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  • 1.
    Boknäs, Niklas
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences.
    Faxälv, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Chemistry.
    Lindahl, Tomas L
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Chemistry.
    Ramström, Sofia
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences.
    Contact activation: important to consider when measuring the contribution of tissue factor-bearing microparticles to thrombin generation using phospholipid-containing reagents2014In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 12, no 4, p. 515-518Article in journal (Refereed)
    Abstract [en]

    Background A commercial MP reagent containing phospholipids is used for thrombin generation (TG) measurements to estimate the procoagulant activity of microparticles (MPs). Previous reports have shown that contact activation affects TG when TF levels are low, and that addition of phospholipids might augment this effect. Objectives To quantify the impact of contact activation on TG in the presence of phospholipids and low/no TF, as is the case using a commercially available MP-reagent. Methods Thrombin generation was analyzed using MP- or platelet-rich plasma (PRP)-reagent in the presence and absence of corn trypsin inhibitor and anti-TF antibodies, respectively. To quantify the impact of different experimental parameters on contact activation, microparticle-depleted plasma was analyzed in the presence of different concentrations of phospholipids, TF and/or contact activating agents (kaolin). Results Even with low contact activating blood collection tubes, substantial thrombin generation was observed with the MP-reagent, but this was completely inhibited by addition of corn trypsin inhibitor. Control experiments illustrate that the phospholipids in the reagent play a major role in enhancing TG initiated by FXIIa. Even with the PRP-reagent, which is recommended for determining the content of phospholipids from MPs, TG was partly dependent on contact activation. Conclusions Contact activation plays a major role in TG when using reagents/samples containing phospholipids but little or no tissue factor. This needs to be considered and accounted for in future clinical studies using TG to assess the procoagulant activity of MPs.

  • 2.
    Egberg, N.
    et al.
    Departments of Clinical Chemistry, Karolinska Hospital, Stockholm.
    Fagerberg, I
    Sahlgrenska University Hospital, Gothenburg.
    Hillarp, A
    Malmö University Hospital, Malmö.
    Lindahl, Tomas
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Stigendal, L
    Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweeden.
    Letter: Guidelines on preparation, certification, and use of certified plasmas for ISI calibration and INR determination - A rebuttal2005In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 3, no 10, p. 2370-2372Article in journal (Other academic)
    Abstract [en]

    [No abstract available]

  • 3.
    Hammarström, Per
    Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Biochemistry.
    The bloody path of amyloids and prions2007In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 5, no 6, p. 1136-1138Other (Other academic)
    Abstract [en]

    [No abstract available]

  • 4.
    Hillarp, A.
    et al.
    University and Regional Laboratories Region Skåne, Malmö, Sweden.
    Gustafsson, Kerstin
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Faxälv, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Chemistry.
    Strandberg, K.
    University and Regional Laboratories Region Skåne, Malmö, Sweden.
    Baghaei, F.
    Sahlgrenska University Hospital, Sweden; University of Gothenburg, Sweden.
    Fagerberg Blixter, I.
    Sahlgrenska University Hospital, Sweden; University of Gothenburg, Sweden.
    Berndtsson, M.
    Karolinska University Hospital, Stockholm, Sweden.
    Lindahl, Tomas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Chemistry.
    Effects of the oral, direct factor Xa inhibitor apixaban on routine coagulation assays and anti-FXa assays2014In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 12, no 9, p. 1545-1553Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION:

    Apixaban is an oral direct factor Xa inhibitor developed for the prophylaxis and treatment of thromboembolic disorders. Laboratory monitoring is not necessary, but the effects on common coagulation reagents and assays constitute clinically valuable information.

    OBJECTIVES:

    To investigate the effects of apixaban on commonly used coagulation methods, and to evaluate anti-FXa assays for specific determination of the drug concentration.

    MATERIALS AND METHODS:

    Apixaban was added to plasma from healthy subjects in the concentration range 0-1000 μg L(-1) , and analyses were performed with different reagents for activated partial thromboplastin time (APTT), prothrombin time (PT), antithrombin, protein C, and protein S. A lupus anticoagulant assay and an APTT assay with varying phospholipid concentrations were used to study the phospholipid dependence.

    RESULTS:

    In general, apixaban showed fewer effects in vitro than have been shown for rivaroxaban, another direct FXa inhibitor. The concentration needed to double the APTT varied between 2200 and 4700 μg L(-1) , and the concentration needed to double the PT varied between 700 and 3900 μg L(-1) . The effects on antithrombin, protein C and protein S assays were dependent on the type of reagent. Apixaban did not cause false-positive lupus anticoagulant results. Chromogenic anti-FXa assays showed linear dose-response curves with apixaban.

    CONCLUSIONS:

    Therapeutic concentrations of apixaban variably affect different assay groups, and even different reagents within an assay group. The effects were much smaller than with rivaroxaban. The use of APTT and/or PT assays to screen the anticoagulant activity of apixaban cannot be recommended. A chromogenic anti-FXa assay can be used for reliable measurements of apixaban concentration.

  • 5.
    Järemo, Petter
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Local Health Care Services in the East of Östergötland, Department of Internal Medicine VHN.
    Starkhammar, C
    Östergötlands Läns Landsting, Public Dental Service.
    Lundström, Å
    Östergötlands Läns Landsting, Public Dental Service.
    Lindahl, Tomas
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Richter, Arina
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Inverse relationship between the severity of gingivitis and platelet reactivity in stable angina pectoris [6]2007In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 5, no 2, p. 422-423Article in journal (Other academic)
    Abstract [en]

    [No abstract available]

  • 6.
    Lindahl, Tomas
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Chemistry.
    Macwan, Ankit
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Ramström, Sofia
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Protease-activated receptor 4 is more important than protease-activated receptor 1 for the thrombin-induced procoagulant effect on platelets in JOURNAL OF THROMBOSIS AND HAEMOSTASIS, vol 14, issue 8, pp 1639-16412016In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 14, no 8, p. 1639-1641Article in journal (Other academic)
    Abstract [en]

    n/a

  • 7.
    Schulman, S.
    et al.
    Department of Hematology, Coagulation Unit, Karolinska University Hospital, Stockholm, Sweden, Department of Medicine, McMaster University, Hamilton, Ont., Canada, Thrombosis Service, McMaster Clinic, HHS - General Hospital, Hamilton, Ont. L8L 2X2, Canada.
    Lindmarker, P.
    Department of Emergency Medicine, Karolinska University Hospital, Karolinska, Sweden.
    Holmstrom, M.
    Holmström, M., Department of Hematology, Coagulation Unit, Karolinska University Hospital, Stockholm, Sweden, Department of Medicine, Huddinge Hospital, Huddinge, Sweden.
    Lafars, G.
    Läfars, G., Södersjukhuset, Sweden.
    Carlsson, A.
    Department of Hematology, Coagulation Unit, Karolinska University Hospital, Stockholm, Sweden, Danderyd Hospital, Danderyd, Sweden.
    Nicol, P.
    Köping Hospital, Köping, Sweden.
    Svensson, E.
    Södertälje Hospital, Södertälje, Sweden.
    Ljungberg, B.
    Nyköping Hospital, Nyköping, Sweden.
    Viering, S.
    Norrtälje Hospital, Norrtälje, Sweden.
    Nordlander, S.
    Västerås Central Hospital, Västerås, Sweden.
    Leijd, B.
    St. Göran Hospital, Sweden.
    Jahed, K.
    Östergötlands Läns Landsting.
    Hjorth, M.
    Lidköping Hospital, Lidköping, Sweden.
    Linder, O.
    Örebro Regional Hospital, Örebro, Sweden.
    Beckman, M.
    Department of Radiology, Karolinska University Hospital, Stockholm, Sweden.
    Post-thrombotic syndrome, recurrence, and death 10 years after the first episode of venous thromboembolism treated with warfarin for 6 weeks or 6 months2006In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 4, no 4, p. 734-742Article in journal (Refereed)
    Abstract [en]

    Background: The influence of the duration of anticoagulant therapy after venous thromboembolism (VTE) on the long-term morbidity and mortality is unclear. Aim: To investigate the long-term sequelae of VTE in patients randomized to different duration of secondary prophylaxis. Methods: In a multicenter trial comparing secondary prophylaxis with vitamin K antagonists for 6 weeks or 6 months, we extended the originally planned 2 years follow-up to 10 years. The patients had annual visits and at the last visit clinical assessment of the post-thrombotic syndrome (PTS) was performed. Recurrent thromboembolism was adjudicated by a radiologist, blinded to treatment allocation. Causes of death were obtained from the Swedish Death Registry. Results: Of the 897 patients randomized, 545 could be evaluated at the 10 years follow-up. The probability of developing severe PTS was 6% and any sign of PTS was seen in 56.3% of the evaluated patients. In multivariate analysis, old age and signs of impaired circulation at discharge from the hospital were independent risk factors at baseline for development of PTS after 10 years. Recurrent thromboembolism occurred in 29.1% of the patients with a higher rate among males, older patients, those with permanent gering risk factor - especially with venous insufficiency at baseline - signs of impaired venous circulation at discharge, proximal deep vein thrombosis, or pulmonary embolism. Death occurred in 28.5%, which was a higher mortality than expected with a standardized incidence ratio (SIR) of 1.43 (95% CI 1.28-1.58), mainly because of a higher mortality than expected from cancer (SIR 1.83, 95% CI 1.44-2.23) or from myocardial infarction or stroke (SIR 1.28, 95% CI 1.00-1.56).The duration of anticoagulation did not have a statistically significant effect on any of the long-term outcomes. Conclusion: The morbidity and mortality during 10 years after the first episode of VTE is high and not reduced by extension of secondary prophylaxis from 6 weeks to 6 months. A strategy to reduce recurrence of VTE as well as mortality from arterial disease is needed. © 2006 International Society on Thrombosis and Haemostasis.

  • 8.
    van den Besselaar, A. M. H. P.
    et al.
    Leiden University, Netherlands.
    Chantarangkul, V.
    Fdn Luigi Villa, Italy.
    Angeloni, F.
    Hemostasis Reference Lab, Canada.
    Binder, N. B.
    Technoclone GmbH, Austria.
    Byrne, M.
    St James Hospital, Ireland.
    Dauer, R.
    Alfred Heatlh, Australia.
    Gudmundsdottir, B. R.
    Landspitali University Hospital, Iceland; University of Iceland, Iceland.
    Jespersen, J.
    University of Southern Denmark, Denmark.
    Kitchen, S.
    Royal Hallamshire Hospital, England.
    Legnani, C.
    University Hospital S Orsola Malpighi, Italy.
    Lindahl, Tomas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Chemistry.
    Manning, R. A.
    Imperial Coll Healthcare NHS Trust, England.
    Martinuzzo, M.
    Lab Central Hospital Italiano Buenos Aires, Argentina.
    Panes, O.
    Pontificia University of Catolica Chile, Chile.
    Pengo, V.
    University of Padua, Italy.
    Riddell, A.
    Royal Free Hospital, England.
    Subramanian, S.
    St Johns Medical Coll Hospital, India.
    Szederjesi, A.
    St Istvan and St Laszlo Hospital, Hungary.
    Tantanate, C.
    Mahidol University, Thailand.
    Herbel, P.
    Roche Diagnost GmbH Mannheim, Germany.
    Tripodi, A.
    University of Milan, Italy; IRCCS Ca Granda Maggiore Hospital Fdn, Italy.
    International collaborative study for the calibration of proposed International Standards for thromboplastin, rabbit, plain, and for thromboplastin, recombinant, human, plain2018In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 16, no 1, p. 142-149Article in journal (Refereed)
    Abstract [en]

    Background: The availability of International Standards for thromboplastin is essential for the calibration of routine reagents and hence the calculation of the International Normalized Ratio (INR). Stocks of the current Fourth International Standards are running low. Candidate replacement materials have been prepared. This article describes the calibration of the proposed Fifth International Standards for thromboplastin, rabbit, plain (coded RBT/16) and for thromboplastin, recombinant, human, plain (coded rTF/16). Methods: An international collaborative study was carried out for the assignment of International Sensitivity Indexes (ISIs) to the candidate materials, according to the World Health Organization (WHO) guidelines for thromboplastins and plasma used to control oral anticoagulant therapy with vitamin K antagonists. Results: Results were obtained from 20 laboratories. In several cases, deviations from the ISI calibration model were observed, but the average INR deviation attributabled to the model was not greater than 10%. Only valid ISI assessments were used to calculate the mean ISI for each candidate. The mean ISI for RBT/16 was 1.21 (between-laboratory coefficient of variation [CV]: 4.6%), and the mean ISI for rTF/16 was 1.11 (between-laboratory CV: 5.7%). Conclusions: The between-laboratory variation of the ISI for candidate material RBT/16 was similar to that of the Fourth International Standard (RBT/05), and the between-laboratory variation of the ISI for candidate material rTF/16 was slightly higher than that of the Fourth International Standard (rTF/09). The candidate materials have been accepted by WHO as the Fifth International Standards for thromboplastin, rabbit plain, and thromboplastin, recombinant, human, plain.

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