Seminars in Thrombosis and Hemostasis

Publisher: Georg Thieme Verlag

Journal description

Current impact factor: 3.69

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.693
2012 Impact Factor 4.216
2011 Impact Factor 4.524
2010 Impact Factor 4.169
2009 Impact Factor 3.214
2008 Impact Factor 3.695
2007 Impact Factor 3.202
2006 Impact Factor 2.733
2005 Impact Factor 2.077
2004 Impact Factor 2.018
2003 Impact Factor 1.906
2002 Impact Factor 2.497
2001 Impact Factor 2.147
2000 Impact Factor 2.179
1999 Impact Factor 2.385
1998 Impact Factor 1.577
1997 Impact Factor 1.171
1996 Impact Factor 1.15
1995 Impact Factor 1.175
1994 Impact Factor 1.483
1993 Impact Factor 1.415
1992 Impact Factor 1.542

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.84
Cited half-life 5.20
Immediacy index 2.00
Eigenfactor 0.01
Article influence 1.06
ISSN 1098-9064
OCLC 163849709
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Georg Thieme Verlag

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    • Publisher's version/PDF can be used on author's personal website only
    • Publisher copyright and source must be acknowledged
    • Link to Publisher version (www.thieme-connect.com) must be included if article has been published online
    • Publisher last contacted on 31/03/2015
    • 'Georg Thieme Verlag' is an imprint of 'Thieme Publishing'
  • Classification
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The diversity of integrins and their complex role in many diseases suggests great potential for this superfamily as drug targets. The initial successes of anti-integrin therapeutics in the treatment of thrombotic disorders suggested that similar anti-integrin agents could be developed for the treatment of inflammatory disorders. While initially a promising strategy, inhibition of the integrins proved to be elusive despite the discovery of highly potent inhibitors. This is due to several reasons, including redundancy among the integrins and the importance of integrins in key physiological systems. Further exploration of the selective role for distinct leukocytic integrins indicated that homing of inflammatory cells to select disease sites depends on a highly regulated expression of discrete integrins and their ligands in limited locations. Selective control of integrin function is also regulated by local chemokines permitting exquisite homing of populations of inflammatory cells to disease sites. A more complete understanding of the regulation of integrin activation in disease states will permit the development of more effective and specific anti-integrin therapeutic agents. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556588
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    ABSTRACT: Venous thromboembolic disease often arises as a complication of another pathological condition and/or triggering event. Infectious diseases result from both the direct action of the pathogens themselves and their effect on the immune system. The resulting inflammatory process and the coagulation and fibrinolysis processes share common pathways, explaining why infection is associated with thrombosis. In this brief overview, besides certain chronic infectious diseases, we also consider some acute infections, as the mechanisms are likely to be similar, particularly in the initial infective stage or the more acute episodes of a chronic infection. The infectious agent can be viral, bacterial, fungal, or parasitic. However, the literature on the link between infections and venous thromboembolism (VTE) is uneven, favoring infections that are found in more developed countries where physicians have access to VTE diagnostic tools. Thus, large epidemiological studies in this field are restricted to a limited number of the common chronic infectious diseases such as tuberculosis, while for other infections, particularly parasitic and fungal infections, the link with VTE is only evoked in a few scattered case reports. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556729
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    ABSTRACT: It is well established that inflammation and thrombosis are intricately linked processes, and there is increasing evidence of the importance of their roles in activated complement in the pathogenesis of thromboembolism. The two systems are activated by similar stimuli simultaneously and interact, either directly or through biochemical mediators, to protect the host from microbial invasion. Diseases characterized by complement hyperactivity such as paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome have high rates of thrombosis. This review describes how disease processes where there is excessive complement activation leads to thrombosis, and the specific interactions between the complement and coagulation systems that lead to pathological thrombus formation. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556732
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    ABSTRACT: Endothelial cells are unique multifunctional cells with basal and inducible metabolic and synthetic functions. Various stimuli can induce physiological or pathological changes in endothelial cell biology. Hematopoietic stem cell transplantation (HSCT) requires high-dose irradiation and/or chemotherapy and is associated with increased risk of bacterial infections and immune reactions. These factors can affect endothelial cells. This review provides an overview of the effects of HSCT on endothelial cells, based on findings observed in cultured cells as well as in patients. We first describe to what extent irradiation and chemotherapy constitute direct and indirect triggers for endothelial cell activation and injury. Then, we highlight the role of the endothelium in several complications of HSCT, including capillary leak syndrome, engraftment syndrome, transplant-associated microangiopathy, graft-versus-host disease, and diffuse alveolar hemorrhages. We also analyze in detail available data on sinusoidal obstruction syndrome, previously known as veno-occlusive disease of the liver, where liver sinusoidal endothelial cells are first injured and eventually lead to sinusoid occlusion and liver cell damage. Finally, we open the question of the possible contribution of endothelial damage to cardiovascular events occurring long after HSCT. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556728
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    ABSTRACT: Thrombotic microangiopathy (TMA) is characterized by the presence of microangiopathic hemolytic anemia and thrombocytopenia. There are several disorders with varied etiopathogenesis, both genetic and acquired, that result in TMA. The neutrophils play an important role in inflammation and thrombosis through the formation of neutrophil extracellular traps (NETs). NETs are formed in response to a variety of stimuli including infections, chemical factors, and platelet activation. The classic TMA, thrombotic thrombocytopenic purpura (TTP) is caused by a severe deficiency of ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type-I motif, member 13), mostly acquired due to autoantibodies, whereas atypical hemolytic uremic syndrome (aHUS) is mostly attributed to genetic defects in complement pathway regulatory proteins. The management of these well-known disorders has evolved over the last decade. Similarly, there is also better understanding of diverse and unusual clinical presentations of both of these conditions. Since there are many other causes of TMAs, which may mimic some of the clinical features of TTP or aHUS, it is essential to thoroughly investigate each patient so that appropriate therapy can be offered. This review focuses on some important developments in understanding of etiopathogenesis, diagnosis, and treatment of more commonly encountered TMAs. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556587
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    ABSTRACT: Inflammation has a pivotal role in cardiovascular disease because it contributes to the progression of atherosclerosis, a chronic inflammatory disease of the vessel wall. Microparticles (MPs) have recently emerged as both surrogate markers for different cardiovascular conditions (i.e., biomarkers of vascular inflammation and coagulation) and paracrine biological shuttle modules with influence in target cells. MPs are vesicles that bud off from cells, lack a nucleus, contain a membrane skeleton, and are defined by their size and expression on their surface of antigens specific of parental cells. Interestingly, not only inflammation is one of the main stimuli causing MP release but also MPs, in its turn, can induce, regulate, and even in specific cases reduce inflammation. The present review aims to summarize and update the role of circulating MPs in inflammation and hemostasis with special emphasis on their novel associations and functions. Besides their role as biomarkers of atherosclerotic inflammation, blood-borne MPs possess mechanisms to alter vascular cell milieu, to disseminate proinflammatory mediators, and to spread the inflammatory cascade reaction, causing a chronic inflammation of the vascular wall and aggravating the atherothrombotic process. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556591
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    ABSTRACT: Platelets are well recognized as a key cell component of the hemostatic system. Recently, several additional functions have been discovered for these blood cells but most importantly in the process of inflammation. Numerous research groups have demonstrated crucial roles for platelets in the pathogenesis of varied clinical conditions where inflammation is important. Alterations in both platelet number and function have been observed with these different conditions. The relevance of these findings is their therapeutic implications through simple antiplatelet therapy to more complex, as yet clinically untrialed options, like interfering with platelet-leukocyte or platelet-endothelial interaction. This review focuses on how platelets are relevant in inflammatory conditions with an impetus on the clinical aspects. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556589
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    ABSTRACT: The autoimmune disease antiphospholipid syndrome (APS) is characterized by thrombosis or pregnancy morbidity in patients with persistent antiphospholipid antibodies (aPLs). Although inflammation is not a key feature of the clinical presentation of the syndrome, there are indications that the inflammatory response plays an important role in APS. The major antigen of aPLs, the plasma protein β2-glycoprotein I, is involved in clearance of microparticles and in the innate immune response. In light of these physiological functions, the formation of antibodies against the protein is easily understood, as antibodies might augment the clearance reaction. In addition, inflammatory mediators are thought to play a role in the activation of leukocytes and the induction of endothelial dysfunction in APS. Moreover, evidence for a role of complement activation in the pathogenesis of the syndrome is accumulating. This review will provide an overview of current knowledge on the physiological function of β2-glycoprotein I, the formation of autoantibodies against β2-glycoprotein I and will explore the contribution of inflammation to the clinical manifestations of APS. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556725
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    ABSTRACT: Behçet disease (BD) is a rare multisystem, inflammatory disease of unknown etiology with vascular involvement and associated thrombogenicity. This review aims to describe the involvement of various mediators in endothelial cell damage and in the hypercoagulable state of BD. The scenario of the chronic inflammation present in BD shows an increased oxidative condition that contributes to endothelial cell damage and induces platelet, leukocyte, and endothelial cell activation through the release of proinflammatory cytokines and chemokines. These factors, together with the increased levels of homocysteine observed in BD patients, induce the endothelial cell expression of adhesion molecules (VCAM-1 and ICAM-1) and tissue factor; the release of cytokines, soluble CD40L (sCD40L), matrix metalloproteinase-9, and blood coagulation factor V; the inhibition of fibrinolysis; the disruption of nitric oxide metabolism; and the increase in platelet reactivity and lipid peroxidation. Endothelial cell dysfunction leads to a prothrombotic and antifibrinolytic phenotype in BD patients. Increased levels of homocysteine, fibrinogen, and plasminogen activator inhibitor type 1 seem to be involved in the procoagulant condition of this pathology that has been verified by end-point tests as well as by global coagulation tests. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556727
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    ABSTRACT: Surgery is associated with an increased risk of venous thromboembolic events (VTE) including deep vein thrombosis and pulmonary embolism. Although the current treatment regiments such as mechanical manipulation and administration of pharmacological prophylaxis significantly reduced the incidence of postsurgical VTE, they remain a major cause of postoperative morbidity and mortality worldwide. The pathophysiology of venous thrombosis traditionally emphasizes the series of factors that constitute Virchow triad of factors. However, inflammation can also be a part of this by giving rise to a hypercoagulable state and endothelial damage. The inflammatory response after surgery, which is initiated by a cytokine "storm" and occurs within hours of surgery, creates a prothrombotic environment that is further accentuated by several cellular processes including neutrophil extracellular traps formation, platelet activation, and the generation of tissue factor-bearing microparticles. Although such inflammatory markers are elevated in undergoing surgery, the precise mechanism by which they give rise to venous thrombosis is poorly understood. Here, we discuss the potential mechanisms linking inflammation to thrombosis, and highlight strategies that may minimize surgical inflammation and reduce the incidence of postoperative VTE. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556726
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    ABSTRACT: Prophylactic replacement of factor concentrate is the established optimal treatment to avoid or minimize joint disease in severe hemophilia patients, thus ultimately improving their life expectancy and quality of life toward values matching those in the normal population. Where uncertainty still exists is around the optimal regimen to be prescribed for prophylaxis, and more and more treaters and patients are showing interest in patient tailored approaches to prophylaxis, aiming at matching the prophylaxis regimen to the specific needs of the patient. The rationale behind tailoring the prophylaxis regimen to the individual patient is based on the significant variability that exists between patients (all with the same label of severe hemophilia) with respect to their bleeding phenotype, their pharmacokinetic handling of factor, their levels of physical activity, and a variety of other characteristics that contribute to differential prophylaxis needs of patients. Of course, any form of tailoring of prophylaxis needs to take into consideration the economic resources of the country; for many countries very intense prophylaxis regimens are just not possible. This article will review different concerns and strategies when tailoring prophylaxis, and will address how these issues will apply to the new longer acting factor concentrates in development. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1552563
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    ABSTRACT: Forming an interface with virtually every other organ, endothelium has a strategic role in modulating vascular homeostasis. While its miscellany of functions includes regulation of vasomotor tone, promotion, and prevention of vascular growth, and modulation of inflammatory and hemostatic processes, it functions critically in maintaining the balance of hemostasis in health. Whereas endothelium has been recognized to influence all stages of hemostasis, new evidence suggests it to have a primary role for thrombin generation. Endothelial dysfunction is being increasingly appreciated in several pathological states and particularly, by virtue of its critical role in hemostasis, in causing thrombosis in a multitude of diseases. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 08/2015; DOI:10.1055/s-0035-1556586
  • Seminars in Thrombosis and Hemostasis 07/2015; 41(5):445-446. DOI:10.1055/s-0035-1550441
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    ABSTRACT: Objectives This study aims to determine the risk factors, diagnostic methods employed, treatment modalities, and outcome in patients with splanchnic vein thrombosis (SVT). Methods A retrospective chart review of patients, age 18 to 90 years, diagnosed with SVT at a single institution from January 1, 2010 to November 10, 2012. They were grouped as portal vein thrombosis (PVT)-including those combined with splenic vein thrombosis (SPVT) or mesenteric vein thrombosis (MVT)-and Budd-Chiari syndrome (BCS). Results Overall 246 SVT patients were identified, including 225 PVT and 21 BCS. Risk factors were liver disease, upper abdominal (regional) cancer and surgery, pancreatitis, and hereditary thrombophilia. The most common symptom was abdominal pain and most patients had abnormal liver function. Among those tested, the JAK2 V617F mutation was present in only 20% of the patients with PVT and 14% of the patients with BCS. Most patients were diagnosed by computed tomography. Anticoagulants were given to 30% of the patients with PVT and to 60% of the patients with BCS, with recurrence of SVT in 15% of the patients with PVT and 24% of the patients with BCS, regardless of anticoagulation. Conclusion As compared with published literature on SVT, we found a higher incidence of regional cancer and surgery and a lower incidence of the JAK2 V617F mutation. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 06/2015; 41(05). DOI:10.1055/s-0035-1550429
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    ABSTRACT: Cirrhosis presents with decreased procoagulant factors as a consequence of the impaired synthetic capacity of the liver. This was taken as evidence to explain the abnormalities of the coagulation tests prothrombin time (PT) and activated partial thromboplastin time (aPTT) and the bleeding events that occur in these patients. It was for long time (and probably is still) common practice to test patients with the PT and to treat those with predefined (but arbitrary) cutoff values with plasma or prohemostatic agents to prevent or stop bleeding. However, anticoagulant factors that contrast the procoagulants are also decreased in cirrhosis. It was therefore postulated that the coagulation balance (i.e., the net result between the action of pro- and anticoagulants) is somewhat rebalanced. Subsequent studies supported this view showing that plasma from cirrhotic patients generates normal amounts of thrombin. In addition, primary hemostasis (i.e., platelet-vessel wall interaction) is rebalanced notwithstanding cirrhosis present with thrombocytopenia. It was shown that increased levels of the adhesive protein von Willebrand factor (a typical feature of cirrhosis) compensate for the low number (function) of platelets. The earlier considerations have been instrumental to help dismantle the old paradigms of cirrhosis as the epitome of the acquired hemorrhagic coagulopathies and the traditional coagulation tests PT and aPTT as suitable predictors of bleeding risk. The demise of the old paradigms and the rise of the new one may have important practical implications for the management of patients with cirrhosis and will be discussed in this chapter. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 06/2015; 41(05). DOI:10.1055/s-0035-1550440
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    ABSTRACT: During the last decade, improved surgical and anesthetic management, such as better understanding of coagulation defects and the use of the phlebotomy, has reduced intraoperative blood product transfusions during orthotopic liver transplantation (OLT). The goal of this study was to look at the impact of initial conventional coagulation tests on blood loss and blood product requirement and to evaluate the role of the phlebotomy during liver transplantations. A total of 700 consecutive OLTs were studied. The group of patients was split into two according to the median of starting international normalized ratio to study blood losses and transfusion rate. Logistic regression was used to determine the main predictors of blood loss, intraoperative blood transfusion, and survival. There was no intergroup difference for demographic characteristics. The mean blood loss was 1,184 mL with a median of 920 mL. Overall, 77.4% of the patients did not receive any blood product and the mean transfusion rate of red blood cells (RBCs) was 0.5 ± 1.4 units per patient. Severity of recipients' disease did not correlate with blood loss or transfusion rate. Starting hemoglobin value was the only biochemical variable linked to RBC transfusions. Phlebotomy was linked to decrease in blood loss, RBC transfusions, and increased survival rate. It is concluded that bleeding did not correlate with traditional coagulation defects or the severity of recipient's disease. Preemptive phlebotomy was linked to a decreased blood loss, a decreased transfusion rate, and an increased 1-year survival rate. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 06/2015; 41(05). DOI:10.1055/s-0035-1550428
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    ABSTRACT: Bleeding frequently complicates end-stage chronic liver disease, and may follow procedures which are required for effective care of patients with liver failure. Thrombosis is increasingly recognized as common, important, and potentially preventable. Standard laboratory tests may not be useful in predicting bleeding or thrombotic risk or guiding therapy, and functional testing serves a more useful role. A state of rebalanced hemostasis exists in many patients, with hypocoagulability present only in a minority. Approaches to management are poorly supported by high-quality evidence; in this review, a practical pragmatic approach to care and minimization of procedure-related risk is discussed. General measures include the correction of systemic factors that may affect coagulation status, prevention and treatment of infection, and individualized coagulation support therapies for specific clinical situations and procedures. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 06/2015; 41(05). DOI:10.1055/s-0035-1550431
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    ABSTRACT: Splanchnic vein thrombosis includes thrombosis of the hepatic venous system (Budd-Chiari syndrome) and thrombosis of the portal venous system. Both conditions share uncommon prothrombotic disorders as causal factors, among which myeloproliferative neoplasms rank first. Budd-Chiari syndrome presents with acute or chronic, asymptomatic or severe liver disease. Diagnosis depends on noninvasive imaging of the obstructed hepatic venous outflow tract. A spontaneously fatal course can be prevented by a stepwise approach: (1) anticoagulation therapy, specific therapy for underlying disease, and medical or endoscopic management of liver-related complications, (2) angioplasty/stenting in a second step, and (3) eventually the insertion of transjugular intrahepatic stent shunt or liver transplantation. Recent portal vein thrombosis mostly jeopardizes the gut. Early anticoagulation prevents thrombus extension but is incompletely successful in achieving recanalization. Chronic portal vein thrombosis is complicated by bleeding related to portal hypertension, which can be prevented by usual pharmacological and endoscopic means. The prevention of recurrent thrombosis is achieved by anticoagulation therapy the impact of which on the risk of bleeding remains unclear. Portal vein thrombosis in patients with cirrhosis is likely neither a direct consequence of nor a direct cause for liver disease progression. Therefore, the indications and effects of anticoagulation therapy for portal vein thrombosis in patients with cirrhosis remain uncertain. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 06/2015; 41(05). DOI:10.1055/s-0035-1550439