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  • 51.
    Olsson, A.
    et al.
    Blekinge Institute of Technology, Karlskrona, Sweden; Linköping University, Linköping, Sweden; Blekinge Hospital, Karlskrona, Sweden.
    Alfredsson, J.
    Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Linköping University, Linköping, Sweden.
    Svedjeholm, R.
    Linköping University, Linköping, Sweden.
    Kenny, D.
    Clinical Research Centre, Royal College of Surgeons in Ireland, Dublin, Ireland.
    Håkansson, E.
    Linköping University, Linköping, Sweden.
    Berglund, J. S.
    Blekinge Institute of Technology, Karlskrona, Sweden.
    Berg, S.
    Linköping University, Linköping, Sweden.
    Better platelet function, less fibrinolysis and less hemolysis in re-transfused residual pump blood with the Ringer’s chase technique: a randomized pilot study2018In: Perfusion, ISSN 0267-6591, E-ISSN 1477-111X, Vol. 33, no 3, p. 185-193Article in journal (Refereed)
    Abstract [en]

    Introduction: Residual pump blood from the cardiopulmonary bypass (CPB) circuit is often collected into an infusion bag (IB) and re-transfused. An alternative is to chase the residual blood into the circulation through the arterial cannula with Ringer’s acetate. Our aim was to assess possible differences in hemostatic blood quality between these two techniques.

    Methods: Forty adult patients undergoing elective coronary artery bypass graft surgery with CPB were randomized to receive the residual pump blood by either an IB or through the Ringer’s chase (RC) technique. Platelet activation and function (impedance aggregometry), coagulation and hemolysis variables were assessed in the re-transfused blood and in the patients before, during and after surgery. Results are presented as median (25-75 quartiles).

    Results: Total hemoglobin and platelet levels in the re-transfused blood were comparable with the two methods, as were soluble platelet activation markers P-selectin and soluble glycoprotein VI (GPVI). Platelet aggregation (U) in the IB blood was significantly lower compared to the RC blood, with the agonists adenosine diphosphate (ADP) 24 (10-32) vs 46 (33-65), p<0.01, thrombin receptor activating peptide (TRAP) 50 (29-73) vs 69 (51-92), p=0.04 and collagen 24 (17-28) vs 34 (26-59), p<0.01. The IB blood had higher amounts of free hemoglobin (mg/L) (1086 (891-1717) vs 591(517-646), p<0.01) and D-dimer 0.60 (0.33-0.98) vs 0.3 (0.3-0.48), p<0.01. Other coagulation variables showed no difference between the groups. Conclusions: The handling of blood after CPB increases hemolysis, impairs platelet function and activates coagulation and fibrinolysis. The RC technique preserved the blood better than the commonly used IB technique.

  • 52.
    Oskarsson, T.
    et al.
    Karolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
    Duun-Henriksen, A. K.
    Danish Cancer Society Research Centre, Survivorship Unit, Copenhagen, Denmark.
    Harila-Saari, A.
    Karolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden; Uppsala University, Department of Women's and Children's Health, Uppsala, Sweden.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Örebro University Hospital. Karolinska Institutet, Clinical Epidemiology Unit, Stockholm, Sweden; University College London, Department of Epidemiology and Public Health, London, United Kingdom; Örebro University, Clinical Epidemiology and Biostatistics‐ Faculty of Medicine and Health, Örebro, Sweden.
    Niinimaki, R.
    Turku University Hospital, Department of Pediatrics, Turku, Finland.
    Madanat-Harjuoja, L.
    Finnish Cancer Registry, Statistics and Research, Helsinki, Finland.
    Tryggvadottir, L.
    Icelandic Cancer Registry, Statistics and Research, Reykjavik, Iceland; University of Iceland, Faculty of Medicine, Reykjavik, Iceland.
    Wesenberg, F.
    Norwegian Cancer Registry, Statistics and Research, Oslo, Norway; University of Oslo, Faculty of Medicine, Oslo, Norway.
    Holmqvist, A. S.
    Skane University Hospital, Division of Pediatric Oncology and Haematology, Lund, Sweden; Lund University, Department of Clinical Sciences, Lund, Sweden.
    Hasle, H.
    Aarhus University Hospital, Department of Pediatrics, Aarhus, Denmark.
    Heyman, M.
    Karolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
    Winther, J. F.
    Danish Cancer Society Research Centre, Survivorship Unit, Copenhagen, Denmark.
    Osteoporotic Fractures in Childhood Cancer Survivors - ALICCS Cohort Study2018In: Pediatric Blood & Cancer, ISSN 1545-5009, E-ISSN 1545-5017, Vol. 65, no Suppl.2, p. S693-S694Article in journal (Other academic)
    Abstract [en]

    Background/Objectives: Children and adolescents undergoing treatment for cancer are exposed to multiple factors that impact the development of peak bone mass and bone quality. The aims of this study were to examine the risks and cumulative incidence of osteoporotic fractures in childhood cancer survivors and identify subgroups at higher risk.

    Design/Methods: In the national cancer registries of Denmark, Finland, Iceland and Sweden we identified patients diagnosed with cancer before 20 years of age from the start of registration in the 1940s and 1950s through 2008. We compared 26.334 one‐year survivors with a cohort of 162.372 age‐ and sex‐matched population comparison subjects selected from the national population registries. With data derived from national hospital registries we estimated the standardized hospitalization rate ratios (SHRR) and the mean cumulative count (MCC) of hospital admissions for osteoporotic fractures. To identify subgroups at risk we used Cox regression models to generate hazard ratios (HR) for osteoporotic fractures. Death and new cancer were treated as competing risks.

    Results: The estimated SHRR for the first osteoporotic fracture was 1.41 (95% CI; 1.27‐1.58) but the MCC for recurrent osteoporotic fractures did not differ between the survivors and the comparison group. The SHRR for isolated hip fractures was 2.90 (2.32‐3.63). The adjusted HR for osteoporotic fracture as the first event was 1.53 (1.09‐2.16) if cancer was diagnosed 15‐19 years and 2.10 (1.48‐2.98) for long‐term survivors of CNS tumors. Survivors 15‐19 years at cancer diagnosis and long‐term survivors of CNS tumors were also at higher risk of experiencing a second fracture, HR 3.29 (1.65‐6.55) and HR 2.71 (1.45‐5.05), respectively.

    Conclusions: Childhood cancer survivors are at higher risk of being hospitalized for osteoporotic fractures but the burden of recurrent fractures is not higher. For subgroups at risk, surveillance of bone health and measures to increase bone strength and prevent fractures should be encouraged.

  • 53.
    Oskarsson, Trausti
    et al.
    Department of Pediatric Oncology, Astrid Lindgren Children’s Hospital, Stockholm, Sweden; Childhood Cancer Research Unit, Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Söderhäll, Stefan
    Department of Pediatric Oncology, Astrid Lindgren Children’s Hospital, Stockholm, Sweden; Childhood Cancer Research Unit, Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Arvidson, Johan
    Department of Pediatric Oncology, Uppsala University Hospital, Uppsala, Sweden.
    Forestier, Erik
    Department of Pediatrics, Umeå University Hospital, Umeå, Sweden.
    Montgomery, Scott
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Bottai, Matteo
    Unit of Biostatistics, Institutet för miljömedicin, Karolinska Institutet, Stockholm, Sweden.
    Lausen, Birgitte
    Department of Pediatric Oncology, Rigshospitalet University Hospital, Copenhagen, Denmark.
    Carlsen, Niels
    Department of Pediatrics, Odense University Hospital, Odense, Denmark.
    Hellebostad, Marit
    Department of Pediatrics, Ullevål Hospital, Oslo, Norway.
    Lähteenmäki, Päivi
    Department of Pediatrics, Turku University Hospital, Turku, Finland.
    Saarinen-Pihkala, Ulla M
    Children’s Hospital, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
    Jónsson, Ólafur G
    Children’s Hospital, Landspitali University Hospital, Reykjavik, Iceland.
    Heyman, Mats
    Department of Pediatric Oncology, Astrid Lindgren Children’s Hospital, Stockholm, Sweden; Childhood Cancer Research Unit, Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Relapsed childhood acute lymphoblastic leukemia in the Nordic countries: prognostic factors, treatment and outcome2016In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 101, no 1, p. 68-76Article in journal (Refereed)
    Abstract [en]

    Relapse is the main reason for treatment failure in childhood acute lymphoblastic leukemia. Despite improvements in the upfront therapy, survival after relapse is still relatively poor, especially for high-risk relapses. The aims of this study were to assess outcomes following ALL relapse after common initial Nordic Society of Paediatric Haematology and Oncology protocol treatment; to validate currently used risk stratifications; and identify additional prognostic factors for overall survival. In total 516 of 2735 patients (18.9%) relapsed between 1992 and 2011 and were included. There were no statistically significant differences in outcome between the upfront protocols or between the relapse-protocols used, but an improvement over time was observed. The 5-year overall survival for patients relapsing 2002-2011 was 57.5 +/- 3.4% but 44.7 +/- 3.2% (p<0.001) if relapse occurred 1992-2001. Factors independently predicting mortality after relapse included short duration of first remission, bone marrow involvement, age ≥10 years, unfavorable cytogenetics and Down syndrome. T-cell immunophenotype was not an independent prognostic factor unless in combination with hyperleukocytosis at diagnosis. The outcome for early combined pre-B relapses was unexpectedly poor (5-year overall survival 38.0 +/- 10.6%) which supports the notion that these patients need further risk adjustment. Although survival outcomes have improved over time, development of novel approaches is urgent to increase survival in relapsed childhood acute lymphoblastic leukemia.

  • 54.
    Osterborg, Anders
    et al.
    Dept Haematol, Karolinska Univ Hosp, Stockholm, Sweden.
    Wierda, William G.
    M D Anderson Canc Ctr, Univ Texas, Houston TX, USA; Canc Therapy Res Ctr, San Antonio TX, USA.
    Mayer, Jiri
    Fac Hosp Brno, Dept Internal Med Haematooncol, University Hospital, Brno, Czech Republic.
    Hess, Georg
    Johannes Gutenberg Univ, Mainz, Germany.
    Hillmen, Peter
    Leeds Teaching Hosp, Leeds, England.
    Schetelig, Johannes
    Univ Klinickum Carl Gustav Carus, Dresden, Germany.
    Schuh, Anna
    Churchill Hosp, Oxford, England.
    Smolej, Lukas
    Fac Med Hradec Kralove, Univ Hosp, Hradec Kralove, Czech Republic; Charles Univ Prague, Hradec Kralove, Czech Republic.
    Beck, Christian
    Haematol Onkolog Inst, Moenchengladbach, Germany.
    Dreyfus, Brigitte
    Hop Jean Bernanrd, Poitiers, France.
    Hellman, Andrzej
    Akad Med Gdansku, Gdansk, Poland.
    Kozlowski, Piotr
    Örebro University Hospital.
    Pfreundschuh, Michael
    Univ Saarlandes Kliniken, Homburg, Germany.
    Rizzi, Rita
    Azienda ospedaliero-universitaria consorziale policlinico, Bari, Italy.
    Spacek, Martin
    Fak Nemocnice, Prague, Czech Republic..
    Phillips, Jennifer L.
    GlaxoSmithKline, Collegeville PA, USA.
    Gupta, Ira V.
    Williams, Vanessa
    Glaxo SmithKline, Durham NC, USA.
    Jewell, Roxanne C.
    Glaxo SmithKline, Durham NC ,USA..
    Nebot, Noelia
    Glaxo SmithKline, Durham NC, USA.
    Lisby, Steen
    Genmab AS, Copenhagen, Denmark.
    Dyer, Martin J. S.
    Ernest & Helen Scott Haematol Res Inst, Univ Leicester, Leicester, England.
    Ofatumumab retreatment and maintenance in fludarabine-refractory chronic lymphocytic leukaemia patients2015In: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 170, no 1, p. 40-49Article in journal (Refereed)
    Abstract [en]

    There are limited data on retreatment with monoclonal antibodies (mAb) in patients with chronic lymphocytic leukaemia (CLL). In a pivotal study, ofatumumab (human anti-CD20 mAb) monotherapy demonstrated a 47% objective response rate (ORR) in fludarabine refractory CLL patients. From this study, a subset of 29 patients who had at least stable disease and then progressed were retreated with eight weekly ofatumumab infusions (induction treatment period), followed by monthly infusions for up to 2years (maintenance treatment period). The ORR after 8weeks of induction retreatment was 45% and 24% had continued disease control after maintenance at 52weeks. Efficacy and safety of the retreated patients were compared with their initial results in the pivotal study. Response duration was 241months vs. 68months; time to next therapy was 148months vs. 123months; and progression-free survival was 74months vs. 79months (medians). Upon retreatment, 72% had infusion reactions, mostly Grade 1-2. Three patients had fatal infections. In summary, ofatumumab retreatment and maintenance therapy was feasible in patients with heavily pretreated CLL and appeared to result in more durable disease control than initial ofatumumab treatment in this subset of patients who may have a more favourable disease profile.

  • 55.
    Peng, Xiang
    et al.
    Department of Nephrology, Qingyuan City Hospital of Jinan University, Guangdong, China; Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Kurz, Tino
    Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Grenegård, Magnus
    Örebro University, School of Medicine, Örebro University, Sweden. Department of Medical and Health Sciences, Linköping University, Linköping, Sweden; .
    Segelmark, Mårten
    Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    The neutrophil serine protease PR3 induces shape change of platelets via the Rho/Rho kinase and Ca2+ signaling pathways2014In: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 134, no 2, p. 418-425Article in journal (Refereed)
    Abstract [en]

    Introduction: Proteinase 3 (PR3) is released from neutrophil azurophilic granules and exerts complex effects on the inflammatory process. PR3 catalyzes the degradation of a number of macromolecules, but the consequences on blood cells are less well defined. In the present study, the effect of PR3 on human platelets was thoroughly investigated.

    Methods: The experiments were performed on washed platelets freshly isolated from blood donated by healthy human volunteers. Platelets shape change and aggregation was measured on a Chrono-Log aggregometer. The phosphorylated form of MYPT1 was visualized by immunostaining. Platelet activation was further evaluated by flow cytometry.

    Results: PR3 induced platelet shape change but not aggregation. Flow cytometry analysis showed that PR3 induced no P-selectin expression or binding of fibrinogen to the platelets, and it did not change the activation in response to PAR1- or PAR4-activating peptides or to thrombin. Furthermore, Fura-2 measurement and immuno-blotting analysis, respectively, revealed that PR3 stimulated small intracellular Ca2+ mobilization and Thr696-specific phosphorylation of the myosin phosphatase target subunit 1 (MYPT1). Separate treatment of platelets with the Rho/Rho kinase inhibitor Y-27632 and the intracellular Ca2+ chelator BAPTA/AM reduced the shape change induced by PR3 whereas concurrent treatment completely inhibited it.

    Conclusion: The data shows that the neutrophil protease PR3 is a direct modulator of human platelets and causes shape change through activation of the Rho/Rho kinase and Ca2+ signaling pathways. This finding highlights an additional mechanism in the complex interplay between neutrophils and platelets.

  • 56.
    Singh, Sukhi
    et al.
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Damén, Tor
    Department of Anaesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Cardiothoracic Anaesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Nygren, Andreas
    Department of Anaesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Cardiothoracic Anaesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Shams Hakimi, Caroline
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Ramström, Sofia
    Örebro University, School of Medical Sciences. Cardiovascular Research Centre, School of Medical Sciences, Örebro University, Örebro, Sweden; Department of Clinical Chemistry and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Dellborg, Mikael
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Lindahl, Tomas L.
    Department of Clinical Chemistry and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Hesse, Camilla
    Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Regional Blood Bank, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Jeppsson, Anders
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Cardiothoracic Surgery, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Adrenaline Improves Platelet Reactivity in Ticagrelor-Treated Healthy Volunteers2019In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 119, no 5, p. 735-743Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Administration of agents that enhance platelet reactivity may reduce the perioperative bleeding risk in patients treated with the adenosine diphosphate (ADP)-receptor antagonist ticagrelor. Adrenaline potentiates ADP-induced aggregation and activation in blood samples from ticagrelor-treated patients, but it has not previously been evaluated in vivo.

    METHODS: Ten healthy male subjects were included in an interventional study. A loading dose of ticagrelor (180 mg) was administered, followed 2 hours later by a gradually increased intravenous adrenaline infusion (0.01, 0.05, 0.10 and 0.15 µg/kg/min; 15 minutes at each step). Blood pressure, heart rate, platelet aggregation (impedance aggregometry), platelet activation (flow cytometry), clot formation (rotational thromboelastometry) and adrenaline plasma concentration were determined before and after ticagrelor administration and at the end of each adrenaline step.

    RESULTS:  = 0.007).

    CONCLUSION: Infusion of adrenaline at clinically relevant doses improves in vivo platelet reactivity and clot formation in ticagrelor-treated subjects. Adrenaline could thus potentially be used to prevent perioperative bleeding complications in ticagrelor-treated patients. Studies in patients are necessary to determine the clinical importance of our observations.

    TRIAL REGISTRY NUMBER: ClinicalTrials.gov NCT03441412.

  • 57.
    Singh, Sukhi
    et al.
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Malm, Carl Johan
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Ramström, Sofia
    Örebro University, School of Medical Sciences. Department of Clinical Chemistry and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Hesse, Camilla
    Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Regional Blood Bank, Sahlgrenska University Hospital, Gothenburg, Sweden .
    Jeppsson, Anders
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Adrenaline enhances in vitro platelet activation and aggregation in blood samples from ticagrelor-treated patients2018In: Research and Practice in Thrombosis and Haemostasis, E-ISSN 2475-0379, Vol. 2, no 4, p. 718-725Article in journal (Refereed)
    Abstract [en]

    Background: Temporarily improved platelet reactivity may reduce the bleeding in patients on antiplatelet therapy who have ongoing bleeding or who are in need of acute surgery. Adrenaline can bind to adrenergic alpha(2A)-receptors on platelets and potentially enhance platelet reactivity.

    Objective: To assess if adrenaline can improve adenosine diphosphate (ADP)-induced platelet aggregation and activation in blood samples from patients on dual antiplatelet therapy with acetylsalicylic acid (ASA) and the ADP-receptor antagonist ticagrelor.

    Methods: Blood samples were collected from a total of forty acute coronary syndrome patients on dual antiplatelet therapy with ASA and ticagrelor. ADP-induced platelet aggregation (by impedance aggregometry) and activation (by flow cytometry) were assessed before and after supplementation with adrenaline and/or platelet concentrate.

    Results: Adrenaline supplementation (770 nmol L-1) increased median ADP-induced aggregation from 15 (25-75th percentiles: 10-20) to 26 (18-38) aggregation units. The effect was independent of concomitant platelet supplementation. Adrenaline also increased ADP-induced platelet activation: from 40% (36-54%) to 83% (74-88%) platelets with active fibrinogen receptor (binding PAC-1) and from 13% (7-21%) to 35% (18-50%) P-selectin-expressing platelets.

    Conclusions: Adrenaline potentiated ADP-induced platelet aggregation and activation in blood samples from ticagrelor-treated patients. Adrenaline infusion may be a new method to enhance platelet function in ticagrelor-treated patients who are in need of acute surgery or have ongoing bleeding. In vivo studies are needed to confirm the present results.

  • 58.
    Sodergren, Anna L.
    et al.
    Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Holm, Ann-Charlotte B. Svensson
    Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Lindström, Eva G.
    Department of Medical and Health Sciences, Faculty of Health Sciences, Linkoöping University, Linköping, Sweden.
    Grenegård, Magnus
    Örebro University, School of Medical Sciences. Department of Medical and Health Sciences, Faculty of Health Sciences, Linkoöping University, Linköping, Sweden; Department of Clinical Medicine, Örebro University Hospital, Örebro, Sweden.
    Öllinger, Karin
    Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Thrombin-induced lysosomal exocytosis in human platelets is dependent on secondary activation by ADP and regulated by endothelial-derived substances2016In: Platelets, ISSN 0953-7104, E-ISSN 1369-1635, Vol. 27, no 1, p. 86-92Article in journal (Refereed)
    Abstract [en]

    Exocytosis of lysosomal contents from platelets has been speculated to participate in clearance of thrombi and vessel wall remodelling. The mechanisms that regulate lysosomal exocytosis in platelets are, however, still unclear. The aim of this study was to identify the pathways underlying platelet lysosomal secretion and elucidate how this process is controlled by platelet inhibitors. We found that high concentrations of thrombin induced partial lysosomal exocytosis as assessed by analysis of the activity of released N-acetyl--glucosaminidase (NAG) and by identifying the fraction of platelets exposing the lysosomal-associated membrane protein (LAMP)-1 on the cell surface by flow cytometry. Stimulation of thrombin receptors PAR1 or PAR4 with specific peptides was equally effective in inducing LAMP-1 surface expression. Notably, lysosomal exocytosis in response to thrombin was significantly reduced if the secondary activation by ADP was inhibited by the P2Y(12) antagonist cangrelor, while inhibition of thromboxane A(2) formation by treatment with acetylsalicylic acid was of minor importance in this regard. Moreover, the NO-releasing drug S-nitroso-N-acetyl penicillamine (SNAP) or the cyclic AMP-elevating eicosanoid prostaglandin I-2 (PGI(2)) significantly suppressed lysosomal exocytosis. We conclude that platelet inhibitors that mimic functional endothelium such as PGI(2) or NO efficiently counteract lysosomal exocytosis. Furthermore, we suggest that secondary release of ADP and concomitant signaling via PAR1/4- and P2Y(12) receptors is important for efficient platelet lysosomal exocytosis by thrombin.

  • 59.
    Södergren, A. L.
    et al.
    Linköping University, Linköping, Sweden.
    Ollinger, K.
    Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Linköping University, Linköping, Sweden.
    Subdivision according to size is necessary for correct interpretation of data regarding platelet expression of active GPIIb/IIIa and phosphatidylserine2013In: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 11, no S1, p. 498-498Article in journal (Refereed)
  • 60.
    Södergren, A.L.
    et al.
    Linlöåin University, Linköping, Sweden.
    Ramström, Sofia
    Örebro University, School of Medical Sciences. Linköping University, Linköping, Sweden.
    Platelet reactivity and receptor density in platelets with different MPV2017In: Research and Practice in Thrombosis and Haemostasis, ISSN 2475-0379, Vol. 1, no S1, p. 1235-1236, article id PB 1273Article in journal (Refereed)
  • 61.
    Tynngård, N.
    et al.
    Transfusion Medicine, Clinical and Experimental Medicine, Linköpings University, Linköping, Sweden.
    Ramström, Sofia
    Clinical Chemistry, Clinical and Experimental Medicine, Linköpings University, Linköping, Sweden.
    Berlin, G.
    Transfusion Medicine, Clinical and Experimental Medicine, Linköpings University, Linköping, Sweden.
    Adhesion Capacity of Platelets During Storage: Evaluation of a Flow Cytometric Adhesion Assay2012In: Transfusion, ISSN 0041-1132, E-ISSN 1537-2995, Vol. 52, no S3, p. 70A-70AArticle in journal (Refereed)
  • 62.
    Vaht, Krista
    et al.
    Section of Hematology and Coagulation, Sahlgrenska University Hospital, Gothenburg, Sweden; Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.
    Göransson, Magnus
    Section of Hematology and Coagulation, Sahlgrenska University Hospital, Gothenburg, Sweden; Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.
    Carlson, Kristina
    Department of Hematology, Uppsala University Hospital, Uppsala, Sweden.
    Isaksson, Cecilia
    Department of Hematology, Cancer Centre, University Hospital, Uppsala, Sweden.
    Lenhoff, Stig
    Department of Hematology, Skåne University Hospital, Lund University, Malmö, Sweden.
    Sandstedt, Anna
    Department of Hematology, Linköping University Hospital, Linköping, Sweden.
    Uggla, Bertil
    Örebro University, School of Medical Sciences. Department of Medicine, Section of Hematology, , Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Winiarski, Jacek
    Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Ljungman, Per
    Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Brune, Mats
    Section of Hematology and Coagulation, Sahlgrenska University Hospital, Gothenburg, Sweden; Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.
    Andersson, Per-Ola
    South Älvsborg Hospital, Borås, Sweden; Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.
    Incidence and outcome of acquired aplastic anemia: real-world data from patients diagnosed in Sweden from 2000-20112017In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 102, no 10, p. 1683-1690Article in journal (Refereed)
    Abstract [en]

    A plastic anemia is a rare life-threatening disease. However, since the introduction of immunosuppressive therapy and allogeneic stem cell transplantation, the outcome has improved considerably, and the 5-year survival is reported to be 70-80% in selected patient cohorts. Yet, contemporary population-based data on incidence and survival are lacking. We performed a national retrospective study to determine the incidence, treatment, and survival of patients with aplastic anemia diagnosed in Sweden from 2000-2011. Patients were included via the National Patient Registry, and diagnosed according to the Camitta criteria. In total, 257 confirmed cases were identified, with an overall incidence of 2.35 (95% CI: 2.06-2.64) cases per million inhabitants per year. Median age was 60 years (range: 2-92), and median follow up was 76 (0-193) months. Primary treatments included immunosuppressive therapy (63%), allogenic stem cell transplantation (10%), or single-agent cyclosporine/no specific therapy (27%). The 5-year survival was 90.7% in patients aged 0-18 years, 90.5% in patients aged 19-39 years, 70.7% in patients aged 40-59 years, and 38.1% in patients aged ≥60 years. Multivariate analysis showed that age (both 40-59 and ≥60 age groups), very severe aplastic anemia and single-agent cyclosporine/no specific therapy were independent risk factors for inferior survival. In conclusion, younger aplastic anemia patients experience a very good long-term survival, while that of patients ≥60 years in particular remains poor. Apparently, the challenge today is to improve the management of older aplastic anemia patients, and prospective studies to address this medical need are warranted.

  • 63.
    Vaht, Krista
    et al.
    Section of Haematology and Coagulation, Sahlgrenska University Hospital, Gothenburg, Sweden; Institute of Medicine, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden.
    Göransson, Magnus
    Department of Pediatrics, The Queen Silvia Children's Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Carlson, Kristina
    Department of Haematology, Uppsala University Hospital, Uppsala, Sweden.
    Isaksson, Cecilia
    Department of Haematology, Cancer Centre, University Hospital, Umeå, Sweden.
    Lenhoff, Stig
    Department of Haematology, Skåne University Hospital, Lund University, Lund, Sweden.
    Sandstedt, Anna
    Department of Haematology, Linköping University Hospital, Linköping, Sweden.
    Uggla, Bertil
    Örebro University, School of Medical Sciences. Section of Haematology Department of Medicine.
    Winiarski, Jacek
    Astrid Lindgren Children's Hospital, Karolinska Institutet, Karolinska University Hospital and CLINTEC, Stockholm, Sweden.
    Ljungman, Per
    Centre of Allogeneic Stem Cell Transplantation Unit (CAST), Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Brune, Mats
    Section of Haematology and Coagulation, Sahlgrenska University Hospital, Gothenburg, Sweden; Institute of Medicine, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden.
    Andersson, Per-Ola
    Institute of Medicine, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden; Department of Medicine, Södra Älvsborg Hospital Borås, Borås, Sweden.
    Low response rate to ATG-based immunosuppressive therapy in very severe aplastic anaemia: A Swedish nationwide cohort study2018In: European Journal of Haematology, ISSN 0902-4441, E-ISSN 1600-0609, Vol. 100, no 6, p. 613-620Article in journal (Refereed)
    Abstract [en]

    Objectives: Antithymocyte globulin (ATG)-based immunosuppression remains a cornerstone in aplastic anaemia (AA) treatment. However, most ATG studies are not population-based and knowledge about real-world results concerning response and outcome could offer important information for treating physicians.

    Methods: We have recently performed a nationwide retrospective cohort study on all AA patients diagnosed in Sweden in 2000–2011 and now present treatment and outcome data on patients receiving first-line ATG. In total, 158 patients showed a 47.0% response rate which was similar in all age groups (range 41.5%-51.7%) with no difference regarding ATG formulation. The response was significantly associated with severity grade—especially at time of treatment initiation: very severe (VSAA) 22.7%; severe (SAA) 54.5% (P <.001); and non-severe 88.5% (P <.001). A logistic regression-based predictive model indicated that VSAA patients with an absolute reticulocyte count <25 × 109/L had only a 19% probability of response. In a multivariable analysis, age and VSAA at the time of treatment were the independent factors for inferior survival.

    Conclusions: Real-world VSAA patients respond poorly to ATG which indicates the need for a different treatment approach. Our findings suggest that age alone should not be a discriminating factor for administering ATG treatment.

  • 64.
    Vedin, Inger
    et al.
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Cederholm, Tommy
    Department of Public Health and Caring Sciences, Uppsala University Hospital, Uppsala, Sweden; Division of Clinical Nutrition and Metabolism, Uppsala University Hospital, Uppsala, Sweden .
    Freund-Levi, Yvonne
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Basun, Hans
    Department of Public Health and Caring Sciences, Uppsala University Hospital, Uppsala, Sweden; Division of Geriatrics, Uppsala University Hospital, Uppsala, Sweden .
    Garlind, Anita
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Irving, Gerd Faxén
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Eriksdotter-Jönhagen, Maria
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Wahlund, Lars-Olof
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Dahlman, Ingrid
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Palmblad, Jan
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden .
    Effects of DHA-rich n-3 fatty acid supplementation on gene expression in blood mononuclear leukocytes: the OmegAD study2012In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 7, no 4, article id e35425Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Dietary fish oil, rich in n-3 fatty acids (n-3 FAs), e.g. docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), regulate inflammatory reactions by various mechanisms, e.g. gene activation. However, the effects of long-term treatment with DHA and EPA in humans, using genome wide techniques, are poorly described. Hence, our aim was to determine the effects of 6 mo of dietary supplementation with an n-3 FA preparation rich in DHA on global gene expression in peripheral blood mononuclear cells.

    METHODS AND FINDINGS: In the present study, blood samples were obtained from a subgroup of 16 patients originating from the randomized double-blind, placebo-controlled OmegAD study, where 174 Alzheimer disease (AD) patients received daily either 1.7 g of DHA and 0.6 g EPA or placebo for 6 months. In blood samples obtained from 11 patients receiving n-3 FA and five placebo, expressions of approximately 8000 genes were assessed by gene array. Significant changes were confirmed by real-time PCR. At 6 months, the n-3 FAs group displayed significant rises of DHA and EPA plasma concentrations, as well as up- and down-regulation of nine and ten genes, respectively, was noticed. Many of these genes are involved in inflammation regulation and neurodegeneration, e.g. CD63, MAN2A1, CASP4, LOC399491, NAIP, and SORL1 and in ubiqutination processes, e.g. ANAPC5 and UBE2V1. Down-regulations of ANAPC5 and RHOB correlated to increases of plasma DHA and EPA levels.

    CONCLUSIONS: We suggest that 6 months of dietary n-3 FA supplementation affected expression of genes that might influence inflammatory processes and could be of significance for AD.

    TRIAL REGISTRATION: ClinicalTrials.gov NCT00211159.

  • 65.
    Vigren, P.
    et al.
    Linköping University Hospital, Linköping, Sweden.
    Ström, Jakob O.
    Linköping University, Linköping, Sweden.
    Petrini, P.
    Karolinska University Hospital, Stockholm, Sweden.
    Callander, M.
    Linköping University, Linköping, Sweden.
    Theodorsson, A.
    Linköping University Hospital, Linköping, Sweden.
    Treatment of spontaneous intracerebral haemorrhage in Glanzmann's thrombasthenia2012In: Haemophilia, ISSN 1351-8216, E-ISSN 1365-2516, Vol. 18, no 5, p. e381-e383Article in journal (Refereed)
  • 66.
    Walker, Alex J.
    et al.
    Div Epidemiol & Publ Hlth, City Hosp Nottingham, Univ Nottingham, Nottingham, England; Nottingham Digestive Diseases Centre, National Institute for Health Research (NIHR) Biomed Res Unit, Nottingham, England.
    Grainge, Matthew J.
    Div Epidemiol & Publ Hlth, City Hosp Nottingham, Univ Nottingham, Nottingham, England; Nottingham Digestive Diseases Centre, National Institute for Health Research (NIHR) Biomed Res Unit, Nottingham, England.
    Card, Tim R.
    Div Epidemiol & Publ Hlth, City Hosp Nottingham, Univ Nottingham, Nottingham, England; Nottingham Digestive Diseases Centre, National Institute for Health Research (NIHR) Biomed Res Unit, Nottingham, England.
    West, Joe
    Div Epidemiol & Publ Hlth, City Hosp Nottingham, Univ Nottingham, Nottingham, England; Nottingham Digestive Diseases Centre, National Institute for Health Research (NIHR) Biomed Res Unit, Nottingham, England.
    Ranta, Susanna
    Childhood Canc Res Unit, Karolinska Inst, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet Sockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Venous thromboembolism in children with cancer: A population-based cohort study2014In: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 133, no 3, p. 340-344Article in journal (Refereed)
    Abstract [en]

    Introduction: Cancer is a known risk factor for venous thromboembolism (VTE) in adults, but population-based data in children are scarce.

    Materials and methods: We conducted a cohort study utilising linkage of the Clinical Practice Research Database (primary care), Hospital Episodes Statistics (secondary care), UK Cancer Registry data and Office for National Statistics cause of death data. From these databases, we selected 498 children with cancer diagnosed between 1997 and 2006 and 20,810 controls without cancer. We calculated VTE incidence rates in children with cancer vs. controls, and hazard ratios (HRs) using Cox regression.

    Results: We identified four VTE events in children with cancer compared with four events in the larger control population corresponding to absolute risks of 1.52 and 0.06 per 1000 person-years respectively. The four children with VTE and cancer were diagnosed with hematological, bone or non-specified cancer. Childhood cancer was hence associated with a highly increased risk of VTE (HR adjusted for age and sex: 28.3; 95% CI = 7.0-114.5).

    Conclusions: Children with cancer are at increased relative risk of VTE compared to those without cancer. Physicians could consider thromboprophylaxis in children with cancer to reduce their excess risk of VTE however the absolute risk is extremely small and the benefit gained therefore would need to be balanced against the risk invoked of implementing such a strategy.

    Novelty & Impact Statements: While there is a reasonable level of knowledge about the risk of VTE in adult populations, it is not well known whether this risk is reflected in paediatric patients. We found a substantial increase in risk of VTE in children with cancer compared to a child population without cancer. While this finding is important, the absolute risk of VTE is still low and must be balanced with the risks of anticoagulation. (C) 2014 The Authors. Published by Elsevier Ltd. All rights reserved.

  • 67. Welander, Edward
    et al.
    Åström, Maria
    Örebro University, School of Medical Sciences. Örebro University, School of Health Sciences.
    Enonge Fotabe, Leslie
    Kardeby, Caroline
    Örebro University, School of Medical Sciences.
    Tina, Elisabet
    Örebro University, School of Medical Sciences.
    Elgbratt, Kristina
    Örebro University, School of Health Sciences.
    Pourlofti, Arvid
    Abawi, Akram
    Romild, Alma
    Kruse, Robert
    Örebro University, School of Medical Sciences.
    Repsilber, Dirk
    Örebro University, School of Medical Sciences.
    Crafoord, Jakob
    Ahlstrand, Erik
    Ivarsson, Mikael
    Örebro University, School of Health Sciences.
    Integrated analysis indicates reciprocal immune response dysregulations between bone marrow multipotent stromal cells and granulocytes at the mRNA but not at the protein level in myelofibrosis2018Conference paper (Refereed)
  • 68.
    Åström, Maria
    Dpt of medicine and laboratory medicine, Örebro University Hospital, Örebro, Sweden.
    Clinical cases: Presentation, diagnosis, treatment and follow-up: Case 2 - Chuvash polycythemia2015In: Congenital Erythrocytosis and Hereditary Thrombocytosis: Clinical presentation, diagnosis, treatment and follow-up. A practical guide with clinical cases. / [ed] Sylvie Hermouet, Portugal: European cooperation in science and technology , 2015Chapter in book (Other academic)
  • 69.
    Åström, Maria
    Örebro University, School of Medical Sciences. Örebro University Hospital.
    Undersökningar av X-bunden trombocytopeni med talassemi (XLTT) och jämförelser med andra former av myelofibros2010In: Oss hematologer emellan, Vol. 4, no 22, p. 39-40Article in journal (Other academic)
  • 70.
    Åström, Maria
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Hahn-Strömberg, Victoria
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Zetterberg, Eva
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Vedin, Inger
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Merup, Mats
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Palmblad, Jan
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis2015In: American Journal of Hematology, ISSN 0361-8609, E-ISSN 1096-8652, Vol. 90, no 3, p. E44-E48Article in journal (Refereed)
    Abstract [en]

    X-linked thrombocytopenia with thalassemia (XLTT) is caused by the mutation 216R > Q in exon 4 of the GATA1 gene. Male hemizygous patients display macrothrombocytopenia, splenomegaly, and a β-thalassemia trait. We describe two XLTT families where three males were initially misdiagnosed as having primary myelofibrosis (PMF) and all five investigated males showed mild-moderate bone marrow (BM) reticulin fibrosis. Comparative investigations were performed on blood samples and BM biopsies from males with XLTT, PMF patients and healthy controls. Like PMF, XLTT presented with high BM microvessel density, low GATA1 protein levels in megakaryocytes, and elevated blood CD34+ cell counts. But unlike PMF, the BM microvessel pericyte coverage was low in XLTT, and no collagen fibrosis was found. Further, as evaluated by immunohistochemistry, expressions of the growth factors VEGF, AGGF1, and CTGF were low in XLTT megakaryocytes and microvessels but high in PMF. Thus, although the reticulin fibrosis in XLTT might simulate PMF, opposing stromal and megakaryocyte features may facilitate differential diagnosis. Additional comparisons between these disorders may increase the understanding of mechanisms behind BM fibrosis in relation to pathological megakaryopoiesis.

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