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  1. Article: Role of von Willebrand factor in vascular disease.

    Paulinska, P / Spiel, A / Jilma, B

    Hamostaseologie

    2009  Volume 29, Issue 1, Page(s) 32–38

    Abstract: Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thromboembolic cardiovascular events, ischaemic stroke as well as with peripheral ... ...

    Abstract Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thromboembolic cardiovascular events, ischaemic stroke as well as with peripheral arterial occlusive disease. In the general population, there is only a weak association between VWF levels and future cardiovascular events or stroke. In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients with increased VWF suffer a higher incidence of major adverse cardiac events including death. The extent of the VWF release and its levels independently predict clinical outcome in patients with acute coronary syndromes. Elevated VWF levels have also been observed in patients with atrial fibrillation compared to controls and predict outcome. This may at least in part be attributable to the association of VWF with underlying cardiovascular risk factors. Hence, VWF correlates with Framingham and CHADS stroke risk stratification score and can be used as a marker in patients with AF. However, VWF is not only a predictor; it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in ACS, ischaemic stroke and peripheral arterial disease and the relevance of therapeutic interventions targeting VWF for ACS patients.
    MeSH term(s) Arterial Occlusive Diseases/blood ; Binding Sites ; Collagen/metabolism ; Coronary Disease/blood ; Coronary Disease/physiopathology ; Factor VIII/metabolism ; Heparin/metabolism ; Humans ; Platelet Membrane Glycoproteins/metabolism ; Reference Values ; Stroke/blood ; Thrombosis/blood ; Thrombosis/physiopathology ; Vascular Diseases/blood ; von Willebrand Factor/metabolism ; von Willebrand Factor/physiology
    Chemical Substances Platelet Membrane Glycoproteins ; von Willebrand Factor ; Factor VIII (9001-27-8) ; Heparin (9005-49-6) ; Collagen (9007-34-5)
    Language English
    Publishing date 2009-01
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 801512-0
    ISSN 0720-9355
    ISSN 0720-9355
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Role of von Willebrand factor in vascular disease

    Paulinska, P. / Spiel, A. / Jilma, B.

    Hämostaseologie

    2009  Volume 29, Issue 1, Page(s) 32

    Language German
    Document type Article
    ZDB-ID 801512-0
    ISSN 0720-9355
    Database Current Contents Medicine

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  3. Article: Role of von Willebrand factor in vascular disease

    Paulinska, P. / Spiel, A. / Jilma, B.

    Hämostaseologie

    2009  Volume 29, Issue 01, Page(s) 32–38

    Abstract: Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thrombo - embolic cardiovascular events, ischaemic stroke as well as with peripheral ... ...

    Abstract Plasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thrombo - embolic cardiovascular events, ischaemic stroke as well as with peripheral arterial occlusive disease. In the general population, there is only a weak association between VWF levels and future cardiovascular events or stroke. In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients with increased VWF suffer a higher incidence of major adverse cardiac events including death. The extent of the VWF release and its levels independently predict clinical outcome in patients with acute coronary syndromes. Elevated VWF levels have also been observed in patients with atrial fibrillation compared to controls and predict outcome. This may at least in part be attributable to the association of VWF with underlying cardiovascular risk factors. Hence, VWF correlates with Framingham and CHADS stroke risk stratification score and can be used as a marker in patients with AF. However, VWF is not only a predictor; it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in ACS, ischaemic stroke and peripheral arterial disease and the relevance of therapeutic interventions targeting VWF for ACS patients.
    Keywords Von Willebrand factor
    Language English
    Publishing date 2009-01-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 801512-0
    ISSN 2567-5761 ; 0720-9355
    ISSN (online) 2567-5761
    ISSN 0720-9355
    DOI 10.1055/s-0037-1616936
    Database Thieme publisher's database

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  4. Article: A randomised pilot trial of the anti-von Willebrand factor aptamer ARC1779 in patients with type 2b von Willebrand disease.

    Jilma, Bernd / Paulinska, Petra / Jilma-Stohlawetz, Petra / Gilbert, James C / Hutabarat, Renta / Knöbl, Paul

    Thrombosis and haemostasis

    2010  Volume 104, Issue 3, Page(s) 563–570

    Abstract: Desmopressin aggravates thrombocytopenia in type 2B von Willebrand disease (VWF type 2B) by release of large and hyper-adhesive von Willebrand Factor (VWF) multimers. This pilot study investigated whether the anti-VWF aptamer ARC1779 can prevent ... ...

    Abstract Desmopressin aggravates thrombocytopenia in type 2B von Willebrand disease (VWF type 2B) by release of large and hyper-adhesive von Willebrand Factor (VWF) multimers. This pilot study investigated whether the anti-VWF aptamer ARC1779 can prevent desmopressin-induced thrombocytopenia and interferes with the excessive VWF turnover in patients with VWF type 2B. Concentration effect curves of ARC1779 were established for five patients in vitro and two patients with VWF type 2B were treated by infusion of ARC1779, desmopressin, or their combination in a randomised, controlled, double-blind design. ARC1779 concentrations in the range of 1-3 microg/ml blocked free A1 domain binding sites by 90% in vitro. In vivo, desmopressin alone induced a profound (-90%) drop in platelet counts in one of the patients. ARC1779 (4-5 microg/ml) completely inhibited VWF A1 domains and prevented this desmopressin-induced platelet drop. Desmopressin alone increased VWF antigen two- to three-fold, accompanied by concordant changes in VWF Ristocetin cofactor activity (RCo) and coagulation factor VIII activity. ARC1779 substantially enhanced the desmopressin-induced maximal increase in these parameters, and improved multimer patterns. No treatment related adverse events were observed and no bleeding occurred despite marked thrombocytopenia. These data provide first proof of concept in humans and evidence that ARC1779 is a potent inhibitor of VWF. ARC1779 prevented the rapid consumption of VWF multimers together with agglutinated platelets that occurred in response to desmopressin challenge in patients with VWD type 2B.
    MeSH term(s) Adult ; Aged ; Aptamers, Nucleotide/administration & dosage ; Aptamers, Nucleotide/adverse effects ; Aptamers, Nucleotide/pharmacokinetics ; Aptamers, Nucleotide/therapeutic use ; Austria ; Binding Sites ; Deamino Arginine Vasopressin/administration & dosage ; Deamino Arginine Vasopressin/adverse effects ; Double-Blind Method ; Factor VIII/metabolism ; Female ; Hemostatics/administration & dosage ; Hemostatics/adverse effects ; Hemostatics/pharmacokinetics ; Hemostatics/therapeutic use ; Humans ; Infusions, Intravenous ; Male ; Middle Aged ; Partial Thromboplastin Time ; Pilot Projects ; Platelet Count ; Platelet Function Tests ; Protein Multimerization ; Thrombocytopenia/blood ; Thrombocytopenia/chemically induced ; Time Factors ; Treatment Outcome ; von Willebrand Disease, Type 2/blood ; von Willebrand Disease, Type 2/drug therapy ; von Willebrand Factor/antagonists & inhibitors ; von Willebrand Factor/metabolism
    Chemical Substances ARC 1779 ; Aptamers, Nucleotide ; Hemostatics ; von Willebrand Factor ; Factor VIII (9001-27-8) ; Deamino Arginine Vasopressin (ENR1LLB0FP)
    Language English
    Publishing date 2010-09
    Publishing country Germany
    Document type Journal Article ; Randomized Controlled Trial
    ZDB-ID 518294-3
    ISSN 0340-6245
    ISSN 0340-6245
    DOI 10.1160/TH10-01-0027
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    Uh III Zs.192: Show issues Location:
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  5. Article: A randomised pilot trial of the anti-von Willebrand factor aptamer ARC1779 in patients with type 2b von Willebrand disease

    Jilma, Bernd / Paulinska, Petra / Jilma-Stohlawetz, Petra / Gilbert, James C. / Hutabarat, Renta / Knöbl, Paul

    Thrombosis and Haemostasis

    2010  Volume 103, Issue 09, Page(s) 563–570

    Abstract: Desmopressin aggravates thrombocytopenia in type 2B von Willebrand disease (VWF type 2B) by release of large and hyper-adhesive von Wille-brand Factor (VWF) multimers. This pilot study investigated whether the anti-VWF aptamer ARC1779 can prevent ... ...

    Abstract Desmopressin aggravates thrombocytopenia in type 2B von Willebrand disease (VWF type 2B) by release of large and hyper-adhesive von Wille-brand Factor (VWF) multimers. This pilot study investigated whether the anti-VWF aptamer ARC1779 can prevent desmopressin-induced thrombocytopenia and interferes with the excessive VWF turnover in patients with VWF type 2B. Concentration effect curves of ARC1779 were established for five patients in vitro and two patients with VWF type 2B were treated by infusion of ARC1779, desmopressin, or their combination in a randomised, controlled, double-blind design. ARC1779 concentrations in the range of 1–3 μg/ml blocked free A1 domain binding sites by 90% in vitro In vivo, desmopressin alone induced a profound (-90%) drop in platelet counts in one of the patients. ARC1779 (4–5 μg/ml) completely inhibited VWF A1 domains and prevented this desmopress-in-induced platelet drop. Desmopressin alone increased VWF antigen two- to three-fold, accompanied by concordant changes in VWF Ristocetin cofactor activity (RCo) and coagulation factor VIII activity. ARC1779 substantially enhanced the desmopressin-induced maximal increase in these parameters, and improved multimer patterns. No treatment related adverse events were observed and no bleeding occurred despite marked thrombocytopenia. These data provide first proof of concept in humans and evidence that ARC1779 is a potent inhibitor of VWF. ARC1779 prevented the rapid consumption of VWF multimers together with agglutinated platelets that occurred in response to desmopressin challenge in patients with VWD type 2B. Clinical Trial registration number: NCT00632242.
    Keywords Clinical trials ; antiplatelet drugs ; von Willebrand factor ; thrombocytopenia ; desmopressin
    Language English
    Publishing date 2010-01-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH10-01-0027
    Database Thieme publisher's database

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  6. Article ; Conference proceedings: Discrepant results between routine screening for latent tuberculosis (TB) and Quantiferon® in patients with inflammatory bowel diseases (IBD)

    Papay, P / Eser, A / Paulinska, P / Lichtenberger, C / Mikulits, A / Miehsler, W / Dejaco, C / Novacek, G / Vogelsang, H / Reinisch, W

    Zeitschrift für Gastroenterologie

    2008  

    Abstract: Background/Aim: Screening for latent TB is part of the routine management in patients with IBD before starting therapy with any anti-Tumor Necrosis Factor (TNF)! compound. Recently, the whole blood interferon “ assay (QuantiFERON®) has been introduced ... ...

    Event/congress 41. Jahrestagung und 19. Fortbildungskurs der österreichischen Gesellschaft für Gastroenterologie und Hepatologie (ÖGGH), Millstatt, 2008
    Abstract Background/Aim: Screening for latent TB is part of the routine management in patients with IBD before starting therapy with any anti-Tumor Necrosis Factor (TNF)! compound. Recently, the whole blood interferon “ assay (QuantiFERON®) has been introduced as additional test to routine screening consisting of tuberculin skin test (TST) and chest X-ray. Our aim was to compare these diagnostic methods in consecutive IBD patients with the indication of anti TNF! therapy.
    Patients/Methods: To date, 78 patients with IBD, who started treatment with infliximab, adalimumab or certolizumab were screened for latent tuberculosis by performing chest x-ray, TST and QuantiFERON®. Signs indicative of latent TB from chest x-ray included granuloma, bihilar lymphadenopathy and pleura scarring. TST was assessed positive if induration >5mm appeared after 48–72h of intracutan application of tuberculin/5 units in 0,1ml/. QuantiFERON® was positive if quantitative measurement revealed >0,35.
    Results: QuantiFERON® test failed on samples from 12/78 patients, resulting in 66/78 (85%) patients on whom results from all 3 screening tests were available. Chest X-ray revealed findings indicative for latent TB in 3/78 (4%) subjects. All of them were positive for TST, but negative for QuantiFERON®. Of note, 2 of those patients received INH previously. Table shows proportion of dis-/concordance between TST and QuantiFERON®. Concordance between TST and QuantiFERON® was observed in 51 cases (77%), discordance in 15 (23%). A positive result in any of the 3 tests prompted prophylactic therapy for latent TB with isoniazid in 15/66 (19%) patients. No single case of active TB was reported by now.
    Conclusion: Our results reveal frequently discordant findings from TST and QuantiFERON®. Hence, we speculate that with current guidelines for TB screening, consisting of chest X-ray and TST, substantial proportions of patients may receive over- or under-treatment with isoniazid. Larger studies on the prognostic impact of those findings are urgently warranted. QuantiFERON® positive QuantiFERON® negative TST positive 4/66 (6%) 11/66 (17%) 15 TST negative 4/66 (6%) 47/66 (71%) 51 8 58 66
    Language English
    Publishing date 2008-06-18
    Publishing place Stuttgart ; New York
    Document type Article ; Conference proceedings
    ZDB-ID 201387-3
    ISSN 1439-7803 ; 0044-2771 ; 0172-8504
    ISSN (online) 1439-7803
    ISSN 0044-2771 ; 0172-8504
    DOI 10.1055/s-2008-1081514
    Database Thieme publisher's database

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