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Arnold Berstad - One of the best experts on this subject based on the ideXlab platform.

  • Interaction between Heparin and Acetylsalicylic Acid on Gastric Mucosal and Skin Bleeding in Humans
    Scandinavian journal of gastroenterology, 1992
    Co-Authors: C. J. Bang, B. Riedel, I. Talstad, Arnold Berstad
    Abstract:

    The haemorrhagic effect of unfractionated heparin and of the low molecular weight heparin, enoxaparin, on gastric mucosal Bleeding induced by acetylsalicylic acid (ASA) and on Skin Bleeding induced by the Simplate technique was investigated in healthy human volunteers. Endoscopic estimation of gastric Bleeding by visual analogue scores was more sensitive than biochemical quantitation of blood in the gastric washing by a modified HaemoQuant method. Contrary to what was expected, the ASA-induced gastric mucosal Bleeding was not increased by heparin pretreatment, whereas heparin in combination with ASA, but not ASA alone, significantly increased the Skin Bleeding time. In the interaction with ASA, enoxaparin and unfractionated heparin appeared to act similarly.

  • Haemorrhagic Effect of Enoxaparin, a Low Molecular Weight Heparin: Comparison with Unfractionated Heparin in Humans
    Scandinavian journal of gastroenterology, 1992
    Co-Authors: C. J. Bang, B. Riedel, I. Talstad, Arnold Berstad
    Abstract:

    The haemorrhagic effects of unfractionated heparin (UFH) and the low molecular weight heparin (LMWH) enoxaparin were investigated and compared in the gastric mucosa (haemorrhage induced by biopsy) and Skin (haemorrhage induced by Simplate) of 12 healthy volunteers. Administration of UFH and LMWH (given in a dose of 75 anti-Xa U/kg intravenously) increased median gastric Bleeding time (3.5 min) and geometric mean blood loss (11.5 l) to 19 min (p = 0.00003) and 54.1 l (p = 0.0021) after UFH and to 13 min (p = 0.008) and 29.0 l (p = 0.275) after LMWH. Median Skin Bleeding time (4.25 min) increased to 6.0 min after UFH (p = 0.003) and to 6.75 min after LMWH (p = 0.0008). Mean heparin activity in plasma was 20% higher after LMWH than after UFH. The calculated gastric Bleeding time to heparin activity ratio was significantly lower for LMWH than for UFH (0.05).

Emmanuel J. Favaloro - One of the best experts on this subject based on the ideXlab platform.

  • Appropriate laboratory assessment as a critical facet in the proper diagnosis and classification of von Willebrand disorder.
    Best practice & research. Clinical haematology, 2001
    Co-Authors: Emmanuel J. Favaloro
    Abstract:

    The correct diagnosis and classification of von Willebrand disease or disorder (VWD) is crucial because the presenting biological activity of von Willebrand factor (VWF) determines both the haemorrhagic risk and the subsequent clinical management. A variety of laboratory assays may be employed, not necessarily restricted to assessments of VWF. Because of assay limitations and von Willebrand disease heterogeneity, no single test procedure is sufficiently 'robust' to permit the detection of all VWD variants. Classically, the test panel might include any combination of: (a) Skin Bleeding time, (b) von Willebrand factor antigen assay, (c) factor VIII C level, (d) assessment of 'functional' von Willebrand factor (collagen-binding activity or ristocetin co-factor assay), (e) ristocetin-induced platelet aggregation, and (f) multimer analysis. There have also been many new diagnostic developments that have begun to influence the diagnostic process. These include the automation of existing assay procedures, new automated platelet function analyzers such as the PFA-100, and specific von Willebrand factor-factor VIII-binding assays. This chapter focuses on the recommended laboratory process for the investigation of VWD. The selection of an appropriate combination test panel and testing sequence is crucial for the proper diagnosis and classification of congenital von Willebrand disease.

C. J. Bang - One of the best experts on this subject based on the ideXlab platform.

  • Interaction between Heparin and Acetylsalicylic Acid on Gastric Mucosal and Skin Bleeding in Humans
    Scandinavian journal of gastroenterology, 1992
    Co-Authors: C. J. Bang, B. Riedel, I. Talstad, Arnold Berstad
    Abstract:

    The haemorrhagic effect of unfractionated heparin and of the low molecular weight heparin, enoxaparin, on gastric mucosal Bleeding induced by acetylsalicylic acid (ASA) and on Skin Bleeding induced by the Simplate technique was investigated in healthy human volunteers. Endoscopic estimation of gastric Bleeding by visual analogue scores was more sensitive than biochemical quantitation of blood in the gastric washing by a modified HaemoQuant method. Contrary to what was expected, the ASA-induced gastric mucosal Bleeding was not increased by heparin pretreatment, whereas heparin in combination with ASA, but not ASA alone, significantly increased the Skin Bleeding time. In the interaction with ASA, enoxaparin and unfractionated heparin appeared to act similarly.

  • Haemorrhagic Effect of Enoxaparin, a Low Molecular Weight Heparin: Comparison with Unfractionated Heparin in Humans
    Scandinavian journal of gastroenterology, 1992
    Co-Authors: C. J. Bang, B. Riedel, I. Talstad, Arnold Berstad
    Abstract:

    The haemorrhagic effects of unfractionated heparin (UFH) and the low molecular weight heparin (LMWH) enoxaparin were investigated and compared in the gastric mucosa (haemorrhage induced by biopsy) and Skin (haemorrhage induced by Simplate) of 12 healthy volunteers. Administration of UFH and LMWH (given in a dose of 75 anti-Xa U/kg intravenously) increased median gastric Bleeding time (3.5 min) and geometric mean blood loss (11.5 l) to 19 min (p = 0.00003) and 54.1 l (p = 0.0021) after UFH and to 13 min (p = 0.008) and 29.0 l (p = 0.275) after LMWH. Median Skin Bleeding time (4.25 min) increased to 6.0 min after UFH (p = 0.003) and to 6.75 min after LMWH (p = 0.0008). Mean heparin activity in plasma was 20% higher after LMWH than after UFH. The calculated gastric Bleeding time to heparin activity ratio was significantly lower for LMWH than for UFH (0.05).

M. Reers - One of the best experts on this subject based on the ideXlab platform.

  • Reduction of r-hirudin induced Bleeding in pigs by the administration of von Willebrand factor.
    Platelets, 1996
    Co-Authors: G. Dickneite, H.-j. Friesen, G. Kumpe, M. Reers
    Abstract:

    To prevent r-hirudin induced excess Bleeding an animal model was established in pigs for the investigation of an anti-Bleeding strategy. We used the Simplate® device to monitor Skin Bleeding time (SBT) at the inner site of the ear. r-Hirudin infused in a dose of 0.3 mag per h induced a prominent increase of SBT. The aim of our studies was to reverse r-hirudin induced Bleeding by enhancing platelet adhesion to the endothelium via the administration of von Willebrand Factor (vWF). Pigs were treated with vWF containing solutions (Haemate® and a vWF-concentrate) at 3h after the start of the r-hirudin infusion. Both compounds suppressed SBT 1h after administration and significantly prevented Bleeding until the termination of the experiment. SBT values (given in times of baseline) in the placebo group were 3.32 ± 0.9, 1.51 ± 0.14 in the Haemate® and 1.85 ± 0.42 in the vWF concentrate group (P = 0.008 or 0.032, in a two-sided Kruskall-Wallis-test). Coagulation parameters (aPTT, PT) were unaltered by the treatmen...

M. Greaves - One of the best experts on this subject based on the ideXlab platform.

  • Fibrinopeptide A, Thromboxane B(2) and Beta-thromboglobulin Levels in Bleeding Time Blood in Uraemia.
    Platelets, 1991
    Co-Authors: A. Moosa, I. Ford, C. B. Brown, M. Greaves
    Abstract:

    The uraemic state is commonly complicated by a haemorrhagic tendency due to an abnormality of the primary haemostatic response. Whilst renal anaemia contributes to the defect, platelet dysfunction has also been implicated. Tests of coagulation and platelet reactivity performed ex vivo on anticoagulated blood samples have not provided an adequate explanation for the haemostatic defect. We have therefore studied events at the site of tissue injury by serial assays of beta-thromboglobulin (BTG), thromboxane B(2) (TxB(2)) and fibrinopeptide A (FPA) in blood samples issuing from a standardised Skin Bleeding time incision in 7 uraemic subjects and matched healthy controls. Generation of TxB(2) and FPA were normal, but the concentration of BTG in Bleeding time blood was markedly reduced throughout the first 5 min in the uraemic subjects. We conclude that a defect of platelet release occurring at the site of tissue injury may contribute to the haemostatic abnormality in uraemia and this finding could be relevant to the therapeutic strategy adopted in the management of Bleeding episodes.