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1
Weitz, Jeffrey I., Saskia Middeldorp, William Geerts, and John A. Heit. "Thrombophilia and New Anticoagulant Drugs." Hematology 2004, no. 1 (January 1, 2004): 424–38. http://dx.doi.org/10.1182/asheducation-2004.1.424.
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Abstract Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is the result of an imbalance among procoagulant, anticoagulant and profibrinolytic processes. This imbalance reflects a complex interplay between genetic and environmental or acquired risk factors. Genetic thrombophilic defects influence the risk of a first episode of thrombosis. How these defects influence the risk of recurrence in patients whose first episode of venous thromboembolism was unprovoked is less certain. Thus, when anticoagulants are stopped, patients with unprovoked venous thromboembolism have a risk of recurrence of at least 7% to 10% per year, even in the absence of an underlying thrombophilic defect. Consequently, there is a trend toward longer durations of anticoagulation therapy for these patients, which is problematic given the limitation of existing anticoagulants. This chapter provides an overview of the thrombophilic defects and how they influence the risk of venous thromboembolism. The chapter also details advances in anticoagulant therapy, focusing on new inhibitors of factor Xa and thrombin. In Section I, Dr. Saskia Middeldorp describes the various thrombophilic defects and reviews their relative importance in the pathogenesis of a first episode of venous thromboembolism. She then discusses the influence of these defects on the risk of recurrent thrombotic events in patients with unprovoked venous thromboembolism and in those whose thrombosis occurred in association with a known risk factor, such as surgery. In Section II, Dr. William Geerts reviews the pharmacology of new parenteral and oral factor Xa inhibitors and describes the results of the Phase II and III clinical trials with these agents. He then provides perspective on the potential advantages and drawbacks of these drugs for the prevention and treatment of venous thromboembolism. In Section III, Dr. John Heit focuses on direct thrombin inhibitors. He discusses their mechanism of action and compares and contrasts their pharmacological profiles prior to describing the results of Phase II and III clinical trials. Dr. Heit then provides perspective on the potential advantages and limitations of these drugs relative to existing anticoagulants.
2
Kumano, Osamu, Kohei Akatsuchi, and Jean Amiral. "Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants." Biomedicines 9, no. 3 (March 7, 2021): 264. http://dx.doi.org/10.3390/biomedicines9030264.
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Anticoagulant drugs have been used to prevent and treat thrombosis. However, they are associated with risk of hemorrhage. Therefore, prior to their clinical use, it is important to assess the risk of bleeding and thrombosis. In case of older anticoagulant drugs like heparin and warfarin, dose adjustment is required owing to narrow therapeutic ranges. The established monitoring methods for heparin and warfarin are activated partial thromboplastin time (APTT)/anti-Xa assay and prothrombin time – international normalized ratio (PT-INR), respectively. Since 2008, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), have been widely prescribed to prevent and treat several thromboembolic diseases. Although the use of DOACs without routine monitoring and frequent dose adjustment has been shown to be safe and effective, there may be clinical circumstances in specific patients when measurement of the anticoagulant effects of DOACs is required. Recently, anticoagulation therapy has received attention when treating patients with coronavirus disease 2019 (COVID-19). In this review, we discuss the mechanisms of anticoagulant drugs—heparin, warfarin, and DOACs and describe the methods used for the measurement of their effects. In addition, we discuss the latest findings on thrombosis mechanism in patients with COVID-19 with respect to biological chemistry.
3
Srinivasan, Divyamani, and Bree Watzak. "Anticoagulant Use in Real Time." Journal of Pharmacy Practice 26, no. 3 (November 25, 2012): 270–79. http://dx.doi.org/10.1177/0897190012465950.
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Venous thromboembolism (VTE) encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE). Each year, VTE affects about 300 000 to 600 000 people in the United States, and death is the first manifestation in one-fourth of this population.1{Beckman, 2010 #79} Moreover, approximately 10% of the US population has genetic factors that increase their risk for developing thrombosis.1 In addition to inherited disorders, factors that contribute to VTE include prolonged immobilization, trauma, surgery, cancer, and critically ill patients.2 Routine assessment and prophylaxis are recommended in these groups to avoid DVT-related complications.2 Anticoagulants are the mainstay of drugs used in DVT/PE prevention and treatment. Despite the availability of evidence-based guidelines for anticoagulant therapy, there is suboptimal implementation of DVT prophylaxis in hospitalized patients.3 All anticoagulants are “high-alert” drugs, and judicious use is mandatory to prevent bleeding complications.4 This review discusses treatment guidelines, monitoring, side effects, and reversal agents available for some anticoagulant drugs approved for VTE. Dissemination of the knowledge via pharmacy education programs significantly improves the adherence to VTE prophylaxis.5 Understanding the clinical aspects of anticoagulant dispensing as presented in this review is hoped to facilitate implementation of the theoretical knowledge as well as evidence-based guidelines in order to maximize patient benefit.
4
Konkle, Barbara A. "Monitoring target-specific oral anticoagulants." Hematology 2014, no. 1 (December 5, 2014): 329–33. http://dx.doi.org/10.1182/asheducation-2014.1.329.
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Abstract Target-specific oral anticoagulants are approved for use for the prevention of stroke in atrial fibrillation and for the prevention and treatment of venous thrombosis without the need for laboratory monitoring. However, there are clinical settings in which laboratory measurement of anticoagulant effect is needed. These may include patients with life-threatening bleeding or those requiring emergency surgery, in the setting of renal or hepatic failure, or patients with thrombosis on therapy. This chapter reviews the use of laboratory testing to assess the anticoagulant effect of these drugs. In addition, because these drugs can interfere with other laboratory testing, available data on these interactions are presented.
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Liesdek, Omayra C. D., Rolf T. Urbanus, Linda M. de Heer, Kathelijn Fischer, Willem J. L. Suyker, and Roger E. G. Schutgens. "Alternatives for Vitamin K Antagonists as Thromboprophylaxis for Mechanical Heart Valves and Mechanical Circulatory Support Devices: A Systematic Review." Seminars in Thrombosis and Hemostasis 47, no. 06 (May 31, 2021): 724–34. http://dx.doi.org/10.1055/s-0041-1722846.
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AbstractThe holy grail of anticoagulation in patients with intracardiac devices, such as mechanical heart valves (MHVs) and left ventricular assist devices (LVADs), comprises safe prevention of thrombosis without interrupting normal hemostasis. Device-induced thrombosis and anticoagulant-related bleeding problems are dreaded complications that may cause a significantly reduced quality of life and increased morbidity and mortality. Vitamin K antagonists are the current standard for oral anticoagulation therapy in patients with MHVs and LVADs. Even within the therapeutic range, hemorrhage is the primary complication of these drugs, which emphasizes the need for safer anticoagulants for the prevention of device-induced thrombosis. Device-induced thrombosis is a complex multifactorial phenomenon that likely requires anticoagulant therapy targeting multiple pathways. Here, we review the preclinical and clinical data describing the efficacy of a variety of anticoagulants as thromboprophylaxis after implantation of intracardiac devices.
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Ansell, Jack E., Jeffrey I. Weitz, and Anthony J. Comerota. "Advances in Therapy and the Management of Antithrombotic Drugs for Venous Thromboembolism." Hematology 2000, no. 1 (January 1, 2000): 266–84. http://dx.doi.org/10.1182/asheducation.v2000.1.266.20000266.
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This review focuses on antithrombotic therapy for venous thromboembolism and covers a diverse range of topics including a discussion of emerging anticoagulant drugs, a renewed focus on thrombolytic agents for selected patients, and an analysis of the factors leading to adverse events in patients on warfarin, and how to optimize therapy. In Section I Dr. Weitz discusses new anticoagulant drugs focusing on those that are in the advanced stages of development. These will include drugs that (a) target factor VIIa/tissue factor, including tissue factor pathway inhibitor and NAPc2; (b) block factor Xa, including the synthetic pentasaccharide and DX9065a; (c) inhibit factors Va and VIIIa, i.e., activated protein C; and (d) block thrombin, including hirudin, argatroban, bivalirudin and H376/95. Oral formulations of heparin will also be reviewed.In Section II, Dr. Comerota will discuss the use of thrombolysis for selected patients with venous thromboembolism. Fibrinolytic therapy, which has suffered from a high risk/benefit ratio for routine deep venous thrombosis, may have an important role to play in patients with iliofemoral venous thrombosis. Dr. Comerota presents his own results with catheter-directed thrombolytic therapy and the results from a large national registry showing long-term outcomes and the impact on quality of life.In Section III, Dr. Ansell presents a critical analysis of the factors responsible for adverse events with oral anticoagulants and the optimum means of improving outcomes. The poor status of present day anticoagulant management is reviewed and the importance of achieving a high rate of “time in therapeutic range,” is emphasized. Models of care to optimize outcomes are described, with an emphasis on models that utilize patient self-testing and patient self-management of oral anticoagulation which are considered to be the ultimate in anticoagulation care. The treatment of venous and arterial thromboembolism is undergoing rapid change with respect to the development of new antithrombotic agents, an expanding list of new indications, and new methods of drug delivery and management. In spite of these changes, many of the traditional therapeutics are still with us and continue to play a vital role in the treatment of thromboembolic disease. The following discussion touches on a wide range of therapeutic interventions, from old to new, exploring the status of anticoagulant drug development, describing a new intervention for iliofemoral venous thrombosis, and analyzing the critical factors for safe and effective therapy with oral anticoagulants.
7
Ansell, Jack E., Jeffrey I. Weitz, and Anthony J. Comerota. "Advances in Therapy and the Management of Antithrombotic Drugs for Venous Thromboembolism." Hematology 2000, no. 1 (January 1, 2000): 266–84. http://dx.doi.org/10.1182/asheducation.v2000.1.266.266.
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Abstract This review focuses on antithrombotic therapy for venous thromboembolism and covers a diverse range of topics including a discussion of emerging anticoagulant drugs, a renewed focus on thrombolytic agents for selected patients, and an analysis of the factors leading to adverse events in patients on warfarin, and how to optimize therapy. In Section I Dr. Weitz discusses new anticoagulant drugs focusing on those that are in the advanced stages of development. These will include drugs that (a) target factor VIIa/tissue factor, including tissue factor pathway inhibitor and NAPc2; (b) block factor Xa, including the synthetic pentasaccharide and DX9065a; (c) inhibit factors Va and VIIIa, i.e., activated protein C; and (d) block thrombin, including hirudin, argatroban, bivalirudin and H376/95. Oral formulations of heparin will also be reviewed. In Section II, Dr. Comerota will discuss the use of thrombolysis for selected patients with venous thromboembolism. Fibrinolytic therapy, which has suffered from a high risk/benefit ratio for routine deep venous thrombosis, may have an important role to play in patients with iliofemoral venous thrombosis. Dr. Comerota presents his own results with catheter-directed thrombolytic therapy and the results from a large national registry showing long-term outcomes and the impact on quality of life. In Section III, Dr. Ansell presents a critical analysis of the factors responsible for adverse events with oral anticoagulants and the optimum means of improving outcomes. The poor status of present day anticoagulant management is reviewed and the importance of achieving a high rate of “time in therapeutic range,” is emphasized. Models of care to optimize outcomes are described, with an emphasis on models that utilize patient self-testing and patient self-management of oral anticoagulation which are considered to be the ultimate in anticoagulation care. The treatment of venous and arterial thromboembolism is undergoing rapid change with respect to the development of new antithrombotic agents, an expanding list of new indications, and new methods of drug delivery and management. In spite of these changes, many of the traditional therapeutics are still with us and continue to play a vital role in the treatment of thromboembolic disease. The following discussion touches on a wide range of therapeutic interventions, from old to new, exploring the status of anticoagulant drug development, describing a new intervention for iliofemoral venous thrombosis, and analyzing the critical factors for safe and effective therapy with oral anticoagulants.
8
Jain, Nishank, and Robert F. Reilly. "Clinical Pharmacology of Oral Anticoagulants in Patients with Kidney Disease." Clinical Journal of the American Society of Nephrology 14, no. 2 (May 25, 2018): 278–87. http://dx.doi.org/10.2215/cjn.02170218.
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Oral anticoagulants are commonly used drugs in patients with CKD and patients with ESKD to treat atrial fibrillation to reduce stroke and systemic embolism. Some of these drugs are used to treat or prevent deep venous thrombosis and pulmonary embolism in patients with CKD who undergo knee and hip replacement surgeries. Warfarin is the only anticoagulant that is approved for use by the Food and Drug Administration in individuals with mechanical heart valves. Each oral anticoagulant affects the coagulation profile in the laboratory uniquely. Warfarin and apixaban are the only anticoagulants that are Food and Drug Administration approved for use in patients with CKD and patients with ESKD. However, other oral anticoagulants are commonly used off label in this patient population. Given the acquired risk of bleeding from uremia, these drugs are known to cause increased bleeding events, hospitalization, and overall morbidity. Each anticoagulant has unique pharmacologic properties of which nephrologists need to be aware to optimally manage patients. In addition, nephrologists are increasingly asked to aid in the management of adverse bleeding events related to oral anticoagulant use in patients with CKD and patients with ESKD. This article summarizes the clinical pharmacology of these drugs and identifies knowledge gaps in the literature related to their use.
9
Nieto, Elena, Marcelo Suarez, Ángela Roco, Juan Carlos Rubilar, Francisca Tamayo, Mario Rojo, Gabriel Verón, et al. "Anticoagulation Management With Coumarinic Drugs in Chilean Patients." Clinical and Applied Thrombosis/Hemostasis 25 (January 1, 2019): 107602961983434. http://dx.doi.org/10.1177/1076029619834342.
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Warfarin and acenocoumarol are used in various cardiovascular disorders to improve the prognosis of patients with thromboembolic disease. However, there is a lack of substantial efficacy and safety data on antithrombotic prophylaxis in several countries, particularly in Latin America. The aim of this study was to provide information about the efficacy of anticoagulants in Chilean patients. Data were collected from databases of the Western Metropolitan Health Service, Santiago, Chile. We identified 6280 records of patients receiving anticoagulant treatment. The three most common diagnoses were rhythm disorder (43.7%), venous thrombosis (22%), and valvular prosthesis (10.7%). The majority of patients (98.5%) received acenocoumarol while 1.5% of patients received warfarin, at weekly therapeutic doses of 13.6 mg and 30.4 mg, respectively. For total diagnoses, the median time in the therapeutic range was 50%. However, better results, 66.7%, were observed when a telemedicine strategy was used only in Santiago Province. Our findings emphasize that in Chile, where the number of patients receiving anticoagulant treatment increases every year, telemedicine, by committed teams, improves the use of oral anticoagulants and is able to increase quality indicators of anticoagulant treatment care.
10
Fredenburgh, James C., and Jeffrey I. Weitz. "Factor XI as a Target for New Anticoagulants." Hämostaseologie 41, no. 02 (April 2021): 104–10. http://dx.doi.org/10.1055/a-1384-3715.
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AbstractDespite advances in anticoagulant therapy, thrombosis remains the leading cause of morbidity and mortality worldwide. Heparin and vitamin K antagonists (VKAs), the first anticoagulants to be used successfully for the prevention and treatment of thrombosis, are associated with a risk of bleeding. These agents target multiple coagulation factors. Thus, by activating antithrombin, heparin mainly inhibits factor Xa and thrombin, whereas VKAs lower the levels of the vitamin K–dependent clotting factors. Direct oral anticoagulants, which have replaced VKAs for many indications, inhibit only factor Xa or thrombin. Although the direct oral anticoagulants are associated with less bleeding than VKAs, bleeding remains their major side effect. Epidemiological and animal studies have identified factor XI as a target for potentially safer anticoagulant drugs because factor XI deficiency or inhibition protects against thrombosis and is associated with little or no bleeding. Several factor XI–directed strategies are currently under investigation. This article (1) reviews the rationale for the development of factor XI inhibitors, (2) identifies the agents in most advanced stages of development, (3) describes the results of completed clinical trials and provides a summary of those underway, and (4) highlights the opportunities and challenges for this next generation of anticoagulants.
11
Ageno, Walter, Francesco Dentali, and Alessandro Squizzato. "How I treat splanchnic vein thrombosis." Blood 124, no. 25 (December 11, 2014): 3685–91. http://dx.doi.org/10.1182/blood-2014-07-551515.
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Abstract Antithrombotic treatment of splanchnic vein thrombosis (SVT) is a clinical challenge. Depending on the site of thrombosis, patients are at risk of developing liver insufficiency, portal hypertension, or bowel infarction and may experience recurrence in both the splanchnic veins and other vein segments. To prevent recurrence, anticoagulant therapy should be started as soon as possible after diagnosis and is often continued for an indefinite period of time. However, active bleeding is not infrequent at the time of SVT diagnosis, and major risk factors for bleeding, such as esophageal varices or a low platelet count, are frequently present in these patients. In real-world clinical practice, a proportion of SVT patients are left untreated because the risks associated with anticoagulant therapy are felt to exceed its benefits. However, the majority of patients receive anticoagulant drugs, with heterogeneous timing of initiation, drug choice, and dosages. Evidence to drive treatment decisions is limited because no randomized controlled trials have been carried out in these patients. This review provides practical guidance for the use of anticoagulant drugs in patients presenting with SVT, including symptomatic as well as incidentally detected events.
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Ribic, Christine, and Mark Crowther. "Thrombosis and anticoagulation in the setting of renal or liver disease." Hematology 2016, no. 1 (December 2, 2016): 188–95. http://dx.doi.org/10.1182/asheducation-2016.1.188.
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Abstract Thrombosis and bleeding are among the most common causes of morbidity and mortality in patients with renal disease or liver disease. The pathophysiology underlying the increased risk for venous thromboembolism and bleeding in these 2 populations is distinct, as are considerations for anticoagulation. Anticoagulation in patients with kidney or liver disease increases the risk of bleeding; this risk is correlated with the degree of impairment of anticoagulant elimination by the kidneys and/or liver. Despite being in the same pharmacologic category, anticoagulant agents may have varied degrees of renal and liver metabolism. Therefore, specific anticoagulants may require dose reductions or be contraindicated in renal impairment and liver disease, whereas other drugs in the same class may not be subject to such restrictions. To minimize the risk of bleeding, while ensuring an adequate therapeutic effect, both appropriate anticoagulant drug choices and dose reductions are necessary. Renal and hepatic function may fluctuate, further complicating anticoagulation in these high-risk patient groups.
13
AlDallal, Salma. "Elevated Coagulation Factor IX and Risk of Thrombosis Development." Oncology & Hematology Review (US) 12, no. 01 (2016): 15. http://dx.doi.org/10.17925/ohr.2016.12.01.15.
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Coagulation involves the regulated sequence of proteolytic activation of a series of zymogens to achieve an appropriate and timely hemostasis in an injured vessel in an environment that favors an anticoagulant state. Alteration of hemostatic balance between the prothrombotic and antithrombotic factors can result in insufficient inhibition of coagulation ‘thrombosis’ or bleeding due to excessive antithrombotic treatment. Fibrin is the key component of thrombi and anticoagulant drugs that reduce thrombin formation are effective in both prevention and treatment of thrombosis. Therefore, an increased circulating level of coagulation factor is a must for treatment mechanisms of both venous and arterial thrombosis. The existing anticoagulants may have only limited effects due to their modest therapeutic benefits, increased bleeding risks, narrow clinical applications, and drug-induced thrombophilia. However, some new oral anticoagulants, when administered optimally, are associated with significant anti-ischemic benefits and lower bleeding risk when compared with heparin and vitamin K antagonists. Since factor IX (FIX) plays a key role in tissue factor-mediated thrombin production, it may represent a promising target for drug development. This review aims to summarize the current data for FIX and its role in the development of thrombosis (although thrombosis is a platelet-centric process and FIX may not have any direct and specific effect on platelets).
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Pagès, Arnaud, Rémi Sabatier, and Brigitte Sallerin. "Factors Associated With the Choice of Oral Anticoagulant Class in the Older Patients: An Observational Study." Journal of Cardiovascular Pharmacology and Therapeutics 25, no. 4 (April 8, 2020): 332–37. http://dx.doi.org/10.1177/1074248420917811.
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Aim: Oral anticoagulants are the first-line drugs for treating thrombotic disorders related to nonvalvular atrial fibrillation and for treating deep vein thrombosis, diseases that increase in prevalence with age. Older patients have a greater risk of thrombotic and hemorrhagic events and are more prone to drug interactions. Given this backdrop, we wanted to determine the factors associated with the prescription of direct oral anticoagulants and vitamin K antagonists in older patients. Methods: We performed a cross-sectional observational study using a hospital prescription database. The study population consists of 405 older patients who were given oral anticoagulants. The 2 variables of interest were the prescription of 1 of the 2 classes of oral anticoagulants (direct oral anticoagulants vs vitamin K antagonists) and appropriateness of oral anticoagulant prescribing according to Summary of Product Characteristics (potentially inappropriate vs appropriate). Results: The factors associated with direct oral anticoagulant prescribing were the female gender (odds ratio [OR]: 1.87, 95% confidence interval [CI]: 1.22-2.88) and initiation during hospital stay (OR: 2.56, 95% CI: [1.52-4.32]). Stage 4 and 5 chronic kidney diseases (OR: 0.39, 95% CI: [0.19-0.79] and OR: 0.07, 95% CI: [0.01-0.53]) were factors favoring vitamin K antagonist prescription. Being 90 years of age or more (OR: 2.05, 95% CI: [1.06-3.98]) was a factor for potentially inappropriate anticoagulant prescribing. The gastroenterology department (OR: 2.91, 95% CI: [1.05-8.11]) was associated with potentially inappropriate anticoagulant prescribing. Conclusions: Direct oral anticoagulants are the drugs of choice for anticoagulant treatment, including in older adults. The female gender and the initiation during hospital stay increased the chances of being prescribed a direct oral anticoagulant in older adults. Stage 4 and 5 chronic kidney disease increased the likelihood of having a vitamin K antagonist prescribed. Our study also revealed a persistence of potentially inappropriate oral anticoagulant prescriptions in older patients.
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Lentz, Steven R. "Thrombosis in the setting of obesity or inflammatory bowel disease." Hematology 2016, no. 1 (December 2, 2016): 180–87. http://dx.doi.org/10.1182/asheducation-2016.1.180.
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Abstract Obesity and inflammatory bowel disease (IBD) are systemic inflammatory disorders that predispose to arterial and venous thrombosis through similar prothrombotic mechanisms. Obesity and IBD are chronic risk factors that lead to a persistently elevated risk of thrombosis, although the thrombotic risk with IBD appears to wax and wane with disease severity. Because of the lack of high-quality evidence to guide management decisions, approaches to the prevention and treatment of thrombosis in patients with obesity or IBD are based on extrapolation from general guidelines for antithrombotic therapy. Obesity alters the pharmacokinetics of some anticoagulant drugs, and IBD patients present the added management challenge of having a high risk of gastrointestinal bleeding while taking anticoagulants. An extended duration of anticoagulant therapy is often recommended for obese or IBD patients with unprovoked venous thromboembolism unless there is a high risk of bleeding, although more data and better biomarkers are needed to determine whether anticoagulation can be safely stopped in a subset of IBD patients during remission of active disease. Most patients with obesity or IBD require thromboprophylaxis in conjunction with hospitalization or surgery, with adjustment of anticoagulant dosing in patients with severe obesity.
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Lentz, Steven R. "Thrombosis in the setting of obesity or inflammatory bowel disease." Blood 128, no. 20 (November 17, 2016): 2388–94. http://dx.doi.org/10.1182/blood-2016-05-716720.
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Abstract Obesity and inflammatory bowel disease (IBD) are systemic inflammatory disorders that predispose to arterial and venous thrombosis through similar prothrombotic mechanisms. Obesity and IBD are chronic risk factors that lead to a persistently elevated risk of thrombosis, although the thrombotic risk with IBD appears to wax and wane with disease severity. Because of the lack of high-quality evidence to guide management decisions, approaches to the prevention and treatment of thrombosis in patients with obesity or IBD are based on extrapolation from general guidelines for antithrombotic therapy. Obesity alters the pharmacokinetics of some anticoagulant drugs, and IBD patients present the added management challenge of having a high risk of gastrointestinal bleeding while taking anticoagulants. An extended duration of anticoagulant therapy is often recommended for obese or IBD patients with unprovoked venous thromboembolism unless there is a high risk of bleeding, although more data and better biomarkers are needed to determine whether anticoagulation can be safely stopped in a subset of IBD patients during remission of active disease. Most patients with obesity or IBD require thromboprophylaxis in conjunction with hospitalization or surgery, with adjustment of anticoagulant dosing in patients with severe obesity.
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Rosengren, Bengt. "The value of anticoagulant drugs in thrombosis of the retina." Acta Medica Scandinavica 130, S206 (April 24, 2009): 212–16. http://dx.doi.org/10.1111/j.0954-6820.1948.tb12038.x.
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Rodziewicz, Mia, and David P. D’Cruz. "An update on the management of antiphospholipid syndrome." Therapeutic Advances in Musculoskeletal Disease 12 (January 2020): 1759720X2091085. http://dx.doi.org/10.1177/1759720x20910855.
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Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by recurrent venous or arterial thrombosis with or without pregnancy morbidity in the presence of persistent antiphospholipid (aPL) autoantibodies. Anticoagulation has, until now, formed the cornerstone of treatment but a significant proportion of patients continue to experience thrombosis and pregnancy morbidity despite this treatment. Thrombosis is the most common cause of mortality and accounts for two fifths of deaths. Direct oral anticoagulant drugs represent an attractive alternative to conventional vitamin K antagonist drugs but emerging evidence suggests these may not be suitable for high-risk patients with thrombotic APS. Laboratory studies and case reports of the successful use of different classes of drugs in APS is increasing our understanding of the other pathophysiological mechanisms which may contribute to the high morbidity of APS. This review summarizes current accepted anticoagulant treatment for APS and examines other potential drugs such as immunomodulating agents, statins and novel agents such as sirolimus and defibrotide.
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Maksimova, M. Yu, A. V. Fonyakin, and L. A. Geraskina. "Ischemic stroke and antithrombotic therapy: key aspects." Medical Council, no. 18 (December 1, 2019): 10–17. http://dx.doi.org/10.21518/2079-701x-2019-18-10-17.
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The paper considers the key areas of antithrombotic therapy for ischemic stroke (IS). Antiplatelet therapy is shown to be a multistage and multidisciplinary strategy of treatment for patients with IS, which begins with the appearance of the first symptoms of the disease and continues throughout life. Each stage, including fibrinolytic therapy, early use of antithrombotic and anticoagulant drugs, and personalized antithrombotic prevention of recurrent cerebral disorders, is important in itself and serves a common goal. As a result, all efforts should be aimed at reducing mortality rates in the acute phase of stroke and the functional dependence of a patient and at preventing venous thromboses, recurrent stroke, and all cardiovascular events to increase life expectancy and to improve quality of life. Fibrinolytic therapy increases the patient’s chances of a full neurologic recovery and improves the quality of later life. Antithrombotic drugs reduce the risk of cardiovascular death, early recurrences of stroke, and recurrent noncardioembolic stroke. Parenteral anticoagulants in acute stroke decrease the risk of venous thrombosis/thromboembolism, oral anticoagulants reduce that of recurrent cardioembolic stroke.
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Levine, Mark N. "New Antithrombotic Drugs: Potential for Use in Oncology." Journal of Clinical Oncology 27, no. 29 (October 10, 2009): 4912–18. http://dx.doi.org/10.1200/jco.2009.24.7346.
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For more than 50 years, heparin and vitamin K antagonists (VKAs) have been the anticoagulant drugs used to prevent and treat thrombosis. Low molecular weight heparins (LMWHs) are more recent and have been available for approximately 20 years. Patients with cancer are members of a unique patient population because of their high risk for thrombosis and the risk of anticoagulant-related bleeding. With the currently available antithrombotic agents, patients with cancer still have unmet needs in terms of the prevention and treatment of thrombosis. Although long-term LMWH is the treatment of choice for patients with cancer who have acute, symptomatic venous thromboembolism (VTE), some patients still experience recurrent VTE. More effective antithrombotic agents are needed for such patients. Convenient (ie, oral and with no laboratory monitoring), effective, and safe agents are needed to prevent thrombosis in patients taking chemotherapy and antiangiogenic drugs and in patients with central vein catheters. There are a number of new antithrombotic agents that have been studied in recent years and will soon be available for certain diseases. They target either activated factor X (ie, factor Xa) or activated thrombin, and some of them have potential therapeutic value in patients with cancer. In this article, the clinical research model used for the development of a new antithrombotic agent is discussed along with the results of recent trials that evaluate these new agents in high-risk populations.
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Franchini, Massimo, and Pier Mannuccio Mannucci. "Direct oral anticoagulants and venous thromboembolism." European Respiratory Review 25, no. 141 (August 31, 2016): 295–302. http://dx.doi.org/10.1183/16000617.0025-2016.
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Venous thromboembolism (VTE), consisting of deep vein thrombosis and pulmonary embolism, is a major clinical concern associated with significant morbidity and mortality. The cornerstone of management of VTE is anticoagulation, and traditional anticoagulants include parenteral heparins and oral vitamin K antagonists. Recently, new oral anticoagulant drugs have been developed and licensed, including direct factor Xa inhibitors (e.g. rivaroxaban, apixaban and edoxaban) and thrombin inhibitors (e.g. dabigatran etexilate). This narrative review focusses on the characteristics of these direct anticoagulants and the main results of published clinical studies on their use in the prevention and treatment of VTE.
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Lee, Agnes Y. Y. "Prevention and treatment of venous thromboembolism in patients with cancer." Hematology 2014, no. 1 (December 5, 2014): 312–17. http://dx.doi.org/10.1182/asheducation-2014.1.312.
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Abstract Robust evidence remains scarce in guiding best practice in the prevention and treatment of venous thromboembolism in patients living with cancer. Recommendations from major consensus guidelines are largely based on extrapolated data from trials performed mostly in noncancer patients, observational studies and registries, studies using surrogate outcomes, and underpowered randomized controlled trials. Nonetheless, a personalized approach based on individual risk assessment is uniformly recommended for inpatient and outpatient thromboprophylaxis and there is consensus that anticoagulant prophylaxis is warranted in selected patients with a high risk of thrombosis. Prediction tools for estimating the risk of thrombosis in the hospital setting have not been validated, but the use of prophylaxis in the ambulatory setting in those with a high Khorana score is under active investigation. Symptomatic and incidental thrombosis should be treated with anticoagulant therapy, but little is known about the optimal duration. Pharmacologic options for prophylaxis and treatment are still restricted to unfractionated heparin, low molecular weight heparin, and vitamin K antagonists because there is currently insufficient evidence to support the use of target-specific, non-vitamin K-antagonist oral anticoagulants. Although these agents offer practical advantages over traditional anticoagulants, potential drug interaction with chemotherapeutic agents, gastrointestinal problems, hepatic and renal impairment, and the lack of rapid reversal agents are important limitations that may reduce the efficacy and safety of these drugs in patients with active cancer. Clinicians and patients are encouraged to participate in clinical trials to advance the care of patients with cancer-associated thrombosis.
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Cacciapuoti, Federico. "Thrombophilias: therapeutic employment of direct oral anticoagulants in venous hypercoagulable states." Italian Journal of Medicine 14, no. 3 (September 17, 2020): 136–42. http://dx.doi.org/10.4081/itjm.2020.1296.
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Thrombophilia or hypercoagulable state is a predisposition to form clots. Thrombophilia can be inherited or acquired, and prevalently involves venous vessels. Inherited thrombophilia consists of congenital conditions, as methylenetetrahydrofolate reductase polymorphism, Factor V Leiden and prothrombin gene mutations, natural anticoagulant deficiencies, high level of factor VIII, or dysfibrinogenemia. These congenital disorders can be responsible for venous thromboembolism, particularly deep venous thrombosis, pulmonary embolism, and, less frequently, mesenteric veins thrombosis, kidneys’ veins thrombosis or retinal vein occlusion. Acquired thrombophilia can be associated both with venous and arterial thrombosis and may be caused by antiphospholipid syndrome, aging, some malignancies, oral contraceptive use, heparin-induced thrombocytopenia, and human immunodeficiency virus. Antiplatelets’ drugs are employed in arterial thrombosis, while, heparins/oral vitamin K antagonists are indicated for acute and long-term anticoagulation. However, new oral anticoagulants can be usefully used for venous thromboembolic events. Recent experiences demonstrated that their employment is useful in some thrombophilias only, whereas other investigations are requested to evaluate their use in all hypercoagulable disorders.
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Ageno, Walter, Nicoletta Riva, Soo-Mee Bang, Maria Teresa Sartori, Elvira Grandone, Jan Beyer-Westendorf, Giovanni Barillari, et al. "Antithrombotic Treatment of Splanchnic Vein Thrombosis: Results of an International Registry." Blood 120, no. 21 (November 16, 2012): 499. http://dx.doi.org/10.1182/blood.v120.21.499.499.
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Abstract Abstract 499 Background: Treatment of splanchnic vein thrombosis (SVT) is a clinical challenge due to heterogeneity of clinical presentations, increased bleeding risk and lack of evidences from clinical trials. We carried out an international registry aimed to describe current treatment strategies and factors associated with therapeutic decisions in a large prospective cohort of SVT patients. Methods: Between May 2008 and January 2012, consecutive SVT patients were enrolled in the registry and information on clinical presentation, risk factors, and therapeutic strategies was collected in an electronic database. Clinical outcomes during the first month of treatment were documented. A two-year follow up is ongoing. Results: 613 patients from 12 countries were enrolled in the registry. Mean age was 53.1 (SD ± 14.8) years (range 16–85); 62.6% were males, 74.4% Caucasians. SVT occurred in the portal vein in 470 patients, in the mesenteric vein in 266, in the splenic vein in 139, and in the supra-hepatic veins in 56; 38.8% of patients had multiple vein segments involved. In 29.8% of patients SVT diagnosis was incidental. Most common risk factors included cirrhosis (27.8%), solid cancer (22.3%), intra-abdominal inflammation/infection (11.5%), surgery (8.9%), and myeloproliferative neoplasm (MPN)(8.2%); in 27.6% of patients SVT was idiopathic. During the acute phase, 471 (76.8%) patients were treated with anticoagulant drugs: unfractionated heparin (10.4%), low molecular weight heparin or fondaparinux (66.4%), vitamin K antagonists (VKA) (48.5%). Four patients received aspirin, 9 received thrombolysis. A total of 135 patients (22.0%) remained untreated. Of patients with incidentally diagnosed SVT, 61.1% received anticoagulant treatment. Incidental diagnosis (p<0.0001), single vein thrombosis (p<0.0001), gastrointestinal bleeding (p0.008), thrombocytopenia (p0.0003), cancer (p0.009) and cirrhosis (p<0.0001) were significantly associated with no anticoagulant treatment. History of venous thrombosis (p0.003), myeloproliferative neoplasm (p0.003), surgery (p0.001), and hormonal treatment (p0.013) were significantly associated with the use of anticoagulant treatment. Decision to start patients on VKA was significantly associated with younger age (p<0.0001), symptomatic onset (p<0.0001), multiple veins involvement (p0.012) and unprovoked thrombosis (p<0.0001). Continued treatment with parenteral anticoagulants was significantly associated with anaemia (p0.013), thrombocytopenia (p<0.0001), cancer (p<0.0001), and cirrhosis (p<0.0001). During the first month after diagnosis, 2 patients on anticoagulant treatment (0.4%) and 3 untreated patients (2.2%) had thrombosis extension, 2 (0.4%) treated and 2 (1.5%) untreated patients had major bleeding, 11 patients died (7 and 4, respectively). Conclusions: Despite the increased bleeding risk and recent guidelines suggesting not to treat incidentally detected SVT, 76.8% of newly diagnosed SVT receive anticoagulant therapy in clinical practice. Treatment strategies vary according to patients characteristics, with this patient selection resulting safe and effective during the acute phase of therapy. The ongoing two-year follow up will provide additional information. Disclosures: No relevant conflicts of interest to declare.
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Caprini, Joseph A. "Thrombosis Risk Assessment In The COVID-19 Era." REVISTA CIÊNCIAS EM SAÚDE 10, no. 3 (June 23, 2020): 1–2. http://dx.doi.org/10.21876/rcshci.v10i3.1006.
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The appearance of the coronavirus pandemic has prompted a renewed interest in thrombosis risk assessment, particularly since this disease is associated with a high risk of thrombotic events. It is known that the number one preventable cause of death in hospitalized patients including those having surgical procedures is fatal pulmonary emboli. There is also high-quality data that the use of anticoagulant drugs in the proper dose, and for the period of time shown to be efficacious, will prevent most fatal events. It is true that even with the use of the best anticoagulant regimes venous thromboembolic events (VTE) can still occur but are rarely fatal. We also realize that providing adequate anticoagulant prophylaxis for the entire period of risk is the key to preventing these deaths. Thrombosis risk scoring identifies who's at risk for these emboli and guides physician choices for appropriate preventive measures.
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Kini, R. Manjunatha. "Anticoagulant proteins from snake venoms: structure, function and mechanism." Biochemical Journal 397, no. 3 (July 13, 2006): 377–87. http://dx.doi.org/10.1042/bj20060302.
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Over the last several decades, research on snake venom toxins has provided not only new tools to decipher molecular details of various physiological processes, but also inspiration to design and develop a number of therapeutic agents. Blood circulation, particularly thrombosis and haemostasis, is one of the major targets of several snake venom proteins. Among them, anticoagulant proteins have contributed to our understanding of molecular mechanisms of blood coagulation and have provided potential new leads for the development of drugs to treat or to prevent unwanted clot formation. Some of these anticoagulants exhibit various enzymatic activities whereas others do not. They interfere in normal blood coagulation by different mechanisms. Although significant progress has been made in understanding the structure–function relationships and the mechanisms of some of these anticoagulants, there are still a number of questions to be answered as more new anticoagulants are being discovered. Such studies contribute to our fight against unwanted clot formation, which leads to death and debilitation in cardiac arrest and stroke in patients with cardiovascular and cerebrovascular diseases, arteriosclerosis and hypertension. This review describes the details of the structure, mechanism and structure–function relationships of anticoagulant proteins from snake venoms.
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İnce, Birsen. "New Oral Anticoagulant Drugs for the Treatment of Cerebral Venous Sinus Thrombosis." Turkish Journal of Cerebrovascular Diseases 22, no. 2 (2016): 49–51. http://dx.doi.org/10.5505/tbdhd.2016.83097.
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Wan, Mimi, Qi Wang, Rongliang Wang, Rui Wu, Ting Li, Dan Fang, Yangyang Huang, et al. "Platelet-derived porous nanomotor for thrombus therapy." Science Advances 6, no. 22 (May 2020): eaaz9014. http://dx.doi.org/10.1126/sciadv.aaz9014.
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The treatment difficulties of venous thrombosis include short half-life, low utilization, and poor penetration of drugs at thrombus site. Here, we develop one kind of mesoporous/macroporous silica/platinum nanomotors with platelet membrane (PM) modification (MMNM/PM) for sequentially targeting delivery of thrombolytic and anticoagulant drugs for thrombus treatment. Regulated by the special proteins on PM, the nanomotors target the thrombus site and then PM can be ruptured under near-infrared (NIR) irradiation to achieve desirable sequential drug release, including rapid release of thrombolytic urokinase (3 hours) and slow release of anticoagulant heparin (>20 days). Meantime, the motion ability of nanomotors under NIR irradiation can effectively promote them to penetrate deeply in thrombus site to enhance retention ratio. The in vitro and in vivo evaluation results confirm that the synergistic effect of targeting ability from PM and motion ability from nanomotors can notably enhance the thrombolysis effect in both static/dynamic thrombus and rat model.
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Lupi, Saturnino Marco, and Arianna Rodriguez y Baena. "Patients Taking Direct Oral Anticoagulants (DOAC) Undergoing Oral Surgery: A Review of the Literature and a Proposal of a Peri-Operative Management Protocol." Healthcare 8, no. 3 (August 20, 2020): 281. http://dx.doi.org/10.3390/healthcare8030281.
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Patients on anticoagulant therapy for the prevention of cardiovascular accidents present an increased risk of bleeding following dental and oral surgery. Four recently introduced non-vitamin K antagonist oral anticoagulants, namely dabigatran etexilate (direct thrombin inhibitor), rivaroxaban, apixaban, and edoxaban (Xa factor direct inhibitor), are widely spreading for convenience of use compared to the older drug class. Dental management of patients taking these drugs has substantial differences compared to patients on vitamin K antagonist therapy. Anticoagulation is not assessed directly through a hematological test, but indirectly by renal function. The interventions must be scheduled at the time of minimum blood concentration of the drug. Bleeding can occur even after several days following the surgery. The interaction with drugs administered for dental care must be carefully evaluated. The peri-operative diet can influence the risk of bleeding. Local measures favoring coagulation must be adopted. The interventions with higher risk must be divided into multiple less invasive interventions. Although antidotes exist for these drugs, their use does not seem necessary for dental interventions that have been planned optimally. Furthermore, in this review of the literature a decision protocol is proposed for the evaluation of the suspension of the anticoagulant drug before oral surgery. Cessation of any anticoagulant should only be made in consultation with the patient’s general practitioner/cardiologist, who will weigh up the risk of bleeding from the proposed procedure with the risk of thrombosis/stroke in each individual patient.
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Golovko, L. S., A. V. Safronenko, N. V. Sukhorukova, and E. V. Gantsgorn. "Clinical and pharmacological risk assessment for thrombohaemorrhagic complications after total lower limb arthroplasty." Kuban Scientific Medical Bulletin 27, no. 5 (October 14, 2020): 74–87. http://dx.doi.org/10.25207/1608-6228-2020-27-5-74-87.
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Background. Anticoagulant and haemostatic drugs are used to prevent thrombosis and bleeding after arthroplasty. Combined therapy with these divergent agents, especially in comorbid patients, is not regulated in relevant clinical guidelines and may lead to a reduced effi cacy.Objectives. Assessment of the effect of time interval (TI) in variant combined settings of haemostatic and anticoagulant drugs and concomitant pathology on the development of thrombohaemorrhagic complications after hip or knee arthroplasty.Мethods. In a retrospective study, we analysed patients’ somatic status, haemostatic and anticoagulant drug regimes and their combined impact on the development of thrombohaemorrhagic complications in early postoperative period.Results. We analysed 253 case histories with total replacement of main lower limb joints. Two cohorts were defi ned with respect to TI between haemostatic and anticoagulant drug applications. TI was 17 h or less (n = 145; 57.31%) in cohort 1 and 18–24 h (n = 108; 42.68%) — in cohort 2. A total of 29 drug combinations were tested. Thrombohaemorrhagic complications were observed in 27 (10.67%) patients, with 22 (81.48%) in cohort 1. Thromboses in regimes with tranexamic acid developed in cohort 1 (p = 0.038) at a 2.2-folds higher rate than in cohort 2 (p < 0.05). Thrombosis development was infl uenced by grade 2 obesity (relative risk = 8.75, p = 0.037), type 2 diabetes (relative risk = 21, p = 0.00001), myocardial infarction (relative risk = 16.875, p = 0.00002), venous pathology (relative risk = 8.1, p = 0.045) and the patient’s age over 75 (relative risk = 6.8, p = 0.029). Age over 75 years increased the risk of bleeding by a factor of 12 (relative risk = 12, p = 0.015).Conclusion. After main joint arthroplasty, differential measures to prevent thrombohaemorrhagic complications include a minimal 18-h TI between haemostatic and anticoagulant agent applications, especially in tranexamic acid regimes, and the consideration of concomitant risk factors, such as grade 2 obesity, type 2 diabetes, myocardial infarction in history, venous pathology and age over 75 years.
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Ofosu, Frederick. "Review: Laboratory markers quantifying prothrombin activation and actions of thrombin in venous and arterial thrombosis do not accurately assess disease severity or the effectiveness of treatment." Thrombosis and Haemostasis 96, no. 11 (2006): 568–77. http://dx.doi.org/10.1160/th06-05-0278.
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SummaryThrombin is normally produced for hemostasis and physiological wound healing. Increased thrombin production in vivo, cell activation and inflammation mediated in part by thrombin are hallmarks of both arterial and venous thrombosis. Thrombin generates (pro) coagulant, mitogenic, inflammatory and anticoagulant responses by interacting witha variety of cells in vivo.Both direct and indirect thrombin inhibitors are effective drugs for preventing and treating the consequences of arterial and venous thrombosis. For these reasons, measurements of the production and activities of thrombin in vivo have the potential for gauging the extent of thromboembolism and the responses of patients to anticoagulant, antiplatelet and anti-inflammatory drugs. How-ever, a critical review of published information suggests that measurement of thrombin production and activity in patients at risk for and in patients with significant thrombosis generally does not provide information useful for clinical decision-making. This lack of clinical utility of levels of thrombin production in vivo may arise from two causes: the inability of the measurement to differentiate between physiological (hemostatic) and disease-related (pathological) sources and/or causes of thrombin production in vivo, and the inability of antithrombotic treatment modalities to permanently eliminate the stimuli that cause increased thrombin production evident in venous and arterial thrombosis.
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Fareed, Jawed, Debra Hoppensteadt, Omer Iqbal, Josephine Cunanan, Vinod Bansal, Schuharazad Abro, and Rakesh Wahi. "Defibrotide Interactions with Newer Oral Anticoagulants and Antithrombotic Agents." Blood 120, no. 21 (November 16, 2012): 3411. http://dx.doi.org/10.1182/blood.v120.21.3411.3411.
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Abstract Abstract 3411 Defibrotide is a polydisperse mixture of porcine-derived single-stranded oligonucleotides which has been used for multiple clinical indications. Recent clinical trials of defibrotide indicate that this drug may provide benefits both for the treatment and prophylaxis of hepatic veno-occlusive disease (VOD) in hematopoietic stem cell therapy. In VOD it is believed that defibrotide exerts two distinct effects; 1. Endothelial cell protection and 2. Restoration of the thrombotic-fibrinolytic balance. Although antithrombotic in nature, defibrotide does not produce any systemic anticoagulant effects atthe selected dose of 25 mg/kg/day Conventional oral anticoagulants are routinely not used in veno-occlusive disease however heparin is often used in the management of these patients. More recently, newer oral anticoagulant drugs such as dabigatran, apixiban and rivaroxiban have been approved for the management of post orthopaedic surgical venous thrombosis and stroke prevention in atrial fibrillation. The current study was undertaken to investigate the effect of defibrotide on the anticoagulant and antiprotease effects of the newer oral anticoagulant drugs in the whole blood, plasma and platelet rich plasma based systems. Materials and Methods Native whole blood was drawn from 25 normal healthy individuals and supplemented with 100 μg/mL defibrotide and 250 ng/mL of each of the individual oral anticoagulant drugs alone and with defibrotide. Activated clotting time (ACT) measurements were made on a Hemachron instrument using celite ACT tubes. For the plasma based anticoagulant studies, a fixed concentration of defibrotide of 100 μg/mL was supplemented with defibrotide to pool plasma alone and with each of the individual oral anticoagulantagents in a concentration range of 0–1000 ng/mL. To investigate the effect of defibrotide on agonist induced platelet aggregation platelet rich plasma was prepared with varying amounts of defibrotide (0–100ug/ml). Such agonsits as ADP, epinephrine, collagen and arachodonic acid were used. To test the effects of newer oral anticoagulants, each agent was supplemented at 250–500ng/ml to the defibrotide enriched PRP (100ug/ml) and agonist induced aggregation studies were carried out in comparison to saline and defibrotide control. To test the effect of defibrotide on the conventional oral anticoagulant agents, plasma samples from patients with INR range of 1.5–3.0 were supplemented with 100ug/ml and the PT/INR was re-determined using Innovin® reagent. Results In the whole blood studies apixaban and rivaroxaban did not produce any prolongation of the whole blood ACT. However, dabigatran produced a modest increase in the ACT at 250 ng/mL. In the anticoagulant assays, supplementation of these agents did not result in any prolongation of the PT with defibrotide and newer oral anticoagulants. In the aPTT assay, the apixaban and rivaroxaban did not have any interaction, at a concentration greater than 500 ng/mL. Dabigatran shows a slight interaction in the aPTT assay. Defibrotide, did not produce any alterations of the effect on the agonist (ADP, epinephrine, collagen, arachidonic acid) induced aggregation of platelets in concentrations up to 100 μg/mL. Studies carried out where defibrotide at 100 μg/mL is combined with 250 ng/mL of each of the new anticoagulants does not show any modification of the aggregation responses. Defibrotide supplementation to anti-platelet therapy treated patient's blood collected did not result in any augmentation of the observed inhibitory responses. Defibrotide did not produce any changes in the PT/INR values of plasma samples collected from warfarin treated patients at concentrations of up to 100 μg/ml. Conclusions These studies indicate that in a concentration range of 0–1000 ng/mL the new anticoagulants do not exhibit any significant interactions with defibrotide. Since dabigatran exhibits some anticoagulant effect of its own, minor interactions with defibrotide may be observed. Based on the indications for the new oral anticoagulant drugs, their circulating levels and rapid clearance, it is unlikely that defibrotide will produce any interactions with these drugs. Disclosures: No relevant conflicts of interest to declare.
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Iqbal, Omer, Debra Hoppensteadt, Daniel Fareed, and Jawed Fareed. "Synthetic Anti-Xa Drugs Can Be Used for Parenteral Anticoagulation but Not Fondaparinux." Blood 104, no. 11 (November 16, 2004): 4088. http://dx.doi.org/10.1182/blood.v104.11.4088.4088.
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Abstract Targeting at the level of factor Xa and/or prothrombinase complex by synthetic anti-Xa agents such as JTV-803 (Akros Pharma, Princeton, NJ), DX-9065a (Daiichi Pharmaceuticals, Tokyo, Japan), and Fondaparinux (Sanofi-Synthelabo, Toulouse, France) represents an important approach in anticoagulant therapy. Factor Xa is an essential component of the prothrombinase complex and leads to the generation of thrombin. Synthetic heparin pentasaccharide, Fondaparinux (Arixtra®) has been approved by the United States Food and Drug Administration for the prophylaxis of deep vein thrombosis in patients undergoing hip and knee replacement surgeries. There is a rapid stride in the development of newer synthetic inhibitors of factor Xa such as DX-9065a, and JTV-803 in various thrombotic indications. In order to evaluate the parenteral anticoagulant potential of these synthetic factor Xa inhibitors, we used the Hemochron (celite) activated clotting time (ACT) assay. DX-9065a at a final concentration of 5 and 10 μg/ml increased the ACTs to 250 and 300 seconds, respectively. Similar anticoagulant potential was noticed with JTV-803. These findings suggest that these agents may be useful as parenteral anticoagulants during interventional cardiologic procedures, surgical anticoagulation and for the prevention of vascular access occlusion. Fondaparinux requiring antithrombin (AT) for its anticoagulant effect does not increase the celite ACT to the extent as other synthetic factor Xa inhibitors. Fondaparinux even at a final concentration of 100 μg/ml increase the ACT to about 200 seconds and hence are not suitable to be used as parenteral anticoagulants. The concentrations of JTV-803, DX-9065a and fondaparinux required to increase the ACT to near 250 seconds are 6.2, 5 and 125 μg/ml, respectively. While fondaparinux is AT-dependent, the synthetic anti-Xa agents are AT-independent in their actions. The antithrombin sparing effect of direct anti-Xa agents may contribute to an additional anticoagulant effect as reflected by increased ACT levels. Furthermore, there are some other advantages of direct anti-Xa agents when compared to fondaparinux. While direct anti-Xa agents may be used for patients with AT deficiency, fondaparinux being AT-dependent, may not. The inhibition of the clot-bound and prothrombinase-bound factor Xa are additional advantages of direct Xa inhibitors when compared to fondaparinux. Fondaparinux being AT-dependent and upon complexation with AT is not capable of inhibiting the clot-bound factor Xa. Oral Xa inhibitors are being developed and when available patients may have an ideal transition from a parenteral anti-Xa agent to an oral Xa inhibitor. The results clearly suggest that synthetic factor Xa inhibitors except fondaparinux may be used as parenteral anticoagulants. Large-scale clinical studies are warranted to evaluate these findings.
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Spronk, Henri, and Leon Schurgers. "Differential cellular effects of old and new oral anticoagulants: consequences to the genesis and progression of atherosclerosis." Thrombosis and Haemostasis 112, no. 11 (2014): 909–17. http://dx.doi.org/10.1160/th14-03-0268.
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SummaryThe main purpose of anticoagulants is to diminish fibrin formation, thereby decreasing the risk of venous or arterial thrombosis. Vitamin K antagonist have been used for many decades in order to achieve reduced thrombotic risk, despite major drawbacks of this class of drugs such as cumbersome dossing and monitoring of anticoagulant status. To overcome these drawbacks of VKA, new classes of anticoagulants have been developed including oral anticoagulants for direct inhibition of either thrombin or factor Xa, which can be administrated in a fixed dose without monitoring. Coagulation factors can activate cellular protease-activated receptors, thereby inducing cellular processes as inflammation, apoptosis, migration, and fibrosis. Therefore, inhibition of coagulation proteases not only attenuates fibrin formation, but may also influence pathophysiological processes like vascular calcification and atherosclerosis. Animal models revealed that VKA therapy induced both intima and media calcification and accelerated plaque vulnerability, whereas specific and direct inhibition of thrombin or factor Xa attenuated atherosclerosis. In this review we provide an overview of old and new oral anticoagulants, as well discuss potential pleiotropic effects with regard to calcification and atherosclerosis. Although translation from animal model to clinical patients seems difficult at first sight, effort should be made to fully understand the clinical implications of long-term oral anticoagulant therapy on vascular side effects.
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van Montfoort, Maurits, and Joost Meijers. "Anticoagulation beyond direct thrombin and factor Xa inhibitors: indications for targeting the intrinsic pathway?" Thrombosis and Haemostasis 110, no. 08 (2013): 223–32. http://dx.doi.org/10.1160/th12-11-0803.
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SummaryAntithrombotic drugs like vitamin K antagonists and heparin have been the gold standard for the treatment and prevention of thromboembolic disease for many years. Unfortunately, there are several disadvantages of these antithrombotic drugs: they are accompanied by serious bleeding problems, it is necessary to monitor the therapeutic window, and there are various interactions with food and other drugs. This has led to the development of new oral anticoagulants, specifically inhibiting either thrombin or factor Xa. In terms of effectiveness, these drugs are comparable to the currently available anticoagulants; however, they are still associated with issues such as bleeding, reversal of the drug and complicated laboratory monitoring. Vitamin K antagonists, heparin, direct thrombin and factor Xa inhibitors have in common that they target key proteins of the haemostatic system. In an attempt to overcome these difficulties we investigated whether the intrinsic coagulation factors (VIII, IX, XI, XII, prekallikrein and high-molecular-weight kininogen) are superior targets for anticoagulation. We analysed epidemiological data concerning thrombosis and bleeding in patients deficient in one of the intrinsic pathway proteins. Furthermore, we discuss several thrombotic models in intrinsic coagulation factor-deficient animals. The combined results suggest that intrinsic coagulation factors could be suitable targets for anticoagulant drugs.
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Katelnitskiy, Ivan I., Igor I. Katelnitskiy, and Ekaterina S. Livadnyaya. "Advantages of modern methods of prevention of thrombotic complications in patients with critical ischemia of lower limbs after reconstructive operations." I.P. Pavlov Russian Medical Biological Herald 27, no. 4 (January 11, 2020): 487–94. http://dx.doi.org/10.23888/pavlovj2019274487-494.
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Aim. To evaluate and improve the results of reconstructive operations in patients with obliterating atherosclerosis with critical ischemia of the lower limbs through reduction of the rate of thrombotic complications by improvement of diagnosis of risk factors for thrombosis on the basis of coagulogram and Thrombodynamics T-2 test data.
Materials and Methods. In the I group of patients (n=48) reconstructive operations were performed on the arteries of lower limbs and anticoagulant therapy with unfractionated heparin (UFH) with control of hemostasiogram before the operation, in 6 hours and 6 days after the operation and with additional control of APTT 30 minutes before introduction of UNH. In the II group (n=34) reconstructive operations were performed with selection of anticoagulant therapy using parameters of hemostasiogram and laboratory-diagnostic system Thrombodynamics Recorder T-2 with control before the operation, in 6 hours, 6 days after the operation and with additional control of APTT in 30 minutes before introduction of UFH.
Results. Analysis of the data of coagulogram and Thrombodynamics T-2 test showed statistical significance of APTT, fibrinogen, delay and initial speed of clot growth, a combination of which permits a possibility for correction of heparin therapy for prevention of thrombosis.
Conclusions. The dynamics of the parameters of Thrombodynamics T-2 test in selection of UFH dose proves high effectiveness of this method for selection of adequate doses of anticoagulant drugs for prevention of postoperative thromboses in patients with critical ischemia of the lower limbs.
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Nakayama, Satoshi, and Naoya Murashima. "Acute Portal Vein Thrombosis Treated with Recombinant Human Soluble Thrombomodulin Combined with Antithrombin III." Case Reports in Medicine 2020 (April 13, 2020): 1–4. http://dx.doi.org/10.1155/2020/8268016.
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Portal vein thrombosis is a major complication associated with liver cirrhosis. In cirrhotic patients, a decrease in procoagulant and anticoagulant factors and an unstable balance between them is observed, and a relative decrease in the activation of anticoagulant drivers is one of the main causes of portal vein thrombosis (PVT). Herein, we report a case of acute portal thrombosis associated with liver cirrhosis and treated with a recombinant form of soluble thrombomodulin (thrombomodulin alpha, TM-α) in combination with antithrombin III. TM-α was administered in accordance with the dosage and route of administration for disseminated intravascular coagulation therapy and resulted in dissolution of PVT with a gradual decrease in D-dimer levels. No adverse events were observed during the course of treatment. In the future, in addition to conventional anticoagulation therapy using heparin or antivitamin K drugs, novel therapies targeting protein C activation using a recombinant form of soluble thrombomodulin may play an important role in the treatment of acute PVT.
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Geddings, Julia, and Nigel Mackman. "New players in haemostasis and thrombosis." Thrombosis and Haemostasis 111, no. 04 (2014): 570–74. http://dx.doi.org/10.1160/th13-10-0812.
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SummaryThe blood coagulation cascade is essential for haemostasis, but excessive activation can cause thrombosis. Importantly, recent studies have identified factors that contribute to thrombosis but not haemostasis. These include factor XII (FXII), tissue factor-positive microparticles (MPs) and neutrophil extracellular traps (NETs). Studies have shown that FXII plays a role in thrombosis but not haemostasis. FXII is activated in vivo by a variety of negatively-charged polyphosphates, which include extracellular RNA, DNA and inorganic polyphosphate (PolyP) that are released during cell damage and infection. These findings have led to the development of nucleic acid-binding polymers as a new class of anticoagulant drug. Other studies have analysed the role of MPs in experimental thrombosis. MPs are small membrane vesicles released from activated or apoptotic cells. We and others have found that tissue factor-positive MPs enhance thrombosis in mouse models and are elevated in the plasma of pancreatic cancer patients. Finally, NETs have been shown to contribute to experimental venous thrombosis in mouse models and are present in human thrombi. NETs are composed of chromatin fibers that are released from neutrophils undergoing cell death. NETs can capture platelets and increase fibrin deposition. The recent advances in our understanding of the factors contributing to thrombosis in animal models provide new opportunities for the development of safer anticoagulant drugs.
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Ahmad, Quamruddin, Md Mahin Reza, Md Ahosan Habib, Syed Faravee Masud, Nasiruddin, Md Ahsanuzzaman Khan, Ahmed Shahed e. Ambiya, and Sonia Nasreen Ahmad. "New Oral Anticoagulants: An Update." Journal of Bangladesh College of Physicians and Surgeons 37, no. 3 (June 12, 2019): 135–50. http://dx.doi.org/10.3329/jbcps.v37i3.41736.
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One of the most common and useful forms of medical intervention is anticoagulant therapy and it is the mainstay of treatment and prevention of thrombosis in different clinical settings, like atrial fibrillation (AF), acute coronary syndrome (ACS), acute venous thromboembolism (VTE), and in patients undergoing invasive cardiac procedures. More than 6 million patients in the United States receive long-term anticoagulation therapy for the prevention of thromboembolism due to AF, placement of a mechanical heart-valve prosthesis, or VTE.1 For more than 60 years, until 2009, warfarin and other vitamin K antagonists were the only class of oral anticoagulants (OAC) available. Although these drugs are highly effective in prevention of TE, their use is limited by a narrow therapeutic index that necessitates frequent monitoring and dose adjustments. This results in substantial risk and inconvenience, leading to inadequate anticoagulant prophylaxis. Recently some new OAC have been marketed which are effective, easier to use and has less side effects. Dabigatran is a new oral thrombin inhibitor and Rivaroxaban, Apixaban and Edoxaban are oral factor Xa inhibitors. This review outlines why these new OACs were essential and describes in detail about these new drugs.
J Bangladesh Coll Phys Surg 2019; 37(3): 135-150
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Falanga, Anna, and Frederick R. Rickles. "Management of Thrombohemorrhagic Syndromes (THS) in Hematologic Malignancies." Hematology 2007, no. 1 (January 1, 2007): 165–71. http://dx.doi.org/10.1182/asheducation-2007.1.165.
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AbstractThe rate of venous thromboembolism (VTE) in patients with acute leukemia or lymphomas is comparable with that of other “high-risk” cancer types. Chemotherapy and anti-angiogenic drugs increase the thrombotic risk in patients with lymphomas, acute leukemias and multiple myeloma (MM). Patients with hematologic malignancies often present with a hypercoagulable state or chronic disseminated intravascular coagulation (DIC) in the absence of active thrombosis and/or bleeding. Malignant cell procoagulant properties, cytotoxic therapies, and concomitant infections are major determinants for clotting activation in hematologic malignancies. In acute leukemia, clinical manifestations range from localized venous or arterial thrombosis to a diffuse, life-threatening thrombohemorrhagic syndrome (THS). All-trans retinoic acid (ATRA) has greatly improved the management of acute promyelocytic leukemia (APL), but has not significantly changed the rate of early hemorrhagic deaths and may actually promote thrombosis. Randomized, controlled trials (RCTs) of different prophylactic regimens to prevent VTE or THS in hematologic malignancies are urgently needed, particularly in patients with lymphoma or MM during chemotherapy and in patients with APL. Anticoagulant therapy is a particular challenge in patients with hematologic malignancies, since these patients are at very high risk for hemorrhage. No guidelines are available for the prophylaxis or treatment of VTE; extrapolations can be made from existing guidelines for management of patients with other malignancies; prolonged periods of treatment-induced thrombocytopenia in patients with hematologic malignancies, however, require a more judicious application of standard anticoagulant approaches. Use of the newer anticoagulants will require careful assessment of hemorrhagic risk in this group of high-risk patients but may be justified under special circumstances.
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L. Venkatraman, Kalkooru, Azeemullah A. Syed, Parimelazhagan Indumathi, and Alka Mehta. "VITPOR AI, A Coagulation Factor XIIa Inhibitor from Porphyra yezoensis: In Vivo Mode of Action and Assessment of Platelet Function Analysis." Protein & Peptide Letters 27, no. 3 (February 10, 2020): 243–50. http://dx.doi.org/10.2174/0929866526666191026111056.
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Background: Thrombosis represents as the prime contributor to the burden of diseases, worldwide. Conventional anticoagulants for thrombosis therapy have a common bleeding side effect. Bioactive peptides are studied to be an effective alternative for currently available therapeutic drugs. Objective: In this study, VITPOR AI peptide, a previously reported coagulation FXIIa inhibitor from Nori (Porphyra yezoensis), was assessed for its inhibitory activity against FXIIa and its in vivo mode of action. Methods: In vivo efficacy as well as the antithrombotic property of the peptide was evaluated in mice model by ex vivo activated Partial Thromboplastin Time assay, tail transection model and whole blood clotting time. The enzyme kinetics was studied using chromogenic substrate assay. Results: The kinetic behaviour of VITPOR AI showed that the peptide is a competitive inhibitor of FXIIa. Peptide showed significant inhibition of platelet adhesion and aggregation. VITPOR AI exhibited significant antithrombotic activity. Furthermore, ex vivo activated Partial Thromboplastin Time assay revealed that VITPOR AI exhibited potent anticoagulant activity in vivo. Tail bleeding assay revealed that the peptide did not prolong bleeding time in mice even at a higher dose of 5 mg/kg. Cytotoxicity studies of the peptide against human blood leukocytes indicated the safety of the peptide. Conclusion: VITPOR AI could be prospected as a potent anticoagulant with Factor XIIa inhibition, antiplatelet aggregation and antithrombotic activity. It was also studied to have no bleeding side effect.
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Stricker, Hans. "Venous thromboembolism and cancer: pathophysiology and incidence." Vasa 43, no. 4 (June 1, 2014): 239–43. http://dx.doi.org/10.1024/0301-1526/a000358.
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A relationship between tumor and thrombosis is well known. This review covers the aspect of incidence and pathophysio-logy of cancer-related thromboembolism. Cancer patients have an up to 7 % risk of developing venous thrombosis, partly because they are subject to various circumstantial risk factors such as surgical interventions, immobilization or drugs during their illness. On the other hand, tumors frequently generate a prothrombotic state, which may remain without clinical manifestation or result in anticoagulant-resistent venous thromboembolism. Recently discovered thrombosis-generating mechanisms could help to classify patients in categories with high and low thrombotic risk, which will allow tailored prophylactic and therapeutic interventions.
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Zeca, Cristina Elena Berbecar, Madalina Elena Iordache, Iulia Muraru, Dragos Muraru, Elena Luminita Stanciulescu, George Jinescu, Mircea Bogdan Maciuceanu Zarnescu, and Alina Monica Mares. "The Role of Anticoagulant Therapy with Heparine in Treatment of Acute Hand Ischemia." Revista de Chimie 69, no. 3 (April 15, 2018): 752–54. http://dx.doi.org/10.37358/rc.18.3.6192.
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Hand ischaemia has multiple causes. The Methadone (C21H27NO) - opioid family of drugs and Alprazolam (C17H13Cl1N4) microcrystals, available under the trade name Xanax - benzodiazepine anxiolytic, when using in case of drugs abuser, are very powerful embolic agents which can cause thrombosis of small vessels. Microvascular embolization caused by microcrystals of the injectable powder has contributed to the process of ischaemia. This paper brings into discussions a case of acute ischaemia of the right hand due to intra-arterial injection of suspended tablets of Methadone and Alprazolam microcrystals into the right radial artery, in the distal 1/3 of the forearm.The therapeutic management consisted of restoring the arterial circulation at the ischaemic segment to prevent the propagation of thromboembolic complications by using of i.v. heparine and to preserve the function of the hand by preventing delayed ischaemia and compartment syndrome followed by necrosis. Heparin is a drug widely used in the treatment and prevention of arterial and venous thrombosis. The main effect of heparins lies in their anticoagulant activity. Heparins are involved in different pathways of the coagulation cascade with anticoagulant, antithrombotic, profibrinolytic, anti-aggregative, as well as anti-inflammatory effects.This paper aims to discuss a severe case of ischaemia which demonstrates that intra-arterial injection of oral drugs can lead to limb loss with currently accepted therapy.
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Lukinova, Nina, Mano Venkatesan, and Jill White. "Novel Point-Of-Use FXa Assay For Monitoring Anticoagulant Therapy By Oral Factor Xa Inhibitors and Heparin." Blood 122, no. 21 (November 15, 2013): 4816. http://dx.doi.org/10.1182/blood.v122.21.4816.4816.
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Introduction A highly specific, rapid, robust and sensitive assay for Factor Xa (FXa) activity will greatly improve monitoring and optimization of anticoagulant therapy by direct FXa inhibitors and by low molecular weight (LMW) heparins. We have developed a new point-of-use diagnostic system that will provide results in less than 30 minutes, enabling rapid medical decisions based on quantitation of FXa activity and anticoagulant drugs in patients’ blood. Anticoagulant therapy with unfractionated or LMW heparins needs aggressive monitoring in pregnant women, patients with renal insufficiency, and neonates, in particular in cases of treatment-related side effects, including heparin-induced thrombocytopenia and bleeding tendency (Chest, 2008). New oral anticoagulants rivaroxaban (Xarelto®) and apixaban (Eliquis®) have been effective in reducing risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation, and in preventing and treating deep vein thrombosis. Both drugs directly inhibit FXa and have significant therapeutic potential as an alternative to warfarin. Unlike warfarin, these drugs do not require constant monitoring and dose adjustment to maintain anticoagulation within the therapeutic interval. However, excessive anticoagulation and consequent hemorrhage risks have been sufficiently common problems to warrant clinical development of specific antidotes for FXa inhibitors. Currently available anti-Xa heparin assays may not be appropriate for rivaroxaban and apixaban measurements. Additionally, recently published data indicate that new oral anticoagulants interfere with the measurement of common test parameters, expanding the need for more specific diagnostic tests (Clinical Chemistry, February 2013). This novel rapid and specific FXa assay will allow monitoring LMW heparins and the new FXa inhibitors, identify heparin-refractory patients as well as those requiring antidotes to oral Factor Xa inhibitors, in addition to directly measuring FXa activity in patients with inherited deficiency of Factor X, congenital antithrombin deficiency, and acquired FXa deficiencies. Method A diagnostic assay to measure FXa activity in human plasma using electrochemiluminescence (ECL) technology was developed at Wellstat Diagnostics, LLC. The assay utilizes a synthetic peptide containing an FXa substrate sequence that is recognized by specific antibodies (labeled with an ECL-active ruthenium chelate) only after specific cleavage by FXa protease. The resulting ECL signal is directly proportional to FXa activity within the physiological range. The assay has been adapted to also provide quantitative measurement of activity of anticoagulant drugs that inhibit FXa. In the modified format the resulting ECL signal is inversely proportional to the concentration of rivaroxaban, apixaban or heparin in plasma. Results The ECL-based assay measures activity of anticoagulant drugs on FXa in human plasma with high intra- and inter-assay reproducibility, accuracy and specificity. Using FX-deficient plasma spiked with Factor X in the range 1-100 ng/mL, we have demonstrated linear increases of ECL signal directly proportional to the concentration of spiked Factor X activated by a specific Russell Viper Venom activator. Serial dilutions of anticoagulant drugs rivaroxaban, apixaban and enoxaparin (LMW heparin) in normal donor plasma showed exponential decreases of ECL signal in the range of concentrations relevant to the therapeutic doses of all three drugs. The dynamic range of the drug detection was 15 - 500 ng/mL for rivaroxaban and apixaban, and 0.2 - 2 IU/mL of enoxaparin. The assay was specific to activity of FXa, while insensitive to variable concentrations of other clotting factors in human plasma, as well as to the presence of other drugs in plasma that don’t directly inhibit FXa. Conclusions The point-of-use FXa assay is shown to be highly specific, robust, rapid and reproducible for measurements of anticoagulant activity of apixaban, rivaroxaban and enoxaparin in human plasma. Use of this point-of-use system for monitoring anticoagulant therapy may be further extended to measure other blood clotting factors (for example, Factor IXa, VIIa, FVIII), for monitoring activity of drugs acting on these factors and for rapid diagnosis of coagulation disorders. Disclosures: No relevant conflicts of interest to declare.
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Golovko, L. S., A. V. Safronenko, and E. V. Gantsgorn. "Thrombosis and bleeding after endoprosthetics of large joints of the lower extremities: what can increase the risk of thrombohemorrhagic complications?" South Russian Journal of Therapeutic Practice 1, no. 3 (December 20, 2020): 75–83. http://dx.doi.org/10.21886/2712-8156-2020-1-3-75-83.
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Objective: to assess the effect of the baseline hemostasiogram and comorbid background on the development of thrombosis and bleeding in the early postoperative period in patients receiving combined hemostatic and anticoagulant pharmacoprophylaxis after arthroplasty of the knee and hip joints.Materials and Methods: A retrospective analysis of 253 case histories of patients with hip or knee arthroplasty performed. The patients received combined pharmacoprophylaxis with hemostatics and anticoagulants. Two groups were identified according to the time interval (TI) between the appointment of hemostatic and anticoagulant drugs. The first group (57,31%) - n=145 (112 women and 33 men), TI≤17 h, the second group (42,68%) — n=108 (78 women and 30 men), TI 18-24 h. In patients, we analyzed the effect of comorbidity and baseline values of the coagulogram on the risk of thrombosis or bleeding in the early postoperative period.Results: Thrombohemorrhagic complications were registered in 27 (10,67%) patients, of which 22 (81,48%) were in the first group. Thrombosis in the first group developed in the regimens with tranexamic acid (p=0,038), and their frequency was 2,2 times higher than in the second group (p=0,023). In the first group, the risk of thrombosis in women was increased by the initially low level of international normalized ratio (INR) (relative risk (RR)=13,333, p=0,00032) and activated partial thromboplastin time (APTT) (RR=5,8, p=0,037). The risk of bleeding in the first group among men and women increased with an increased preoperative APTT level (RR=18, p=0,0012 and RR=28, p=0,00022, respectively), and separately for women - with a reduced content of fibrinogen (RR=23,25, p=0,00065) and platelets (RR=10,2, p=0,038). The development of thrombosis as influenced by: degree 2 obesity (RR=8,75, p=0,037), type 2 diabetes mellitus (RR=21, p=0,00001), myocardial infarction (RR=16,875, p=0,00002), venous pathology (RR=8,1, p=0,045), moderate decline in renal function (RR=6,231, p=0,0465) and age over 75 years (RR=6,8, p=0,029). Age over 75 years increased the risk of bleeding 12-fold (RR=12, p=0,015).Conclusions: to minimize the risk of thrombosis and bleeding after endoprosthetics of large joints of the lower extremities, especially in patients with the above risk factors, in particular, when using tranexamic acid as a hemostatic, it is recommended to observe the TI between hemostatic and anticoagulant pharmacoprophylaxis of at least 18 hours.
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Deb, Sudip Ranjan, Ahmedul Kabir, Tanzia Khanum, Md Golam Ur Rahman, Anowar Hossain, Md Alamin, and Rafiya Afroz. "Digital Symmetrical Peripheral Gangrene: A Rare Male PresentAtion of AntiPhospholipid Anti Body Syndrome." Journal of Dhaka Medical College 24, no. 2 (September 15, 2016): 152–55. http://dx.doi.org/10.3329/jdmc.v24i2.29628.
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Anti-phospholipid antibody syndrome can be defined as the occurrence of venous and arterial thrombosis with or without recurrent miscarriage in association with laboratory evidence of persistent Antiphospholipid antibody / antibody to beta-2-Glycoprotein-1 / anti cardiolipin antibody /lupus anticoagulant (usually associated with SLE). It occurs usually in female who can present with recurrent miscarriage and fetal loss. Anti-phospholipid Antibody can be also found in some autoimmune diseases and post viral infections. Even certain drugs; e.g. phenothiazine, can cause it. Arterial thrombosis may lead to peripheral limb ischemia, stroke, and myocardial infarct. And venous thrombosis may be found in the form of DVT, pulmonary embolism & thrombosis in vessels supplying the abdominal organ.J Dhaka Medical College, Vol. 24, No.2, October, 2015, Page 152-155
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Janus, Nicolas. "Gastrointestinal Disorders and Toxicities Induced By Anticancer Drugs. Another Risk Factor of Bleeding in Cancer-Associated Thrombosis." Blood 136, Supplement 1 (November 5, 2020): 36. http://dx.doi.org/10.1182/blood-2020-141814.
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Introduction Anticancer treatments has been changing since decades, evolving from chemotherapy (platinum salts) to recent check-point inhibitors. Nausea, vomiting and diarrhoea are common adverse events of anticancer drugs, despites the fact that some supportive care drugs can manage these adverse events. Gastro-intestinal (GI) disorders/toxicities are also important. Such as gastric/duodenal ulcer, gastritis, stomatitis, colitis, esophagitis... Cancer-associated-thrombosis (CAT) patients were also reported to be exposed to such GI disorders/toxicities and several publications recommended to consider these GI disorders/toxicities when choosing an anticoagulant in CAT (Carrier M. Curr Oncol 2018; Moik F. ESMO Open 2020). However, little is known about the nature of the anticancer drugs that CAT patients are receiving. The aim of this work was to check all the anticancer's SmPCs (Summary of Product Characteristics) on the EMA website for GI disorders. Methods All SmPCs of anticancer drugs indicated for lung cancer were checked on the EMA website. All adverse events regarding GI disorders/toxicities were collected. The frequency of adverse events used was the following: very common (≥ 1/10); common (≥ 1/100 to < 1/10); uncommon (≥ 1/1,000 to < 1/100); rare (≥ 1/10,000 to < 1/1000); very rare (< 1/10,000). However, it was decided to mainly focus on very common and common ones. Old anticancer drugs SmPCs (platinium salts...) were checked on electronic medicines compendium (medicines.org.uk), because these old SmPCs are not always available on the EMA website. Generics, biosimilars and drugs without a licence were excluded. Results Twenty-eight anticancer drugs were identified with a mix of traditional chemotherapies (platinum salts...), tyrosine kinase inhibitors (nib) and monoclonal antibodies (mab). Among these 28 anticancer drugs, 26 had at least one very common/common GI disorders/toxicities. Obviously, vomiting (82.1%) and diarrhoea (89.3%) are very well-known, but it was interesting to see that many anticancer drugs were associated with other very common/common GI toxicities such as stomatitis (71.4%) and colitis (10.7%). Additionally, several drugs (35.7%) were exposing to GI bleeding and/or GI perforation but these last adverse events were less common. Unfortunately, the SmPCs did not include data about the GI profile of the patients during the trials. Conclusion Monreal M et al reported in 1991 that acute gastroduodenal lesion was found in 21% of patients with venous thromboembolism, but there are no dedicated study about the incidence of GI disorders in CAT patients. This work reported that GI disorders/toxicities were common in anticancer drug's SmPCs. Consequently, it is important to be aware of this before initiating an anticoagulant treatment. However, this work had limitations. Indeed, these adverse events were reported in the SmPCs, based mainly on cancer trials and not on CAT trials. Furthermore, clinical trials and SmPCs may not always reflect the real clinical setting. Finally, lung cancer patients are usually receiving anticancer regimens that include several anticancer drugs, so the potential impact of GI disorders/toxicities from 2 or 3 anticancer drugs on a single patients could be greater. Nevertheless, it sounds reasonable to check for GI disorders/toxicities risks in order to initiate an adequate anticoagulant treatment in CAT patients and during follow-up. Disclosures Janus: Guerbet:Research Funding;B-Braun:Honoraria;LEO Pharma A/S:Current Employment, Honoraria;Fresenius Medical Care:Honoraria;Amgen:Honoraria, Research Funding;TEVA:Research Funding;Daichii-Sankyo:Honoraria, Research Funding;Roche:Honoraria, Research Funding;Vifor Pharma:Honoraria, Research Funding;Gilead:Honoraria, Research Funding;Novartis:Honoraria;Pierre Fabre Oncology:Research Funding;Bayer:Honoraria, Research Funding;Pfizer:Consultancy, Honoraria;IPSEN:Honoraria.
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Dwivedi, Rohini, and Vitor H. Pomin. "Marine Antithrombotics." Marine Drugs 18, no. 10 (October 13, 2020): 514. http://dx.doi.org/10.3390/md18100514.
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Thrombosis remains a prime reason of mortality worldwide. With the available antithrombotic drugs, bleeding remains the major downside of current treatments. This raises a clinical concern for all patients undergoing antithrombotic therapy. Novel antithrombotics from marine sources offer a promising therapeutic alternative to this pathology. However, for any potential new molecule to be introduced as a real alternative to existing drugs, the exhibition of comparable anticoagulant potential with minimal off-target effects must be achieved. The relevance of marine antithrombotics, particularly sulfated polysaccharides, is largely due to their unique mechanisms of action and lack of bleeding. There have been many investigations in the field and, in recent years, results have confirmed the role of potential marine molecules as alternative antithrombotics. Nonetheless, further clinical studies are required. This review covers the core of the data available so far regarding the science of marine molecules with potential medical applications to treat thrombosis. After a general discussion about the major biochemical steps involved in this pathology, we discuss the key structural and biomedical aspects of marine molecules of both low and high molecular weight endowed with antithrombotic/anticoagulant properties.
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Faioni, Elena M., and Marco Cattaneo. "Inflammation and Thrombosis — Brothers in Arms." European Oncology & Haematology 07, no. 01 (2011): 81. http://dx.doi.org/10.17925/eoh.2011.07.01.81.
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Several interactions occur between inflammation and thrombosis that become more apparent with ageing. It is a two-way process: inflammation promotes aggregation and coagulation, while activated platelets and coagulation factors or peptides promote inflammation by several mechanisms. Recent evidence points to the role played by platelets and possibly coagulation factors in the regulation of innate immunity. Physiological anticoagulant pathways also have anti-inflammatory properties. This strong interdependence has an evolutionary origin. Current viewpoints are that inflammation, and thus coagulation, have a role in ageing. ‘Inflamm-ageing’ is a neologism that denotes a low-grade inflammation that accompanies healthy ageing, but can evolve towards excessive inflammation and clotting. It can thus be associated with thrombosis and early death. These fascinating pathophysiological discoveries provide novel targets for the development of new, potentially efficacious antithrombotic drugs.
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Papaioannou, Georgia, Emmanouil Papadakis, Maria Topalidou, Kyriaki Kokoviadou, Anastasia Karapiperidou, Anna Kioumi, and Ioannis Korantzis. "Antiplatelet Agents as Secondary Thromboprophylaxis after Anticoagulant Treatment for Thrombosis." Blood 108, no. 11 (November 16, 2006): 4127. http://dx.doi.org/10.1182/blood.v108.11.4127.4127.
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Abstract Patients suffering an unprovoked VTE event have high risk of recurrence after anticoagulation cessation especially in the first two-year period. Our study examined whether secondary thromboprophylaxis with antiplatelet drugs reduces the relapse risk. STUDY DESIGN: We studied 53 patients, 25 men and 28 women, (group A), with median age of 41(18–74) years. 31 received aspirin at 100mg while 22 received clopidogrel at 75mg after anticoagulant therapy for VTE. We compared them with 77 patients (group B) who did not receive any thromboprophylaxis after VTE with a median age of 40(18–82) years. Of group B, 56 were men while 21 were women. In 51 out of 130 patients we monitored D-dimers, F1+2 prothrombin fragments, and TAT (thrombin-antithrombin) complexes as prothrombotic and fibrinolysis markers. Failure was determined as VTE recurrence or elevation of prothrombotic markers in the first 2year period. RESULTS: In 4 patients of group A (7,5%) we noticed marked elevation of prothrombotic markers and they were turned to anticoagulation, and in 3 marker elevation subsided by changing the antiplatelet agent (aspirin to clopidogrel). 1 patient stopped prophylaxis due to hemorrhage while none relapsed. In group B VTE recurrence was noticed at 27(36%, p<0,0002). In both groups late recurrence (> 2 years) was observed at 27,6% of 130 patients. CONCLUSIONS: Low dose aspirin or clopidogrel administration is safe and effective as thromboprophylaxis after anticoagulation for first venous thromboembolic event. Markers as D-dimers, F1+2, TAT, have prognostic significance and are valuable tools in patient monitoring. Patient follow-up has to be long-standing because VTE recurrence risk persists through the years.