wiley. - 0042-9007 .- 1423-0410. ; 111:1, s. 3-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Objectives: Point-of-care testing using capillary blood from a finger prick is widely used for predonation haemoglobin testing of blood donors. It is common practice to cover the finger prick with a cotton swab and to instruct the donor to press for few minutes. The finger prick can cause blood contamination of surfaces in contact with the lanced finger, especially door handles, risking infectious disease transmission, particularly if another person touching the contaminated door handle also has a punctured fingertip.Materials and Methods: First, we investigated contamination by blood (benzidine assay) of the door handles of our blood donor clinic, taking 175 samples 3 h after opening of the donation centre (baseline). We then introduced band-aids to cover the finger prick and started an information campaign using educational flyers to sensitize blood donors and staff to this problem (period-1). Thereafter, the staff was instructed to use the non-dominant hand for blood sampling and mandated to replace any discarded band-aids immediately (period-2).Results: At baseline, 82% of the nurse room door handles showed contamination with blood. This decreased somewhat (10-40%) after period-1, but only after immediate mandatory band-aid replacement on any donor finger without a band-aid (period-2), no further blood contaminations were detected.Conclusion: Blood contamination of shared surfaces can occur after finger prick for capillary blood sampling. Application of a band-aid and use of the non-dominant hand for fingertip incision are easy to apply and effective in reducing this iatrogenic health hazard.
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32.
  • Greinacher, A, et al. (författare)
  • Recombinant hirudin in clinical practice : focus on lepirudin.
  • 2001
  • Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 103:10, s. 1479-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical applications for recombinant hirudins have been investigated for the past 10 years. The first indication for which a hirudin-lepirudin-has been approved is treatment of heparin-induced thrombocytopenia (HIT). Also, the recently completed trials for use of lepirudin in unstable angina indicate a potentially new indication. This review describes pharmacology and clinical applications of lepirudin with an emphasis on HIT and unstable angina. An overview of usage of lepirudin in acute coronary syndromes is given, as well as a summary of rare indications for lepirudin, such as extracorporeal circulation, for which comprehensive data are lacking.
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33.
  • Hernandez, Victor Agmo, et al. (författare)
  • The adhesion and spreading of thrombocyte vesicles on electrode surfaces
  • 2008
  • Ingår i: Bioelectrochemistry. - : Elsevier BV. - 1567-5394 .- 1878-562X. ; 74, s. 210-216
  • Tidskriftsartikel (refereegranskat)abstract
    • The interaction of thrombocyte vesicles with the surface of metal electrodes, i.e., mercury, gold and gold electrodes modified with self assembled monolayers (SAM), was studied with the help of chronoamperometry, atomic force microscopy, and quartz crystal microbalance measurements. The experimental results show that the interaction of the thrombocyte vesicles with the surface of the electrodes depends on the hydrophobicity of the latter: whereas on very hydrophobic surfaces (mercury and gold functionalized with SAM) the thrombocyte vesicles disintegrate and form a monolayer of lipids. on the less hydrophobic gold surface a bilayer is formed. The chronoamperometric measurements indicate the possibility of future applications to probe membrane properties of thrombocytes. (C) 2008 Elsevier B.V. All rights reserved.
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34.
  • Kjeldsen-Kragh, Jens, et al. (författare)
  • Fetal/neonatal alloimmune thrombocytopenia : A systematic review of impact of HLA-DRB3∗01:01 on fetal/neonatal outcome
  • 2020
  • Ingår i: Blood Advances. - : American Society of Hematology. - 2473-9529 .- 2473-9537. ; 4:14, s. 3368-3377
  • Forskningsöversikt (refereegranskat)abstract
    • The most common, severe cases of fetal and neonatal alloimmune thrombocytopenia among whites are caused by antibodies against human platelet antigen 1a (HPA-1a). The aims of this systematic review and meta-analysis are to determine the association between maternal HLA-DRB3∗01:01 and: (1) HPA-1a-alloimmunization and (2) neonatal outcome in children born of HPA-1a-immunized women. A systematic literature search identified 4 prospective and 8 retrospective studies. Data were combined across studies to estimate pooled odds ratios (ORs) and the associated 95% confidence intervals (CIs). The population represented by the prospective studies was more than 150 000. In the prospective studies, there were 64 severely thrombocytopenic newborns (platelet count < 50 × 109/L) of whom 3 had intracranial hemorrhage. The mothers of all 64 children were HLA-DRB3∗01:01+. The number of severely thrombocytopenic children born of HPA-1a-alloimmunized women in the retrospective studies was 214; 205 of whom were born of HLA-DRB3∗01:01+ women. For HLA-DRB3∗01:01- women, the OR (95% CI) for alloimmunization was 0.05 (0.00-0.60), and for severe neonatal thrombocytopenia 0.08 (0.02-0.37). This meta-analysis demonstrates that the risk of alloimmunization and of having a child with severe thrombocytopenia are both very low for HPA-1a- women who are HLA-DRB3∗01:01-.
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35.
  • Lubenow, Norbert, et al. (författare)
  • Drugs for the prevention and treatment of thrombosis in patients with heparin-induced thrombocytopenia.
  • 2001
  • Ingår i: American Journal of Cardiovascular Drugs. - 1175-3277 .- 1179-187X. ; 1:6, s. 429-43
  • Tidskriftsartikel (refereegranskat)abstract
    • Most patients with heparin-induced thrombocytopenia (HIT), a serious adverse effect of heparin mediated by platelet-activating heparin-dependent antibodies, require alternative anticoagulation. This is because HIT is highly prothrombotic and is characterized by markedly increased thrombin generation. Unfractionated heparins seem to induce HIT more often than low molecular weight heparins. There are three anticoagulants for which there is an emerging consensus for their efficacy in management of HIT, and which are currently approved for treatment of HIT in several countries: the recombinant hirudin, lepirudin, a direct thrombin inhibitor; the synthetic direct thrombin inhibitor, argatroban; and the heparinoid, danaparoid sodium, mainly exhibiting antifactor-Xa activity. Recommendations for optimal use of these drugs in HIT are given in this review stressing the need for immediate treatment of patients with HIT without awaiting laboratory diagnosis. Hirudin, the drug for which most data from prospective trials exists, can be safely and effectively used in patients with HIT, its dramatically increased elimination half-life in patients with renal failure being the most important drawback. Argatroban, which is mainly eliminated by the liver, could be used preferentially in such patients with renal impairment. Interference with the international normalized ratio makes oral anticoagulation, which is necessary in many patients with HIT, problematic. Activated partial thromboplastin time is sufficient to monitor lepirudin and argatroban treatment in most cases. Danaparoid sodium, with an antifactor-X activity half-life of about 24 hours seems to be best suited for thrombosis prophylaxis in patients with HIT. In some patients monitoring by determining antifactor-Xa activity is necessary. No antidote is available for any of the drugs discussed, and bleeding complications are the most important adverse effects. In situations such as hemodialysis or cardiopulmonary bypass, not only the characteristics of the drug in use itself, but also availability of monitoring methods play an important role. Adjunctive treatments have not been systematically evaluated and should be used cautiously. Recent data suggest that re-exposure of patients with a history of HIT with heparin, for example during cardiopulmonary bypass, can be well tolerated provided no circulating HIT antibodies are detectable at the time of re-exposure, and heparin is strictly avoided pre- and postoperatively.
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36.
  • Lubenow, Norbert, et al. (författare)
  • Heparin-induced thrombocytopenia : recommendations for optimal use of recombinant hirudin.
  • 2000
  • Ingår i: BioDrugs. - 1173-8804 .- 1179-190X. ; 14:2, s. 109-25
  • Tidskriftsartikel (refereegranskat)abstract
    • Recombinant hirudins have a definite role in the treatment of patients with heparin-induced thrombocytopenia (HIT). The most important adverse effects are haemorrhages and the induction of antihirudin antibodies. Major haemorrhages were not significantly increased in patients with HIT compared with a historical control group, but prospective data comparing hirudin and heparinoids such as danaparoid are lacking. The definition of the optimal method for monitoring and the availability of an antidote for hirudin would probably increase safety with this drug. To date, haemofiltration using high-flux filter systems is the only way to remove an overdosage of hirudin from the circulation. In patients with renal impairment requiring hirudin treatment, it therefore seems safer to start with a low dose that is subsequently adjusted according to the activated partial prothromboplastin time or ecarin clotting time. Even in special circumstances, such as cardiopulmonary bypass or dialysis, hirudins can be applied successfully if care is taken to monitor their effects meticulously. There are many other indications in which hirudins have shown feasibility (e.g. acute coronary syndromes) but available data preclude definite conclusions.
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37.
  • Lubenow, Norbert, et al. (författare)
  • [Hirudins in the treatment of heparin-induced thrombocytopenia and in thrombosis prophylaxis].
  • 2002
  • Ingår i: Hämostaseologie. - 0720-9355. ; 22:3, s. 44-54
  • Tidskriftsartikel (refereegranskat)abstract
    • Approved indications for the recombinant hirudins lepirudin (Refludan(R)) und desirudin (Revasc(R)) are therapy of heparin-induced thrombocytopenia (HIT) and thrombosis prophylaxis following knee or hip replacement surgery. Kidney function dependent pharmacokinetics and their capability of inducing antibodies directed against hirudin are characteristic of this class of drugs. However, close dose-monitoring allows safe and effective use of both compounds. While lepirudin is used widely, besides danaparoid, for treatment of HIT, desirudin has not yet been widely accepted for thrombosis prophylaxis following knee or hip replacement surgery.
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38.
  • Lubenow, Norbert, et al. (författare)
  • Lepirudin in patients with heparin-induced thrombocytopenia - results of the third prospective study (HAT-3) and a combined analysis of HAT-1, HAT-2, and HAT-3.
  • 2005
  • Ingår i: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 3:11, s. 2428-36
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To assess efficacy and safety of lepirudin in patients with heparin-induced thrombocytopenia (HIT) in a prospective study (HAT-3) as well as in a combined analysis of all HAT study data. PATIENTS/METHODS: Patients with laboratory-confirmed HIT were treated with lepirudin in three different aPTT-adjusted dose regimen and during cardiopulmonary bypass (CPB). Endpoints were new thromboembolic complications (TEC), limb amputations, and death and major bleeding. A historical control group (n = 120) was used for comparison. RESULTS: After start of lepirudin in 205 patients treated in HAT-3, the combined endpoint occurred in 43 (21.0%). Thirty (14.6%) patients died, 10 (4.9%) underwent limb amputation, and 11 (5.4%) new TECs occurred. Major bleeding occurred in 40 patients (19.5%) (seven during CPB surgery). Combining all prospective HAT trials (n = 403), after start of lepirudin treatment, the combined endpoint occurred in 82 patients (20.3%), with 47 deaths (11.7%), 22 limb amputations (5.5%), 30 new TECs (7.4%), and 71 (17.6%) major bleedings. Compared with the historical control group (log-rank test), the combined endpoint after start of treatment was reduced (29.7% vs. 52.1%, P = 0.0473), primarily because of reduction in new thromboses (11.9% vs. 32.1%, P = 0.0008). Mean lepirudin maintenance doses ranged from 0.07 to 0.11 mg kg(-1) h(-1). Major bleeding was more frequent in the lepirudin-treated patients (29.4% vs. 9.1%, P = 0.0148). CONCLUSIONS: The rate of new TECs in HIT patients is low after start of lepirudin treatment. The rate of major bleeding of 17.6% might be reduced by reducing the starting dose to 0.1 mg kg(-1) h(-1).
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39.
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40.
  • Lubenow, Norbert, et al. (författare)
  • Very low platelet counts in post-transfusion purpura falsely diagnosed as heparin-induced thrombocytopenia. Report of four cases and review of literature.
  • 2000
  • Ingår i: Thrombosis Research. - 0049-3848 .- 1879-2472. ; 100:3, s. 115-25
  • Tidskriftsartikel (refereegranskat)abstract
    • Differential diagnosis between post-transfusion purpura (PTP) and heparin-induced thrombocytopenia (HIT) can be difficult in the initial stages of thrombocytopenia, as the early clinical presentations are often similar. Four patients are described who were suspected clinically of suffering from HIT. All four patients had recent blood transfusions and platelet alloantibodies, thus the diagnosis of PTP was made. One lethal gastrointestinal and one retroperitoneal hemorrhage developed in two of the four patients. Unusually, one patient was male and two different platelet alloantibodies were present in his serum; in another patient platelet alloantibodies and HIT-antibodies were detectable. To arrive at the right diagnosis as quickly as possible is vitally important since treatment, which has to be initiated promptly, is very different for the two syndromes. Thus, we suggest that in patients where HIT is suspected, additional information should be sought. If features consistent with PTP (such as a recent blood transfusion or a marked drop in platelet count to below 15 Gpt/L) are present, we recommend parallel testing for platelet alloantibodies to rule out PTP.
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