Thrombosis and Haemostasis Journal Impact Factor & Information

Publisher: International Society on Thrombosis and Haemostasis, Schattauer

Journal description

Thrombosis and Haemostasis publishes original papers only, as well as reports, news and inside information about current research and science. In addition, it presents innovative results of scientific research which will be the practitioner's tool of tomorrow. Thrombosis and Haemostasis is read by haematologists, angiologists, cardiologists, surgeons, gynaecologists, internal specialists and laboratory physicians. Thrombosis and Haemostasis is published monthly. It is the official journal of the International Society on Thrombosis and Haemostasis (ISTH). All members of the Society receive Thrombosis and Haemostasis as part of their Society membership.

Current impact factor: 4.98

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.984
2013 Impact Factor 5.76
2012 Impact Factor 6.094
2011 Impact Factor 5.044
2010 Impact Factor 4.701
2009 Impact Factor 4.451
2008 Impact Factor 3.803
2007 Impact Factor 3.501
2006 Impact Factor 2.803
2005 Impact Factor 3.056
2004 Impact Factor 3.413
2003 Impact Factor 4.95
2002 Impact Factor 4.357
2001 Impact Factor 4.91
2000 Impact Factor 4.372
1999 Impact Factor 4.983
1998 Impact Factor 3.726
1997 Impact Factor 4.582
1996 Impact Factor 4.267
1995 Impact Factor 4.464
1994 Impact Factor 4.125
1993 Impact Factor 4.352
1992 Impact Factor 4.481

Impact factor over time

Impact factor

Additional details

5-year impact 4.45
Cited half-life 8.10
Immediacy index 1.25
Eigenfactor 0.03
Article influence 1.49
Website Thrombosis & Haemostasis website
Other titles Thrombosis and haemostasis
ISSN 0340-6245
OCLC 2208259
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On authors personal website, institutional repository or centrally organized repository
    • On a non-profit server
    • Publisher copyright and source must be acknowledged with set statement (see policy)
    • Publisher's version/PDF cannot be used
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Annual costs for venous thromboembolism (VTE) have been defined within the United States (US) demonstrating a large opportunity for cost savings. Costs for the European Union-28 (EU-28) have never been defined. A literature search was conducted to evaluate EU-28 cost sources. Median costs were defined for each cost input and costs were inflated to 2014 Euros (€) in the study country and adjusted for Purchasing Power Parity between EU countries. Adjusted costs were used to populate previously published cost-models based on adult incidence-based events. In the base model, annual expenditures for total, hospital-associated, preventable, and indirect costs were €1.5-2.2 billion, €1.0-1.5 billion, €0.5-1.1 billion and €0.2-0.3 billion, respectively (indirect costs: 12 % of expenditures). In the long-term attack rate model, total, hospital-associated, preventable, and indirect costs were €1.8-3.3 billion, €1.2-2.4 billion, €0.6-1.8 billion and €0.2-0.7 billion (indirect costs: 13 % of expenditures). In the multiway sensitivity analysis, annual expenditures for total, hospital-associated, preventable, and indirect costs were €3.0-8.5 billion, €2.2-6.2 billion, €1.1-4.6 billion and €0.5-1.4 billion (indirect costs: 22 % of expenditures). When the value of a premature life-lost increased slightly, aggregate costs rose considerably since these costs are higher than the direct medical costs. When evaluating the models aggregately for costs, the results suggests total, hospital-associated, preventable, and indirect costs ranging from €1.5-13.2 billion, €1.0-9.7 billion, €0.5-7.3 billion and €0.2-6.1 billion, respectively. Our study demonstrates that VTE costs have a large financial impact upon the EU-28's healthcare systems and that significant savings could be realised if better preventive measures are applied.
    Thrombosis and Haemostasis 11/2015; 115(3). DOI:10.1160/TH15-08-0670
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    ABSTRACT: Tissue factor pathway inhibitor (TFPI) down-regulates the extrinsic coagulation pathway by inhibiting FXa and FVIIa. Both TFPI and FXa interact with several plasma proteins (e. g. prothrombin, FV/FVa, protein S) and non-proteinaceous compounds (e. g. phospholipids, heparin). It was our aim to investigate effects of ligands that bind to FXa and TFPI on FXa inhibition by full-length TFPI (designated TFPI) and truncated TFPI (TFPI1-150). Inhibition of FXa by TFPI and TFPI1-150 and effects of phospholipids, heparin, prothrombin, FV, FVa, and protein S thereon was quantified from progress curves of conversion of the FXa-specific chromogenic substrate CS11-(65). Low concentrations negatively charged phospholipids (~10 µM) already maximally stimulated (up to 5- to 6-fold) FXa inhibition by TFPI. Unfractionated heparin at concentrations (0.2-1 U/ml) enhanced FXa inhibition by TFPI ~8-fold, but impaired inhibition at concentrations > 1 U/ml. Physiological protein S and FV concentrations both enhanced FXa inhibition by TFPI 2- to 3-fold. In contrast, thrombin-activated FV (FVa) impaired the ability of TFPI to inhibit FXa. FXa inhibition by TFPI1-150 was not affected by FV, FVa, protein S, phospholipids and heparin. TFPI potently inhibited FXa-catalysed prothrombin activation in the absence of FVa, but hardly inhibited prothrombin activation in the presence of thrombin-activated FVa. In conclusion, physiological concentrations TFPI (0.25-0.5 nM TFPI) inhibit FXa with a t1/2 between 3-15 minutes. Direct FXa inhibition by TFPI is modulated by physiological concentrations prothrombin, FV, FVa, protein S, phospholipids and heparin indicating the importance of these modulators for the in vivo anticoagulant activity of TFPI.
    Thrombosis and Haemostasis 11/2015; 115(3). DOI:10.1160/TH15-04-0354
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    ABSTRACT: Prior studies have shown an association between high on-clopidogrel platelet reactivity (PR) and the risk of major adverse cardiovascular events (MACE). However, large intervention trials on PR-tailored treatments have been neutral. The role and usefulness of PR with regard to levels of cardiovascular risk are unclear. We undertook a systematic review and meta-analysis of individual patient data on MACE outcomes (acute coronary syndromes (ACS), ischaemic strokes, and vascular deaths) in relation to PR and its interaction with cardiovascular risk levels. PR was determined using ADP-induced light transmission aggregometry with a primary concentration of 20 µM ADP.Thirteen prospective studies totaled 6,478 clopidogrel-treated patients who experienced 421 MACE (6.5 %) during a median follow-up of 12 months. The strength of the association between the risk of MACE and PR increased significantly (p=0.04) with the number of risk factors present (age> 75 years, ACS at inclusion, diabetes, and hypertension). No association was detected in patients with no risk factor (p=0.48). In patients presenting one risk factor, only high-PR was associated with an increased risk of MACE (HR 3.2, p=0.001). In patients presenting ≥ 2 risk factors, the increase of risk started from medium-PR (medium-PR: HR=2.9, p=0.0004; high-PR: HR=3.7, p=0.0003). PR allowed the reclassification of 44 % of the total population to a different risk level for the outcome of MACE, mostly in intermediate or high risk patients. In conclusion, the magnitude of the association between PR and MACE risk is strongly dependent on the level of cardiovascular risk faced by patients on clopidogrel.
    Thrombosis and Haemostasis 11/2015; 115(3). DOI:10.1160/TH15-09-0742
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    ABSTRACT: We performed a meta-analysis about the prevalence of left atrial thrombus (LAT) in patients with atrial fibrillation (AF) undergoing trans-esophageal echocardiography (TEE). Studies reporting on LAT presence in AF patients were systematically searched in the PubMed, Web of Science, Scopus and EMBASE databases and the pooled LAT prevalence was evaluated as weighted mean prevalence (WMP). Seventy-two studies (20,516 AF patients) showed a LAT WMP of 9.8 % (95 %CI: 7.6 %-12.5 %). LAT presence was associated with a higher age (mean difference: 2.56, 95 %CI: 1.49-3.62), and higher prevalence of female gender (OR: 1.35, 95 %CI: 1.04-1.75), hypertension (OR: 1.78, 95 %CI: 1.38-2.30), diabetes mellitus (OR: 1.86, 95 %CI: 1.33-2.59) and chronic heart failure (OR: 3.67, 95 %CI: 2.40-5.60). Overall, LAT patients exhibited a higher CHADS2-score (mean difference 0.88, 95 %CI: 0.68-1.07) and a higher risk of stroke/systemic embolism (OR: 3.53, 95 %CI: 2.24-5.56) compared with those without LAT. A meta-regression showed an inverse association between LAT prevalence and the presence of anticoagulation (Z-value: -7.3, p< 0.001). Indeed, studies in which 100 % of patients received oral anticoagulation reported a 3.4 % WMP of LAT (95 %CI: 1.3 %-8.7 %), whereas studies in which 0 % of patients received anticoagulation showed a LAT WMP of 7.4 % (95 %CI: 2.3 %-21.5 %). Our data suggest that LAT is present in ≍10 % of AF patients, and is associated with a 3.5-fold increased risk of stroke/systemic embolism. Interestingly, LAT is also reported in some of patients receiving anticoagulation. The implementation of the screening of LAT in AF patients before cardioversion/ablation could be useful for the prevention of vascular events.
    Thrombosis and Haemostasis 11/2015; 115(3). DOI:10.1160/TH15-07-0532
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    ABSTRACT: Rupture of atherosclerotic plaques is the main cause of acute cardiovascular events. Animal models of plaque rupture are rare but essential for testing new imaging modalities to enable diagnosis of the patient at risk. Moreover, they enable the design of new treatment strategies to prevent plaque rupture. Several animal models for the study of atherosclerosis are available. Plaque rupture in these models only occurs following severe surgical or pharmaceutical intervention. In the process of plaque rupture, composition, biology and mechanics each play a role, but the latter has been disregarded in many animal studies. The biomechanical environment for atherosclerotic plaques is comprised of two parts, the pressure-induced stress distribution, mainly - but not exclusively - influenced by plaque composition, and the strength distribution throughout the plaque, largely determined by the inflammatory state. This environment differs considerably between humans and most animals, resulting in suboptimal conditions for plaque rupture. In this review we describe the role of the biomechanical environment in plaque rupture and assess this environment in animal models that present with plaque rupture.
    Thrombosis and Haemostasis 11/2015; 115(3). DOI:10.1160/TH15-07-0614
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    ABSTRACT: Addition of a potent P2Y12 inhibitor to aspirin is the standard therapy for non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients undergoing percutaneous coronary intervention (PCI). Glycoprotein IIb/IIIa inhibitor, together with antiplatelet therapy, may be considered as part of initial therapy in NSTE-ACS patients with high-risk features. This study investigated the antiplatelet effect of ticagrelor loading dose (LD) versus tirofiban bolus injection with a post-bolus infusion on top of aspirin among NSTE-ACS patients planned to PCI. NSTE-ACS patients were randomised to receive either ticagrelor (n = 47) or tirofiban (n = 48). Platelet reactivity was assessed by light transmittance aggregometry at 0, 2, 8, and 24 hours (h) after treatment initiation. Primary endpoint was inhibition of platelet aggregation (IPA, 20 µM ADP, final extent) at 2 h after LD therapy, with a non-inferiority margin of 10 %. The prevalence of high on-treatment platelet reactivity (HPR) was also compared at 0, 2, 8, and 24 h. The mean difference in IPA between ticagrelor and tirofiban was -9.9 % (95 % confidence interval: -25.7 % to 5.9 %) at 2 h, -1.6 % (-8.0 % to 4.8 %) at 8 h, and -3.3 % (-18.4 % to 12.0 %) at 24 h. The prevalence of HPR did not differ between the two groups at any time point (all p values ≥ 0.059), which was almost abolished by 8 h post-LD (< 5 %). In conclusion, the antiplatelet effect during the early phase (~2 h) after ticagrelor LD appeared to be relatively strong, but it did not reach that of tirofiban in NSTE-ACS patients.
    Thrombosis and Haemostasis 11/2015; 115(1). DOI:10.1160/TH15-02-0180
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    ABSTRACT: The role of anticoagulants and antiplatelet agents in tumour growth and prognosis is not new, and currently under intense investigation. Some randomised data strongly suggest that this association exists, but it is complex, and not necessarily pointed at the same direction. The potential mechanisms responsible for such harmful association include a direct hazard of novel antithrombotics on cancer, indirect promotion of tumour growth, easier metastatic dissemination due to instability of platelet-tumour cell aggregates, or/and inability to keep cancer cells locally in situ are considered. The latest randomised evidence ultimately rejected the drug-specific cancer risks, clearly indicating the class-effect. In lay terms "cancers follow bleeding", which seems to be true for antithrombotic agents in general. Significant excess of solid cancers which was similar after prasugrel in TRITON, and with vorapaxar in TRACER trials was confirmed by the FDA reviews. Later, extra cancer deaths reported following clopidogrel and prasugrel in DAPT, and after ticagrelor in PEGASUS are also of concern. However, there are remaining controversies with regard to published cancer risks after ticagrelor (PLATO), or another vorapaxar trial (TRA2P), while full disclosure of separate clopidogrel and prasugrel cancer data in DAPT is still lacking. In short, if we apply moderate antiplatelet strategies for over two years, or aggressive regimens including triple therapy for much less than one year, the solid cancer risks emerge. Currently, more delicate platelet inhibition, and shorter exposure to dual oral antiplatelet agents should prevail.
    Thrombosis and Haemostasis 11/2015; 114(6). DOI:10.1160/TH15-01-0077

  • Thrombosis and Haemostasis 11/2015; 114(6). DOI:10.1160/TH15-11-0842

  • Thrombosis and Haemostasis 11/2015; 114(6). DOI:10.1160/TH15-10-0825
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    ABSTRACT: A few trials so far have evaluated the effectiveness of algorithms designed to calculate doses in oral anticoagulant therapy, with negative or contradictory results. We compared a genotype-guided algorithm vs physician management for the initiation of acenocoumarol. In a two-arm, prospective, randomised study with patients with atrial fibrillation who started therapy, the first dose was administered to all patients according to the physician's criteria. At 72 hours, the corresponding dose was calculated based on INR in the standard care group (SC, N=92), whereas genetic data (VKORC1, CYP2C9 and CYP4F2) were also considered for the genotype-guided dosing (pharmacogenetic) group (PGx, N=87) by using an algorithm previously validated in 2,683 patients. The primary outcomes were: patients with steady dose, the time needed to reach the same and the percentage of therapeutic INRs. After 90 days, 25 % of the SC and 39 % of the PGx patients reached the steady dose (p=0.038). Kaplan-Meier analysis showed that PGx group needed fewer days to reach therapeutic INR (p=0.033). Additionally, PGx had a higher percentage of therapeutic INRs than SC patients (50 % and 45 %, respectively) (p=0.046). After six months the proportion of steadily anticoagulated patients remained significantly higher in PGx (p=0.010). In conclusion, genotype-guided dosing was associated with a higher percentage of patients with steady dose than routine practice when starting oral anticoagulation with acenocoumarol.
    Thrombosis and Haemostasis 11/2015; 115(1). DOI:10.1160/TH14-09-0814
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    ABSTRACT: The prevalence of both vitamin D deficiency and venous thromboembolism (VTE) is important in the elderly. Previous studies have provided evidence for a possible association between vitamin D status and the risk of VTE. Thus, we aimed to investigate the association between vitamin D levels and VTE in the population aged 75 and over included in the EDITH case-control study. The association between vitamin D status and VTE was analysed. We also analysed the monthly and seasonal variations of VTE and vitamin D. Between May 2000 and December 2009, 340 elderly patients (mean age 81.5 years, 32 % men) with unprovoked VTE and their controls were included. The univariate and multivariate analysis found no significant association between serum levels of vitamin D and the risk of unprovoked VTE. In the unadjusted analysis, a higher BMI was statistically associated with an increased risk of VTE (OR 1.09; 95 % CI 1.05-1.13) whereas a better walking capacity and living at home were associated with a decreased rate of VTE: OR 0.57; 95 % CI 0.36-0.90 and 0.40; 95 % CI 0.25-0.66, respectively. Although not significant, more VTE events occurred during winter (p=0.09). No seasonal variations of vitamin D levels were found (p=0.11). In conclusion, in contrast with previous reports our findings suggest that vitamin D is not associated with VTE in the elderly population.
    Thrombosis and Haemostasis 11/2015; 115(1). DOI:10.1160/TH15-02-0148
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    ABSTRACT: The study aim was to identify predictive factors for major bleeding in patients receiving the novel oral factor Xa inhibitor rivaroxaban or enoxaparin-vitamin K antagonists (VKAs) for the treatment of acute symptomatic venous thromboembolism. We analysed data from patients included in the phase III EINSTEIN DVT and EINSTEIN PE studies. Factors associated with major bleeding events were assessed with best subset variable selection using Cox proportional hazards regression model. Three time windows were considered, i. e. the initial three weeks, after the third week onwards, and the entire duration of the anticoagulant treatment. Model discrimination was estimated using the C-statistic and validated internally by bootstrap techniques. Major bleeding occurred in 40 (1.0 %) of 4130 patients receiving rivaroxaban and in 72 (1.7 %) of 4116 receiving enoxaparin/VKAs, with 44 % of the major bleeding events occurring in the first three weeks of treatment. Significant risk factors for major bleeding were older age, black race, low haemoglobin concentrations, active cancer, and antiplatelet or non-steroidal anti-inflammatory drug therapy. The discrimination of the model for major bleeding was high for the first three weeks (C-statistic 0.73), from the fourth week onwards (C-statistic 0.68), and the entire period of anticoagulant treatment (C-statistic 0.74). This analysis identified risk factors for major bleeding in patients receiving the novel oral anticoagulant rivaroxaban or enoxaparin/VKAs for the treatment of acute venous thromboembolism. The prognostic model based on the combination of identified risk factors may be informative to estimate the risk of major bleeding both during the initial and later phases of anticoagulation.
    Thrombosis and Haemostasis 10/2015; 115(2). DOI:10.1160/TH15-06-0474
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    ABSTRACT: Platelets contain and release matrix metalloproteinase-2 (MMP-2) that in turn potentiates platelet aggregation. Platelet deposition on a damaged vascular wall is the first, crucial, step leading to thrombosis. Little is known about the effects of MMP-2 on platelet activation and adhesion under flow conditions. We studied the effect of MMP-2 on shear-dependent platelet activation using the O`Brien filtration system, and on platelet deposition using a parallel-plate perfusion chamber. Preincubation of human whole blood with active MMP-2 (50 ng/ml, i. e. 0.78 nM) shortened filter closure time (from 51.8 ± 3.6 sec to 40 ± 2.7 sec, p< 0.05) and increased retained platelets (from 72.3 ± 2.3 % to 81.1 ± 1.8 %, p< 0.05) in the O'Brien system, an effect prevented by a specific MMP-2 inhibitor. High shear stress induced the release of MMP-2 from platelets, while TIMP-2 levels were not significantly reduced, therefore, the MMP-2/TIMP-2 ratio increased significantly showing enhanced MMP-2 activity. Preincubation of whole blood with active MMP-2 (0.5 to 50 ng/ml, i.e 0.0078 to 0.78 nM) increased dose-dependently human platelet deposition on collagen under high shear-rate flow conditions (3000 sec-1) (maximum +47.0 ± 11.9 %, p< 0.05, with 50 ng/ml), while pre-incubation with a MMP-2 inhibitor reduced platelet deposition. In real-time microscopy studies, increased deposition of platelets on collagen induced by MMP-2 started 85 sec from the beginning of perfusion, and was abolished by a GPIIb/IIIa antagonist, while MMP-2 had no effect on platelet deposition on fibrinogen or VWF. Confocal microscopy showed that MMP-2 enhances thrombus volume (+20.0 ± 3.0 % vs control) rather than adhesion. In conclusion, we show that MMP-2 potentiates shear-induced platelet activation by enhancing thrombus formation.
    Thrombosis and Haemostasis 10/2015; 115(2). DOI:10.1160/TH15-04-0300
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    ABSTRACT: Introduction: Increased plasma levels of von Willebrand factor Antigen (vWF:Ag) are associated with high risk of coronary artery disease. The effect of statin therapy on vWF:Ag levels remains uncertain. Therefore the aim of this meta-analysis was to evaluate the effect of statin therapy on vWF:Ag Levels. Methods: A systematic multiple-database search was carried out to identify RCTs that investigated the effect of statins on plasma vWF:Ag levels. Results: Random-effect meta-analysis of 21 treatment arms revealed a significant decrease in plasma vWF:Ag levels following statin therapy (SMD:-0.54, 95%CI: -0.87, -0.21, p=0.001). In subgroup analyses, the greatest effect was observed with simvastatin (SMD:-1.54, 95%CI: -2.92, -0.17, p=0.028) and pravastatin (SMD:-0.61, 95%CI: -1.18, -0.04, p=0.035), but not with fluvastatin (SMD:-0.34, 95%CI: -0.69, 0.02, p=0.065), atorvastatin (SMD:-0.23, 95%CI: -0.57, 0.11, p=0.179) and rosuvastatin (SMD:-0.20, 95% CI: -0.71, 0.30, p=0.431). The lowering effect of statins on plasma vWF:Ag levels was greater in the subset of studies lasting ≥12 weeks (SMD:-0.70, 95%CI: -1.19, -0.22, p=0.005) compared with that of studies lasting <12 weeks (SMD:-0.34, 95%CI: -0.67, 0.003, p=0.052). Finally, low-intensity statin therapy was not associated with a significant reduction in vWF:Ag levels (SMD:-0.28, 95%CI: -0.82, 0.27, p=0.320), but a significant effect was observed in high-intensity statin trials (SMD:-0.66, 95%CI: -1.07, -0.24, p=0.002). Conclusions: This meta-analysis of available RCTs demonstrates a significant reduction in plasma vWF:Ag levels following statin therapy.
    Thrombosis and Haemostasis 10/2015;
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    ABSTRACT: Patients with polycythaemia vera (PV), essential thrombocythaemia (ET) and primary myelofibrosis (PMF) are at increased risk of arterial and venous thrombosis. In patients with ET a positive correlation was observed between JAK-2 V617F mutation, that facilitates erythropoietin receptor signalling, and thrombotic events, although the mechanism involved is not clear. We previously demonstrated that heparanase protein forms a complex and enhances the activity of the blood coagulation initiator tissue factor (TF) which leads to increased factor Xa production and subsequent activation of the coagulation system. The present study was aimed to evaluate heparanase procoagulant activity in myeloproliferative neoplasms. Forty bone marrow biopsies of patients with ET, PV, PMF and chronic myelogenous leukaemia (CML) were immunostained to heparanase, TF and TF pathway inhibitor (TFPI). Erythropoietin receptor positive cell lines U87 human glioma and MCF-7 human breast carcinoma were studied. Heparanase and TFPI staining were more prominent in ET, PV and PMF compared to CML. The strongest staining was in JAK-2 positive ET biopsies. Heparanase level and procoagulant activity were higher in U87 cells transfected to over express JAK-2 V617F mutation compared to control and the effect was reversed using JAK-2 inhibitors (Ruxolitinib, VZ3) and hydroxyurea, although the latter drug did not inhibit JAK-2 phosphorylation. Erythropoietin increased while JAK-2 inhibitors decreased the heparanase level and procoagulant activity in U87 and MCF-7 parental cells. In conclusion, JAK-2 is involved in heparanase up-regulation via the erythropoietin receptor. The present findings may potentially point to a new mechanism of thrombosis in JAK-2 positive ET patients.
    Thrombosis and Haemostasis 10/2015; 115(1). DOI:10.1160/TH15-04-0320

  • Thrombosis and Haemostasis 10/2015; 115(3). DOI:10.1160/TH15-08-0643