Academic literature on the topic 'Anticoagulant drugs'
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Journal articles on the topic "Anticoagulant drugs"
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Marija, Marinko, Novakovic Aleksandra, Divac Tatjana, Milojevic Predrag, and Nenezic Dragoslav. "New anticoagulant drugs." Medicinski casopis 46, no. 3 (2012): 145–54. http://dx.doi.org/10.5937/mckg46-1612.
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Weitz, Jeffrey I., and Jack Hirsh. "New Anticoagulant Drugs." Chest 119, no. 1 (January 2001): 95S—107S. http://dx.doi.org/10.1378/chest.119.1_suppl.95s.
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Weitz, Jeffrey I., Jack Hirsh, and Meyer M. Samama. "New Anticoagulant Drugs." Chest 126, no. 3 (September 2004): 265S—286S. http://dx.doi.org/10.1378/chest.126.3_suppl.265s.
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Bates, Shannon M., and Jeffrey I. Weitz. "Emerging Anticoagulant Drugs." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 9 (September 2003): 1491–500. http://dx.doi.org/10.1161/01.atv.0000084827.77945.66.
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Weitz, Jeffrey I. "Emerging Anticoagulant Drugs." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 4 (April 2007): 721. http://dx.doi.org/10.1161/01.atv.0000260470.02821.fe.
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Oates, John A., Alastair J. J. Wood, and Jack Hirsh. "Oral Anticoagulant Drugs." New England Journal of Medicine 324, no. 26 (June 27, 1991): 1865–75. http://dx.doi.org/10.1056/nejm199106273242606.
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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.
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Fareed, Jawed, Michael J. Moorman, Walter Jeske, and Debra Hoppensteadt. "Defibrotide Interaction With Newer Oral Anticoagulant and Antiplatelet Drugs." Blood 122, no. 21 (November 15, 2013): 4804. http://dx.doi.org/10.1182/blood.v122.21.4804.4804.
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Introduction Defibrotide represents a single stranded mammalian DNA derived agent originally developed for anti-thrombotic and anti-ischemic indications. Defibrotide is currently used to treat or prevent failure of normal blood flow (Veno-occlusive disease, VOD) in the liver of patients who had bone marrow transplants or received drugs such as oral estrogens and mercatopurine. Defibrotide is a polypharmocologic agent with multiple sites of actions, which include anti-inflammatory and vaso-facilitatory effects. The purpose of this investigation is to determine potential interactions of defibrotide and some of the newer oral anticoagulant drugs, such as dabigatran, apixaban and rivaroxaban and antiplatelet drugs such as ticagrelor. Materials & Methods Defibrotide (lot no. DV0601) was obtained in powder form from Gentium s.p.A (Villa Guardia, Italy). The active form of dabigatran was purchased from Selleckcham (Houston, TX). Apixaban and rivaroxaban were obtained commercially and were of synthetic origin. The effect of defibrotide on dabigatran, apixaban, rivaroxaban and ticagrelor, on agonists (epinephrine, ADP, collagen, arachidonic acid and 2.5U thrombin) was measured using platelet aggregation techniques. The platelet rich plasma collected from normal healthy donors (n=15) were also supplemented with each of the individual anticoagulant drugs, alone in a range of 0-1000 ng/ml and in combination with defibrotide at 50-250ug/ml. Such clotting times as the PT, aPTT and Heptest and thrombin generation studies were carried out. In addition, whole blood activated clotting time (celite) studies were carried out by supplementing each of the individual oral anticoagulant agents at 1ug/ml, alone and with defibrotide at 100ug/ml. Results Neither defibrotide nor the newer anticoagulants and ticagrelor produced any effects on the epinephrine, ADP, collagen and arachidonic acid induced aggregation of PRP (p>0.05). However, dabigatran at concentrations of >62.5ng/ml produced inhibition of thrombin induced aggregation, all of the other agents did not have any effect on thrombin. Defibrotide at a concentration 100 ug/ml did not alter the aggregation profile in anticoagulant supplemented PRP. In both the plasma and whole blood anticoagulant assays, dabigatran produced stronger anticoagulant effects (306+30sec) than both apixaban (145+12sec) and rivaroxaban(160+15sec). Defibrotide exhibited minimal effects (135+10sec). Ticagrelor did not have any anticoagulant effect. Defibrotide in combination with dabigatran produced modest augmentation of the anticoagulant responses (360+42sec), however, it had much weaker effects on rivaroxaban (168+18sec) and apixaban(152+14sec). All of the anticoagulants in the TGA produced varying degrees of inhibition of thrombin generation in the following order; dabigatran > rivaroxaban > apixaban. Ticagrelor did not produce any inhibition of thrombin generation. Defibrotide did not produce any effects on TGA at concentrations up to 100ug/ml. When combined with oral anticoagulants, it did not show any augmentation of rivaroxaban and apixaban; however, it enhanced dabigatrans inhibitory effects. Conclusions These results suggest that defibrotide itself has weak or negligible anticoagulant effects in the plasma and whole blood assays. All of the new oral anticoagulants produced varying degrees of assay dependent anticoagulant effects in plasma and whole blood systems. However defibrotide did not show any interactions with apixaban and rivaroxaban, it showed some augmentation of the anticoagulant responses of dabigatran. Ticagrelor did not exhibit any interactions with defibrotide. These studies demonstrate that unlike heparins, defibrotide exhibits minimal interactions with newer oral anticoagulant and antiplatelet drugs. Disclosures: No relevant conflicts of interest to declare.
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Tatarsky, B. A., and N. V. Kazyonnova. "Safety and interaction of direct oral anticoagulants with antiarrhythmic drugs." Russian Journal of Cardiology 26, no. 7 (August 8, 2021): 4482. http://dx.doi.org/10.15829/1560-4071-2021-4482.
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The use of direct oral anticoagulants minimized the risks associated with vitamin K antagonist (warfarin) therapy. Currently, direct oral anticoagulants have priority over warfarin for the prevention of thromboembolic events in patients with atrial fibrillation and a number of other conditions requiring anticoagulant therapy. Direct oral anticoagulants along with antiarrhythmic therapy are the accepted strategy for atrial fibrillation treatment. At the same time, the effect of drug-drug interactions (DDI) between direct oral anticoagulants and antiarrhythmic drugs, which have common points of metabolic application, has not been fully elucidated. In order to provide effective and safe anticoagulant and antiarrhythmic therapy in patients with AF, it is important to understand the mechanisms and severity of DDI of direct oral anticoagulants and antiarrhythmic agents. This review discusses the issues of DDI of direct oral anticoagulants and antiarrhythmic drugs used to treat atrial fibrillation.
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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.
Dissertations / Theses on the topic "Anticoagulant drugs"
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Glossop, Paul. "Thrombin inhibition." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244533.
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Cove, Christina Lauren. "Severe renal dysfunction among individuals taking warfarin and implications for new oral anticoagulants." Thesis, Boston University, 2014. https://hdl.handle.net/2144/21140.
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Thesis (M.S.M.) PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.BACKGROUND: Although novel anticoagulant drugs have proven safety and efficacy profiles from Phase III clinical trials, those patients with significant kidney disease were excluded. The lack of knowledge about incidence, severity and risk factors for severe renal dysfunction in patients requiring oral anticoagulation impedes development of strategies to mitigate risks of hemorrhage associated with renally-eliminated novel oral anticoagulants. METHODS: Patients taking warfarin for atrial fibrillation (AF) or venous thromboembolism (VTE) were consecutively enrolled from January 2007 to December 2010. Baseline kidney function was assessed and patients were followed to their first decline in Glomerular Filtration Rate (GFR) to < 30 ml/min estimated by the Cockcroft-Gault calculation. Independent risk factors for development of severe kidney dysfunction were assessed by multivariate analysis. RESULTS: Of 787 patients identified, 34 were excluded for baseline eGFR < 30 ml/min. The mean age of the cohort was 71 years. At baseline, 23% (n=174) had moderate renal impairment, or Stage 3 CKD (eGFR 30-59 ml/min), while 31% had mild disease. Overall, those with hypertension, congestive heart failure (CHF), diabetes mellitus (DM), and coronary artery disease (CAD) were 74%, 33%, 31%, 24%, and 9% of the cohort, respectively. A decline in eGFR to < 30 ml/min (the primary outcome) occurred in 91 patients, 25% of which happened within 5.3 months. Of those with baseline Stage 3 CKD, 37% experienced the primary outcome. In multiple logistic regression analysis, a baseline eGFR 30–59 ml/min conferred a greater than 14-fold increased risk in the development of eGFR < 30 ml/min (OR 14.5, 99% CI: 5.3 to 39.8, P<0.001) during the warfarin exposure period. CAD was associated with a greater than two-fold increased risk (OR 2.2, 95% CI 1.1 to 4.4, P=0.004). After adjusting for baseline kidney function, age was not an independent risk factor for a decline in eGFR to < 30 ml/min. CONCLUSIONS: Acute and chronic renal dysfunction is common among individuals on chronic warfarin therapy. Better understanding of the fluctuations in renal function would inform patient selection and monitoring strategies for optimal use of novel anticoagulants.
2031-01-01
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Henry, Brian Lawrence. "Novel Sulfated 4-Hydroxycinnamic Acid Oligomers as Potent Anticoagulants." VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/1462.
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The occurrence of thrombosis in several pathophysiological conditions creates a huge need for anticoagulation therapy. Thrombin and factor Xa have been prime targets for regulation of clotting through the direct and indirect mechanism of inhibition. This work investigates chemo-enzymatically prepared oligomers of 4-hydroxycinnamic acids (DHPs) as potential anticoagulants. Oligomers were prepared through peroxidase-catalyzed oxidative coupling of 4-hydroxycinnamic acids. The products resulting from this reaction are called CDs, FDs and SDs. Structurally, these sulfated DHPs are unique and do not resemble any of the anticoagulants known in the literature.DHP oligomers were found to increase clotting times at concentrations comparable to heparin. Studies in blood and plasma show that DHPs possess an anticoagulation profile similar to enoxaparin. To understand the mechanism of action of DHPs, we studied the inhibition of thrombin, FXa, FIXa, and FVIIa in the presence and absence of antithrombin. CDs and FDs display a preference for direct inhibition of thrombin and FXa, and exhibit a high level of specificity over FIXa and FVIIa. In the presence of AT, CDs and FDs displayed weaker inhibition of FXa and thrombin suggesting that binding to AT is a competitive side reaction. SDs exhibited potent inhibition of FXa and thrombin in the absence of antithrombin, but was inactive against FIXa and FVIIa representing the best selectivity among the DHPs. For SDs, inhibition of all the pro-coagulant enzymes favored the antithrombin dependent pathway. Binding studies were performed to determine how CDs directly inhibits thrombin. Competitive binding studies suggest that CDs interacts with exosite II and disrupts the catalytic triad of thrombin. These results indicate that the preferred mechanism of CDs action is exosite II mediated allosteric disruption of thrombin. CDs appears to be the first exosite II mediated DTI and this represents a novel mechanism of inhibitor function. The inhibition characteristics of DHPs are unique and radically different in structure from all the current clinically used anticoagulants. To the best of our knowledge this dual mechanism of anticoagulation and unique binding mode has not been described as yet in literature and represents a novel strategy that our laboratory has discovered.
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Costa, Leandro Silva. "Caracteriza??o parcial e atividades farmacol?gicas do extrato rico em polissacar?deos sulfatatos da angiosperma marinha Halodule wrightii." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/12537.
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Previous issue date: 2008-11-25Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior
Sulfated polysaccharides (PS) are biomolecules with a great biotechnological potential. There are few data about PS from high plants. In addition, pharmacological activities of PS from plants have not been carrying out. The aim of this work was extract PS from the angiosperm Halodule wrightii and study their anticoagulant and antioxidant activities. Histological analysis showed the presence of the PS manly in the roots. A polysaccharide-rich extract was obtained from H. wrightii by proteolysis followed by methanol and TCA precipitation. Chemical, infra-red analysis and agarose gel electrophoresis in 1.3 diaminopropane acetate buffer confirmed the presence of sulfated polysaccharides made by glucose, galactose, xylose and sulfate residues in the proportion 1: 0,9: 1: 1. In addition polyacrilamide electrophoresis have shown that extract is mainly compose by 11kDa sulfated polysaccharides. Pharmacological analysis have shown total antioxidant capacity (CAT) that resulted in 15,21 μg for equivalent of ascorbic acid, scavenging activity of the DPPH radical with 41,36 % of scavenging, activity of reducing power with the maximum of 0,290 nm (50 % of vitamin C activity) and scavenging activity superoxide radical (O2-) with a maximum of 32,23 %. Chelating activity of metal less than 4% and scavenging activity of the radical hydroxyl (OH-) less than 2%. Time of activated partial tromboplastin (aPTT) doubling the time of coagulation from 20μg of and protrombin time (PT) was not present. The data indicate that PS from Halodule wrightii could be considered for future applications in medicine, food production or cosmetic industry
Os polissacar?deos sulfatados (PS) s?o biomol?culas com um grande potencial biotecnol?gico por apresentarem uma diversidade estrutural e farmacol?gica muito grande. Poucos s?o os relatos da exist?ncia destes pol?meros em vegetais superiores, al?m disso, ainda n?o se tem relatos da identifica??o de atividades antioxidantes e anticoagulantes com PS extra?dos destes vegetais. Com o intuito de verificar a presen?a destes polissacar?deos em angiospermas marinhas conhecidas popularmente como capim do mar, foi coletada a esp?cie marinha Halodule wrightii. As por??es vegetativas (folha, caule e raiz) n?o foram separadas sendo preparado inicialmente um extrato denominado de extrato bruto (EB). Ap?s descontamina??o prot?ica o material obtido foi chamado de extrato de polissacar?deos totais (EPT). A presen?a destes polissacar?deos foi investigada e confirmada por an?lises qu?micas, espectroscopia de infravermelho e eletroforese em gel de agarose sendo denominados de extrato rico em polissacar?deos sulfatados (EPS). A an?lise histol?gica da localiza??o dos PS resultou na presen?a destes polissacar?deos principalmente na epiderme da por??o vegetativa raiz. As an?lises qu?micas mostraram que os polissacar?deos contem glicose, galactose, xilose e sulfato na propor??o de 1: 0,9: 1: 1 e massa molecular de aproximadamente 11 kDa. Os grupos sulfatos est?o provavelmente ligados principalmente em C2 de um monossacar?deo. Testes de atividade antioxidante demonstraram que os PS de H. wrightii n?o apresentaram resultado para o teste de capacidade antioxidante total pelo m?todo CAT. Desta forma foi utilizada a atividade de seq?estro do radical DPPH indicado na literatura por dosar a capacidade antioxidante total que resultou em 41,36%. O seq?estro do ?on super?xido tamb?m foi realizado e resultou em 32,23% assim como o poder redutor que equivaleu a 50% da atividade da Vit. C. N?o houve atividade de seq?estro do radical hidroxila assim como atividade quelante de metal. O teste de atividade anticoagulante (aPTT) mostrou que EPS dobra o tempo de coagula??o com 20 g, que ? apenas 2,5 vezes a quantidade da Clexane? (heparina de baixo peso molecular). Para o tempo de protrombina (PT) H.wrightii n?o apresentou atividade. Os dados indicam que EPS possuem um potencial biotecnol?gico anticoagulante e antioxidante e que futuras an?lises se fazem necess?rias para confirmarem esse potencial
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Silva, Juliana Maria Costa da. "Caracteriza??o parcial e atividades farmacol?gicas do extrato rico em polissacar?deos sulfatados da angiosperma marinha Halodule wrightii." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/12542.
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Previous issue date: 2008-11-25Sulfated polysaccharides (PS) are biomolecules with a great biotechnological potential. There are few data about PS from high plants. In addition, pharmacological activities of PS from plants have not been carrying out. The aim of this work was extract PS from the angiosperm Halodule wrightii and study their anticoagulant and antioxidant activities. Histological analysis showed the presence of the PS manly in the roots. A polysaccharide-rich extract was obtained from H. wrightii by proteolysis followed by methanol and TCA precipitation. Chemical, infra-red analysis and agarose gel electrophoresis in 1.3 diaminopropane acetate buffer confirmed the presence of sulfated polysaccharides made by glucose, galactose, xylose and sulfate residues in the proportion 1: 0,9: 1: 1. In addition polyacrilamide electrophoresis have shown that extract is mainly compose by 11kDa sulfated polysaccharides. Pharmacological analysis have shown total antioxidant capacity (CAT) that resulted in 15,21 μg for equivalent of ascorbic acid, scavenging activity of the DPPH radical with 41,36 % of scavenging, activity of reducing power with the maximum of 0,290 nm (50 % of vitamin C activity) and scavenging activity superoxide radical (O2-) with a maximum of 32,23 %. Chelating activity of metal less than 4% and scavenging activity of the radical hydroxyl (OH-) less than 2%. Time of activated partial tromboplastin (aPTT) doubling the time of coagulation from 20μg of and protrombin time (PT) was not present. The data indicate that PS from Halodule wrightii could be considered for future applications in medicine, food production or cosmetic industry
Os polissacar?deos sulfatados (PS) s?o biomol?culas com um grande potencial biotecnol?gico por apresentarem uma diversidade estrutural e farmacol?gica muito grande. Poucos s?o os relatos da exist?ncia destes pol?meros em vegetais superiores, al?m disso, ainda n?o se tem relatos da identifica??o de atividades antioxidantes e anticoagulantes com PS extra?dos destes vegetais. Com o intuito de verificar a presen?a destes polissacar?deos em angiospermas marinhas conhecidas popularmente como capim do mar, foi coletada a esp?cie marinha Halodule wrightii. As por??es vegetativas (folha, caule e raiz) n?o foram separadas sendo preparado inicialmente um extrato denominado de extrato bruto (EB). Ap?s descontamina??o prot?ica o material obtido foi chamado de extrato de polissacar?deos totais (EPT). A presen?a destes polissacar?deos foi investigada e confirmada por an?lises qu?micas, espectroscopia de infravermelho e eletroforese em gel de agarose sendo denominados de extrato rico em polissacar?deos sulfatados (EPS). A an?lise histol?gica da localiza??o dos PS resultou na presen?a destes polissacar?deos principalmente na epiderme da por??o vegetativa raiz. As an?lises qu?micas mostraram que os polissacar?deos contem glicose, galactose, xilose e sulfato na propor??o de 1: 0,9: 1: 1 e massa molecular de aproximadamente 11 kDa. Os grupos sulfatos est?o provavelmente ligados principalmente em C2 de um monossacar?deo. Testes de atividade antioxidante demonstraram que os PS de H. wrightii n?o apresentaram resultado para o teste de capacidade antioxidante total pelo m?todo CAT. Desta forma foi utilizada a atividade de seq?estro do radical DPPH indicado na literatura por dosar a capacidade antioxidante total que resultou em 41,36%. O seq?estro do ?on super?xido tamb?m foi realizado e resultou em 32,23% assim como o poder redutor que equivaleu a 50% da atividade da Vit. C. N?o houve atividade de seq?estro do radical hidroxila assim como atividade quelante de metal. O teste de atividade anticoagulante (aPTT) mostrou que EPS dobra o tempo de coagula??o com 20 ug, que ? apenas 2,5 vezes a quantidade da Clexane? (heparina de baixo peso molecular). Para o tempo de protrombina (PT) H.wrightii n?o apresentou atividade. Os dados indicam que EPS possuem um potencial biotecnol?gico anticoagulante e antioxidante e que futuras an?lises se fazem necess?rias para confirmarem esse potencial
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Bolela, Fabiana. "Estado de saúde e adesão ao tratamento de pacientes atendidos em ambulatório especializado em anticoagulação oral." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/22/22132/tde-26092013-193814/.
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Estudo exploratório, de delineamento longitudinal, com 81 pacientes em uso de anticoagulante oral e que foram avaliados durante internação e dois meses após a alta. Os objetivos foram acompanhar a evolução quanto á terapia de anticoagulação oral e adesão ao tratamento; comparar o estado geral de saúde e a presença de sintomas de ansiedade e depressão. Foram utilizados instrumentos específicos para avaliar adesão ao tratamento medicamentoso (Medida de Adesão aos Tratamentos), estado geral de saúde (Escala Visual Analógica) e presença de sintomas de ansiedade (HADS-Ansiedade) e depressão (HADS- Depressão). As análises estatísticas realizadas foram: Teste t de Student pareado para comparar as médias do estado geral de saúde e da HADS; Modelo Linear de Efeitos Mistos para analisar a associação entre estado geral de saúde, ansiedade, depressão e tempo de avaliação no estudo. O nível de significância adotado foi 0,05. Entre os participantes, 54,3% eram mulheres, com idade média de 59,5 anos e nível médio de instrução de 5,1 anos. A principal indicação clínica para uso do medicamento foi formação de trombos (34,6%), sendo a varfarina o anticoagulante oral mais utilizado (97,5%). Dois meses após a alta, todos os pacientes foram classificados como aderentes ao tratamento e 42% mantiveram o INR na faixa terapêutica. As diferenças entre as médias do estado geral de saúde, HADS-Ansiedade e HADS-Depressão durante a internação e dois meses após a alta não foram estatisticamente significantes (p=0,78; p=0,27 e p=0,40, respectivamente). Em relação á presença de ansiedade, quando associamos as duas variáveis de forma categórica, com e sem sintomas, e o tempo de avaliação, 38 (46,9%) pacientes foram classificados como \"sem sintomas\" de ansiedade e 22 (27,1%) \"com sintomas\", sendo esta associação estatisticamente significante (p<0,001). Para depressão, a maioria (55; 67,9%) foi classificada como \"sem sintomas\" e 11 (13,6%) \"com sintomas\", sendo tal associação estatisticamente significante (p<0,001). Ao analisarmos as médias do estado geral de saúde segundo tempo e grupo de sintomas, resultados estatisticamente significantes foram obtidos apenas quando comparamos os valores entre os grupos sem sintomas de depressão (M=80,5; D.P.=23,46) e com sintomas (M=62,5; D.P.=26,07) (p=0,021), dois meses após a alta e quando comparamos as médias do grupo com sintomas de depressão, na internação (M= 75,37; D.P.=25,02) e dois meses após a alta (M=62,5; D.P.=26,07) (p=0,046). Identificar o perfil clínico de pacientes em uso de anticoagulante oral, desde a internação até dois meses de seguimento ambulatorial; conhecer sua percepção sobre estado de saúde, presença de sintomas de ansiedade e de depressão e a adesão ao tratamento são ações importantes a serem consideradas no atendimento desses pacientes. Tais resultados poderão ser utilizados para nortear mudanças na organização do ambulatório de anticoagulação oral e no planejamento da assistência de enfermagem a tais pacientes.This exploratory and longitudinal research involved 81 patients under oral anticoagulation treatment, who were evaluated during hospitalization and two months after discharge. The objectives were to follow the patients\' clinical evolution, considering the oral anticoagulation therapy and treatment adherence; and to compare the general health condition and the presence of anxiety and depression symptoms. Specific instruments were used to assess adherence to medication treatment (Treatment Adherence Measure), general health condition (visual analogue scale) and the presence of anxiety (HADS-Anxiety) and depression symptoms (HADS-depression). For the sake of statistical analysis, the following were applied: Student\'s paired t-test to compare the mean scores for the general health condition and HADS scores; the Linear Fixed Effects Model to analyze the association between general health condition, anxiety, depression and research moment. Significance was set at 0.05. Among the participants, 54.3% were women, with a mean age of 59.5 years and a mean education time of 5.1 years. The main clinical indication for medication use was the formation of thrombi (34.6%), with warfarin as the most used oral anticoagulant drug (97.5%). AT two months after discharge, all patients were classified as adherent to the treatment and 42% maintained their INR within the therapeutic range. The differences between the mean general health, HADS-Anxiety and HADS-Depression scores during hospitalization and two months after discharge were not statistically significant (p=0.78; p=0.27 and p=0.40, respectively). As regards the presence of anxiety, when the two variables are associated categorically, with and without symptoms, and the research moment, 38 (46.9%) patients were classified as \"without symptoms\" of anxiety and 22 (27.1%) \"with symptoms\", with a statistically significant association (p<0.001). As for depression, the majority (55; 67.9%) was classified as \"without symptoms\" and 11 (13.6%) \"with symptoms\", a statistically significant association (p<0.001). The analysis of the mean general health condition scores according to the research moment and group of symptoms only revealed statistically significant results when comparing the groups without (M=80.5; S.D.=23.46) and with symptoms (M=62.5; S.D.=26.07) (p=0.021) two months after the discharge and when comparing the mean scores for the group with depression symptoms during hospitalization (M= 75.37; S.D.=25.02) and two months after the discharge (M=62.5; S.D.=26.07) (p=0.046). Identifying the clinical profile of patients under oral anticoagulant therapy since hospitalization and after two months of outpatient monitoring and getting to know their perceived health condition, presence of anxiety and depression symptoms and treatment adherence are important actions for consideration in care delivery to these patients. These results can be used to guide changes in the organization of the oral anticoagulation outpatient clinic and in nursing care planning for these patients.
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Santos, Nednaldo Dantas dos. "Identifica??o e avalia??o de propriedades de polissacar?deos sulfatados de diferentes fontes naturais que possibilitem sua aplicabilidade biotecnol?gica." Universidade Federal do Rio Grande do Norte, 2012. http://repositorio.ufrn.br:8080/jspui/handle/123456789/13241.
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Previous issue date: 2012-03-19Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico
Sulfated polysaccharides (SP) are widely distributed in animals and seaweeds tissues. These polymers have been studied in light of their important pharmacological activities, such as anticoagulant, antioxidant, antitumoral, anti-inflammatory, and antiviral properties. On other hand, SP potential to synthesize biomaterials like as nanoparticules has not yet been explored. In addition, to date, SP have only been found in six plants and all inhabit saline environments. However, the SP pharmacological plant activities have not been carrying out. Furthermore, there are no reports of SP in freshwater plants. Thus, do SP from marine plants show pharmacological activity? Do freshwater plants actually synthesize SP? Is it possible to synthesize nanoparticles using SP from seaweed? In order to understand this question, this Thesis was divided into tree chapters. In the first chapter a sulfated polysaccharide (SPSG) was successfully isolated from marine plant Halodule wrightii. The data presented here showed that the SPSG is a 11 kDa sulfated heterogalactan contains glucose and xylose. Several assays suggested that the SPSG possessed remarkable antioxidant properties in different in vitro assays and an outstanding anticoagulant activity 2.5-fold higher than that of heparin Clexane? in the aPTT test; in the next chapter using different tools such as chemical and histological analyses, energy-dispersive X-ray analysis (EDXA), gel electrophoresis and infra-red spectroscopy we confirm the presence of sulfated polysaccharides in freshwater plants for the first time. Moreover, we also demonstrate that SP extracted from E. crassipes root has potential as an anticoagulant compound; and in last chapter a fucan, a sulfated polysaccharide, extracted from the brown seaweed was chemically modified by grafting hexadecylamine to the polymer hydrophilic backbone. The resulting modified material (SNFuc) formed nanosized particles. The degree of substitution for hydrophobic chains of 1H NMR was approximately 93%. SNFfuc-TBa125 in aqueous media had a mean diameter of 123 nm and zeta potential of -38.3 ? 0.74 mV, measured bydynamic light scattering. Tumor-cell (HepG2, 786, H-S5) proliferation was inhibited by 2.0 43.7% at SNFuc concentrations of 0.05 0.5 mg/ mL and RAEC non-tumor cell line proliferation displayed inhibition of 8.0 22.0%. On the other hand, nanogel improved CHO and RAW non-tumor cell line proliferation in the same concentration range. Flow cytometric analysis revealed that this fucan nanogel inhibited 786 cell proliferation through caspase and caspaseindependent mechanisms. In addition, SNFuc blocks 786 cell passages in the S and G2-M phases of the cell cycle
Os polissacar?deos sulfatados (PS) s?o amplamente distribu?dos em animais e tecidos de algas. Estes pol?meros t?m sido estudados em fun??o da import?ncia de suas atividades farmacol?gicas, tais como: anticoagulante, antioxidante, antitumoral, anti-inflamat?ria e as propriedades antivirais. Contudo, o potencial dos PS para sintetizar biomateriais, tais como nanopart?culas, ainda ? pouco explorado. At? ent?o, os PS s? foram encontrados em seis plantas e todas habitam ambientes salino. N?o havendo relatos de PS em plantas de ?gua doce. O que nos levou aos seguintes questionamentos: Os PS extraidos de vegetais marinhos n?o apresentam atividades farmacol?gicas? Os vegetais de ?gua doce realmente sintetizam PS? ? poss?vel sintetizar nanopart?culas utilizando PS a partir de algas marinhas? Para melhor entender as quest?es, esta tese foi dividida em tr?s cap?tulos. No primeiro cap?tulo, um polissacar?deo sulfatado (SPSG) foi isolado a partir de um vegetal marinho Halodule wrightii. Os dados aqui apresentados mostram que o SPSG ? uma heterogalactana sulfatada de 11 kDa constituida de glucose e xilose. Os ensaios realizados sugerem que o SPSG possue propriedades antioxidantes not?veis em diferentes ensaios in vitro e uma excelente actividade anticoagulante de 2,5 vezes mais elevadas do que a de heparina Clexane ? no teste APTT. No cap?tulo seguinte, utilizando ferramentas diferentes, tais como an?lises qu?micas e histol?gicas, an?lise de dispers?o de raios-X (EDXA), eletroforese em gel e espectroscopia de infra-vermelho,confirmamos, em primeira m?o, a presen?a de polissacar?deos sulfatados em vegetais de ?gua doce. Al?m de demonstrarmos que o PS extra?do a partir da raiz de E. crassipes tem potencial como um composto anticoagulante.No ?ltimo cap?tulo uma fucana, um polissac?rido sulfatado, extra?do a partir de uma alga marrom, foi quimicamente modificada por adi??o de hexadecilamina ? cadeia principal do pol?mero hidrof?lico. O material resultante (SNFuc) forneceu part?culas nanom?tricas. O grau de substitui??o para as cadeias hidrof?bicas de 1H RMN foi de aproximadamente 93%. SNFuc em meios aquosos tinha um di?metro m?dio de 123 nm e potencial zeta de -38,3 ? 0,74 mV. Os ensaios com c?lulas tumorais (HepG2, 786, H-S5) demonstrou a ocorr?ncia de uma inibi??o que variou de 2,0-43,7% em concentra??es diferentes de SNFuc (0,05-0,5 mg / mL) resultado semelhante foi obtido com a RAEC monstrando uma inibi??o entre 8,0-22,0%. Por outro lado, o nanogel estimulou a prolifera??o de linhagens celulares n?o tumorais como CHO e RAW nas mesmas concentra??es. An?lise por citometria de fluxo revelou que este nanogel de fucana inibiu a prolifera??o celular de 786 por mecanismos dependentes e independentes de caspases. Al?m disso, bloqueou a passagens da c?lula 786 na fase S e G2-M do ciclo celular
2020-01-01
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Chen, Y. Y. "Genetics of the anticoagulant drug warfarin." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597528.
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In this thesis I use the most widely prescribed anticoagulant drug, warfarin, as a model to investigate the effect of genetic determinants on drug efficacy and safety. Following a literature review of all the genes involved in warfarin pharmacokinetics and pharmacodynamics, 35 candidate genes were selected for investigation. Two independent Swedish cohorts of warfarin-treated patients were analysed. First linkage disequilibrium maps were constructed for each gene. Selected SNPs integrated with putative functional variants were genotyped in 201 patients recruited at the Uppsala University. A panel of 216 haplotype tag SNPs were then derived to analyse an independent cohort of 1496 patients from the prospective Warfarin Genetic Study in Sweden. The two studies were analysed separately for genetic association to warfarin dose requirement (single marker and haplotypic tests). Common SNPs in the vitamin K epoxide reductase gene (VKORC1) are significantly associated with dose in the Uppsala and WARG studies (p=1.9 x 10-15 and 6.5 x 10-100, respectively). Cytochrome P450 2C9 (CYP2C9) has been known to affect dose requirement and was confirmed in both Swedish cohorts (p= 2.3 x 10-5 and 4.9 x 10-32). The two genes together explain ~40% of warfarin dose variation. SNPs in microsomal epoxides hydrolase (EPHX1) and orosomucoid 1 (ORM1) genes do not show a broad effect but are associated with dose in both studies. Genes encoding PROC, APOE, CALU, PDIA2 and GGCX showed nominal association with dose in the Uppsala study. Likewise, PROS1, CYP1A1, CYP3A4, PDIA5, PDIA3 and F10 showed nominal association to dose in the WARG study. Most of these minor effects if real are most likely to be population/treatment specific. A model taking in to account genetic factors (VKORC1 and CYP2C9*2/*3) and non genetic factors (age, gender, and drug interaction) together explained more than 50% inter-individual dose variance. We analysed 64 patients from the Uppsala and WARG studies with recorded severe bleeding episodes using the same 216 common SNPs. Case-control analysis found SNPs in PDIA4, P4HB, and NR1I3 to be associated (p≤0.01) with bleeding. Using a recessive model, patients with a gastrointestinal bleeding sub-phenotype in the WARG cohort showed association with common variants in PD1A6 (P=0.0014, odds ratio = 6.98). We sequenced the exons of 11 of the candidate genes in 36 bleeders and 12 non-bleeders (Uppsala study). However, no high prevalence mutation was discovered.
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Tolrà, Rovira Roser. "Nova síntesi d'interès industrial d'un fàrmac genèric." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/462952.
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L'objectiu principal d'aquesta Tesi doctoral ha estat l’obtenció d’una via alternativa a les existents per a l'obtenció d'un intermedi clau, 1, en la síntesi d'un fàrmac anticoagulant. La nova via havia de ser novedosa i patentable per tal de poder obtenir el producte industrialment.
Així doncs inicialment es va fer una cerca bibliogràfica per tal de conèixer els precedents sintètics existents i a partir d'aquests es van proposar una sèrie d’objectius més concrets: una primera aproximació per tal de sintetitzar el ciclohexà central de 1, una altra basada en una reacció de iodolactamització per tal de tenir un dels nitrògens del sistema cis-diamino ja introduït i una tercera basada en una aziridina com a intermedi clau tenint en aquest cas tambè ja un dels nitrògens presents en la molècula.
La primera aproximació es basava en una reacció Diels-Alder com a etapa clau per a formar el ciclohexà central de la molècula objectiu. Tot i arribar a un intermedi força avançat, no es va poder arribar a producte final i es va haver de descartar aquesta aproximació.
La segona via que es va provar consistia en una reacció de iodolactamització com a etapa clau seguida de la formació del derivat de Boc.
A partir d’aquest intermedi es van proposar vàries alternatives per a substituir l’àtom de iode i introduir el segon nitrogen a la molècula, ja fos directament amb amoníac per exemple, o a travès d’un equivalent sintètic del grup amina com podia ser l’azida o bè el grup ftalimida. Tambè es va provar de formar intermedis tipus urea amb isocianats i introduïr així el segon nitrogen de l’anell de sis baules intramolecularment. Malauradament cap d’elles va permetre arribar a obtenir el producte objectiu 1 així que es va passar a estudiar la darrera aproximació.
La tercera via proposada passava per un intermedi clau aziridínic que es formava per reacció d’una olefina amb una sulfamida amb catàlisi de rodi. Desprès de provar la reacció principal a partir de diferents substrats, es va trobar un intermedi de tipus lactona inesperat però que va ser clau en aquesta aproximació. Seguint una sèrie de reaccions senzilles partint de la lactona es va arribar a obtenir 1.
Així doncs es va assolir l’objectiu d’obtenir una via per tal d’obtenir 1. Malaurdament degut a una reivindicació d’una patent que protegeix l’últim intermedi de la síntesi i la transformació d’aquest a 1, no serà possible sintetitzar industrialment 1 seguint aquest nou procès obtingut.
Tot i això, es va decidir seguir les reaccions de l’aproximació que havia permès obtenir 1, però variant el grup dimetilamida per altres grups alternatius. Es va pensar en formar èsters activats amb el 2,2,2-trifluoroetanol, el fenol i la N,N-
dietilhidroxilamina. Aquesta estratègia permetria arribar a obtenir la molècula objectiu però sense infringir la patent ja que, en la darrera etapa, seria on s’introduiria el grup dimetilamida de manera que no es passaria per l’intermedi reivindicat.
Malauradament, amb cap dels grups alternatius utilitzats es va aconseguir arribar a l’objectiu degut a la formació d’ intermedis tipus aziridina, els quals no es van poder transformar a la sulfamida bicíclica desitjada de cinc baules.The main objective of this Thesis was to obtain a novel and alternative route to the existing key intermediate 1 in the synthesis of an anticoagulant drug. The new approach had to be innovative and patentable in order to produce the product industrially. First of all, we searched in the literature the existing synthetic precedents and from these we proposed a series of more specific objectives: a first approach to synthesize the central cyclohexane, another based on a iodolactamization reaction, having one of the nitrogens in the cis-diamino system already introduced, and a third approach based on aziridine as a key intermediate, in this case it has also already one of the nitrogens present in the molecule. The first approach was based on a Diels-Alder reaction as a key step to form the central cyclohexane target molecule. Despite reaching an advanced intermediate, this approach failed to reach the final product and had to discard it. The second route that was tested had a iodolactamization reaction as a key step and followed the synthesis of the Boc derivative of this product . From this intermediate we proposed several alternatives to replace the iodine atom and introduce the second nitrogen in the molecule, either directly with ammonia for example, or through a synthetic equivalent of the amino group for example with an azide or a phthalimide group. We also tried to form an urea intermediate with isocyanate and thus insert the second nitrogen in the six member ring intramolecularly. Unfortunately none of the methods allowed us to arrive at the desired product so we kept on studying the latest approach. The third proposed route passes through a key aziridine intermediate that was formed by the reaction of an olefin with a sulfamide using rhodium catalysts. After testing the main reaction from different substrates, we found a lactone intermediate which was key in this approach. Following a series of simple reactions starting from the lactone we get the objective molecule 1. The main objective was achieved, unfortunately, due to a claim of a patent that protects the last intermediate synthesis and transformation of this to 1, it will not be possible to synthesize 1 industrially following this new process. However, we decided to follow the reactions of the approach that had yielded 1, but varying the dimethylamide group to other alternative groups. We thought about forming activated esters with 2,2,2-trifluoroethanol, phenol and N,N- diethylhydroxylamine. This strategy would reach the target molecule obtained without infringing the patent because it was in the last stage, where it would introduce the dimethylamide group so the route would not pass through the intermediate claimed.
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Bouchnita, Anass. "Mathematical modelling of blood coagulation and thrombus formation under flow in normal and pathological conditions." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1300/document.
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Cette thèse est consacrée à la modélisation mathématique de la coagulation sanguine et de la formation de thrombus dans des conditions normales et pathologiques. La coagulation sanguine est un mécanisme défensif qui empêche la perte de sang suite à la rupture des tissus endothéliaux. C'est un processus complexe qui est règlementé par différents mécanismes mécaniques et biochimiques. La formation du caillot sanguin a lieu dans l'écoulement sanguin. Dans ce contexte, l'écoulement à faible taux de cisaillement stimule la croissance du caillot tandis que la circulation sanguine à fort taux de cisaillement la limite. Les désordres qui affectent le système de coagulation du sang peuvent provoquer différentes anomalies telles que la thrombose (coagulation exagérée) ou les saignements (insuffisance de coagulation). Dans la première partie de la thèse, nous présentons un modèle mathématique de coagulation sanguine. Le modèle capture la dynamique essentielle de la croissance du caillot dans le plasma et le flux sanguin quiescent. Ce modèle peut être réduit à un modèle qui consiste en une équation de génération de thrombine et qui donne approximativement les mêmes résultats. Nous avons utilisé des simulations numériques en plus de l'analyse mathématique pour montrer l'existence de différents régimes de coagulation sanguine. Nous spécifions les conditions pour ces régimes sur différents paramètres pathophysiologiques du modèle. Ensuite, nous quantifions les effets de divers mécanismes sur la croissance du caillot comme le flux sanguin et l'agrégation plaquettaire. La partie suivante de la thèse étudie certaines des anomalies du système de coagulation sanguine. Nous commençons par étudier le développement de la thrombose chez les patients présentant une carence en antihrombine ou l'une des maladies inflammatoires. Nous déterminons le seuil de l'antithrombine qui provoque la thrombose et nous quantifions l'effet des cytokines inflammatoires sur le processus de coagulation. Puis, nous étudions la compensation de la perte du sang après un saignement en utilisant un modèle multi-échelles qui décrit en particulier l'érythropoïèse et la production de l'hémoglobine. Ensuite, nous évaluons le risque de thrombose chez les patients atteints de cancer (le myélome multiple en particulier) et le VIH en combinant les résultats du modèle de coagulation sanguine avec les produits des modèles hybrides (discret-continues) multi-échelles des systèmes physiologiques correspondants. Finalement, quelques applications cliniques possibles de la modélisation de la coagulation sanguine sont présentées. En combinant le modèle de formation du caillot avec les modèles pharmacocinétiques pharmacodynamiques (PK-PD) des médicaments anticoagulants, nous quantifions l'action de ces traitements et nous prédisons leur effet sur des patients individuelsThis thesis is devoted to the mathematical modelling of blood coagulation and clot formation under flow in normal and pathological conditions. Blood coagulation is a defensive mechanism that prevents the loss of blood upon the rupture of endothelial tissues. It is a complex process that is regulated by different mechanical and biochemical mechanisms. The formation of the blood clot takes place in blood flow. In this context, low-shear flow stimulates clot growth while high-shear blood circulation limits it. The disorders that affect the blood clotting system can provoke different abnormalities such thrombosis (exaggerated clotting) or bleeding (insufficient clotting). In the first part of the thesis, we introduce a mathematical model of blood coagulation. The model captures the essential dynamics of clot growth in quiescent plasma and blood flow. The model can be reduced to a one equation model of thrombin generation that gives approximately the same results. We used both numerical simulations and mathematical investigation to show the existence of different regimes of blood coagulation. We specify the conditions of these regimes on various pathophysiological parameters of the model. Then, we quantify the effects of various mechanisms on clot growth such as blood flow and platelet aggregation. The next part of the thesis studies some of the abnormalities of the blood clotting system. We begin by investigating the development of thrombosis in patients with antihrombin deficiency and inflammatory diseases. We determine the thrombosis threshold on antithrombin and quantify the effect of inflammatory cytokines on the coagulation process. Next, we study the recovery from blood loss following bleeding using a multiscale model which focuses on erythropoiesis and hemoglobin production. Then, we evaluate the risk of thrombosis in patients with cancer (multiple myeloma in particular) and HIV by combining the blood coagulation model results with the output of hybrid multiscale models of the corresponding physiological system. Finally, possible clinical applications of the blood coagulation modelling are provided. By combining clot formation model with pharmacokinetics-pharmacodynamics (PK-PD) models of anticoagulant drugs, we quantify the action of these treatments and predict their effect on individual patients
Books on the topic "Anticoagulant drugs"
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Anticoagulants, antiplatelets, and thrombolytics. 2nd ed. New York, NY: Humana, 2010.
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American Society of Health-System Pharmacists, ed. Anticoagulation therapy: A point-of-care guide. Bethesda, MD: American Society of Health-System Pharmacists, Inc., 2011.
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Gulseth, Michael. Managing anticoagulation patients in the hospital: The inpatient anticoagulation service. Bethesda, Md: American Society of Health-System Pharmacists, 2007.
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Handbook of compounds with anti-inflammatory and anti-platelet aggregation activities isolated from plants. New York: Nova Science Publishers, 2008.
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Waksman, Ron, and Andrew E. Ajani. Pharmacology in the catheterization laboratory. Chichester, West Sussex, UK: Wiley-Blackwell, 2009.
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Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York: Oxford University Press, 2006.
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Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York, NY: Oxford University Press, 2005.
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Božič-Mijovski, Mojca, ed. Anticoagulant Drugs. InTech, 2018. http://dx.doi.org/10.5772/intechopen.70971.
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Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0044.
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Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
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Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0044_update_001.
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Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
Book chapters on the topic "Anticoagulant drugs"
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Biswas, Subarna, Jun Sasaki, and Michelle Braunfeld. "Anticoagulant Drugs." In Essentials of Pharmacology for Anesthesia, Pain Medicine, and Critical Care, 397–413. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8948-1_24.
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Woerlee, G. M. "Anticoagulant Drugs & Surgery." In Common Perioperative Problems and the Anaesthetist, 247–52. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1323-3_46.
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Witt, Daniel M., and Nathan P. Clark. "Anticoagulant Drugs: Current and Novel." In Antiplatelet and Anticoagulation Therapy, 113–41. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4297-3_3.
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Green, Laura, and Samuel J. Machin. "Anticoagulant, Antiplatelet, and Thrombolytic Drugs." In Laboratory Hematology Practice, 535–42. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781444398595.ch41.
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Ghosh, Arun K., and Sandra Gemma. "Development of Direct Thrombin Inhibitor, Dabigatran Etexilate, as an Anticoagulant Drug." In Structure-Based Design of Drugs and Other Bioactive Molecules, 337–54. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2015. http://dx.doi.org/10.1002/9783527665211.ch15.
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Witiw, Christopher D., Laureen D. Hachem, and Michael G. Fehlings. "Classes of Drugs and Blood Products for Acute Reversal of Anticoagulant Effect." In Anticoagulation and Hemostasis in Neurosurgery, 227–42. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27327-3_17.
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Özkaya, Esen, and Kurtuluş Didem Yazganoğlu. "Anticoagulants." In Adverse Cutaneous Drug Reactions to Cardiovascular Drugs, 195–206. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6536-1_14.
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Corsini, Alberto, and Nicola Ferri. "Drug–Drug Interaction with DOACs." In Direct Oral Anticoagulants, 41–69. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74462-5_4.
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Pauli, R. M. "Anticoagulants." In Drug Toxicity in Embryonic Development II, 191–229. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60447-8_5.
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Nguyen, Phuong-Tan, Jessica Erin Sandy, and Ricardo Munoz. "Anticoagulants, Antithrombotics, and Antiplatelets." In Handbook of Pediatric Cardiovascular Drugs, 248–79. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-953-8_11.
Full textConference papers on the topic "Anticoagulant drugs"
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Day, H. J., R. Cherrey, D. O'Hara, and J. Carabello. "INCIDENCE OF PROCAINAMIDE-INDUCED LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644241.
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Isolated cases of lupus anticoagulants (LA) in association with procainamide have been reported. This study was done to estimate the frequency of LA in patients taking procainamide. Two groups of patients were evaluated: Group A: 110 hospitalized patients (84 males, 26 females, ages 51-78, mean age 74.3) and Group B: 80 ambulatory patients (54 males, 26 females, ages 36-89, mean 67.5 years). The latter group of patients was on this drug for a period of two-five years, while the former group hadbeen on drug at least two full days. All patients were screened with baseline laboratory data including activated partial thromboplastin time (APTT) and prothrombin time (PT) which were performed using Auto APTT® and Simplastin® on a Coagulamate X2® (General Diagnostics/Organon Teknika). Patients taking drugs known to alter the APTT and PT were excluded. All patients were followed with daily (hospital patients) or weekly (ambulatory patients) APTT and PT. Prolongation of the APTT of 5 sec or PT of 3 sec over baseline was considered as a positive LA screening test. Patients with a positive screening test were further evaluated with tissue thromboplastin inhibitor assay (TTI), platelet neutralization procedure (PNP, anti-nuclear antibodies (ANA) and blood serology (RPR). In Group A. 11 out of 110 (1096) developed prolonged APTT while on procainamide . Of these, 9 developed abnormal TTI and 2 had positive PNP. The ANA was positive (titers of 1:320-1:2560) in 10 patients with the only positive RPR test, being in the patient with the highest ANA titer. In Group B, 12 out of 80 (1596) developed prolonged APTT, 11 had positive TTI. The ANA titer was elevated in all positive cases, although one patient's titer was 1:30. The PNP was positive in 1/12. All blood serologies were negative in this group. The difference in incidence between Groups A and B may reflect longer exposure to drug in the latter group. This difference is not statistically significant. This study indicates that the incidence of procainamide-induced lupus antocoagulant is between 10-1596 when the APTT (or PT) is used as a screening test. The TTI and ANA seem to have equal sensitivity in this syndrome when taking this drug. The failure of the PNP to be sensitive to LA may be due to the minimal prolongation of the APTT arbitrarily chosen as representing a positive screening test.
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Rouvier, J., H. Vidal, J. Gallino, M. Boccia, A. Scazziota, and R. Altman. "ACUTE INTERRUPTION OF ORAL ANTICOAGULANT THERAPY: A THROMBOTIC RISK?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643265.
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It is still on discussion how oral anticoagulant therapy must be interrupted. A progressive diminution of drug intake have been proposed in order to avoid a MreboundM of vitamin K-dependent procoagulant factors. At the present, it is well known that coumarin drugs affect not only the biologic activity of factors II, VII, IX and X but also Protein C (PC), an inhibitor of coagulation kinetics, and their cofactor Protein S. With the aim to determine the recovery level of PC in relation with the others vitamin K-dependent factors, the effect of suppression of anticoagulant therapy in patients under chronic treatment with acenocoumarin was studied.Quick time, functional factors II, VII, X (one stage methods), functional PC (Francis method) and immunological Factor II and Protein C (Laurell) were determined before and 36 hours after suspension of acenocoumarin administration.Results showed that: 1) Recovery levels of functional Protein C (increased from 28.55% ±2.57 to 72.64% ±5.9) were significantly higer than functional Factor II (22.09% ±2.34 to 30.73% ±8.64), Factor VII (22.55% ±2.01 to 40.73% ±4.85) and Factor X (23.27% ±2.66 to 39.18% ±3.19). Statistical analysis (Newmann-Keuls test) showed at least a p<0.01 between PC increase and factors II, VII or X increment.2) No significant differences were seen between immunological levels of Factor II before and after suspension of acenocoumarin.3) Levels of immunological PC in patients under anticoagulant therapy were higer than functional PC. After acenocoumarin suppression, not correlation was seen between immunological and functional Protein C recovery.It is concluded that acute suppression of acenocoumarin does not induce a thrombotic tendency because the recuperation of functional Protein C is more important than factors II, VII and X recovery.
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Heptner, W., J. R. Suárez, and V. Lütgendorf. "STUDIES ON PLATELET AGGREGATION BY IMPEDANCE AGGREGOMETRY AND ATP SECRETION IN NON-ANTICOAGULANT BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644810.
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Investigations in vitro on the time-dependent increase in thrombin activityand platelet function have been used tocharacterize the kinetics of the clotting process in nonanticoagulated blood. The test procedures described involve great effort and expense and therefore are not suitable for routine tests in pharmacology and clinical pharmacology. The present contribution describes the determination of clotting times in ATP secretion in the Chrono-Log Whole Blood Aggregometer.Blood was taken from healthy donors who had not used any drug in the two weeks before the trial. 0.5 ml blood wereimmediately transfered into siliconizedglass cuvettes containing 0.4 ml salineand 0.1 ml luciferin-luciferase cocktail prewarmed to 37°C. Impedance and luminescence were recorded continuously. Clotting at the electrodes is indicated by an immediate steep rise in both impedance and luminescence. Clotting time is defined as the time from diluting the blood in the cuvettes until the point at which marked elevation of these variables begins.In the blood of twelve subjects the mean clotting time was 3.8 min and intersubject variation (SD) was 0.45 min. Drastic interindividual differences in response to collagen and ADP in citratedwhole blood were observed in the study group.In vitro addition of 20 μl Fibraccel(Behringwerke AG, Marburg, FRG),a platelet factor 3 containing plateletextract decreased clotting time by 35 %(n=10). In the presence of 0.2 U heparin a slow and lona-lasting increase in impedance was seen. 1 g oral AspirinR didnot influence clotting time measured ex vivo.The results indicate that whole blood aggregometry is a simple, fast, and precise method of determining blood clotting and the effects of drugs in a medium reflecting almost physiological conditions.
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Roncaglioni, M. C., I. Reyers, A. P. Bolognese Dolessandro, C. Cerletti, M. B. Donati, and G. de Gaetano. "SALICYLATE-WARFARIN INTERACTION: EFFECTS ON SYSTEMIC ANTICOAGULATION, BLEEDING TIME, AND EXPERIMENTAL VENOUS THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643270.
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The potential benefit of the aspirin/warfarin association as an antithrombotic treatment has been matter of debate in view of the major haemorrhagic effect reported with this drug combination. We have tested the effect of such association in a model of venous thrombosis already shown to be prevented by a fully anticoagulant schedule of warfarin. CD-COBS male rats were treated for three days with either warfarin (0.1 mg/kg i.v. once a day) or salicylate (175 mg/kg i.p. twice a day) or their combination (W+S). Systemic anticoagulation (thrombotest), template bleeaing time and occurrence of experimental venous thrombosis (ligature of inferior vena cava) were followed. Treatment with W or S alone did not affect template bleeding time, whereas the association (W+S) did (320+35 sec versus 120± 10 sec in the control group, p<0.01). Thrombotest was only slightly prolonged by single drug treatment (W= 43%, S=48% versus 90% of controls) but strongly prolonged in the association group (S+W=5%; p<0.001). The mechanism of this combined effect may be multifaceted; competition of both drugs for protein binding and the anticoagulant effect of salicylate itself could contribute. In any case, neither the incidence nor the weight of the thrombus were reduced by any drug treatment. Thus, W+S, in contrast to W alone (<5% thrombotest), was unable to prevent or reduce venous thrombosis, while prolonging bleeding time. Bleeding complications reported in clinical trials by the association of W and aspirin might not be solely due to the antiplatelet effect of aspirin.
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Merton, R. E., T. W. Barrowcliffe, and D. P. Thomas. "A COMPARISON OF DERMATAN SULPHATE AND HEPARIN AS ANTITHROMBOTIC DRUGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642933.
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Dermatan sulphate (DS) has been shown to accelerate thrcmbin inhibition by its action on heparin cofactor II (HCII) but has no effect on anti thrombin III (Tollefson et al., 1983). In this study, we have examined the in vitro anticoagulant effect of a purified preparation of DS (free from heparin and heparan sulphate), m comparison with that of unfractionated heparin (UEH). We have also studied the effect of DS and UEH in preventing experimental venous thrombosis in rabbits and in inhibiting thrombin generation, both in vitro and in ex vivo plasma samples.Dermatan had low activity in vitro by APTT and anti-Xa assays (< 5 iu/ mg). When thrombin generation was measured in vitro, 1 μg/ml UEH was sufficient to inhibit thrombin formation. Although 1 μg/ml DS reduced thrombin generation to 40% of control values, there was no further reduction when the concentration of DS was increased to 8 μg/ml.When DS was injected into rabbits (n = 10), a dose of 150 μg/kg inpaired thrombogenesis m a Wessler stasis model. The mean thrombus score was reduced to 25% of the control values, although thrombosis could not be completely prevented, even after an eight-fold increase m dose (1250 μg/kg). When the duration of stasis was extended from 10 to 20 minutes, there was no impairment of thrombosis (mean thrombus score 100%) following 1250 μg/kg of DS. Thrombin generation measured in ex vivo plasma after 150 μg/kg of DS was 72% (s.e.m. 63-81) of that measured in pre-injection plasma. In contrast, 150 μg/kg of heparin prevented thrombosis after both 10 and 20 minutes stasis (mean score 0%) and thrombin generation was reduced to 17% (s.e.m. 12-23) of control values m ex vivo plasma samples.Unlike heparin, DS does not completely abolish thrcmbin generation in vitro and is not as potent as UEH in inhibiting thrombin generation m ex vivo plasma. While DS has demonstrable antithrombotic activity under defined conditions, it is less effective than heparin and increasing doses of DS do not improve antithrombotic effectiveness in this model.
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Poort, S. R., C. Krommenhoek-van Es, I. K. van der Linden, N. H. van Tilburg, and R. M. Bertina. "DEFECTS OF VITAMIN K-DEPENDENT FACTORS IN CA(11)-STABILI ZED STRUCTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644320.
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Vitamin K-dependent (anti)coagulation factors (factor II, VII, IX, X protein C and S) undergo a conformational transition upon binding of Ca(II), which is a prerequisite for their normal function. Abnormalities in these properties occur during vitamin K deficiency or treatment with anti vitamin K drugs and in some genetic variants of coagulation factors. Immunological assays utilizing antibodies against the Ca(II)-stabilized structure are useful to detect such abnormalities.Starting from specific rabbit antisera antibody populations specific for the Ca(II)-dependent conformation of factor II, VII, IX, X and protein C and S were isolated using immuno-affinity procedures. Subsequently immunoradiometric assays specific for the Ca(II)-dependent (Ca(II)Ag) and Ca(II)-independent (NonCa(II)Ag) conformations of the different proteins were developed. These assays were used for the analysis of plasmas of patients stably treated with oral anticoagulants; Ca(II)Ag, NonCa(II)Ag and their ratio were measured as function of the intensity of the treatment (INR 2.4 to 4.8). The same parameters were measured in plasmas of patients with hereditary coagulation disorders. After treatment with oral anticoagulation with an antivitamin K drug reduced ratios of Ca(II)Ag/-NonCa(II)Ag were observed for factor II, VII, IX, protein C and protein S. However, the actual degree of reduction and its dependence on the intensity of treatment varied for the different vitamin K-dependent proteins. In general Ca(II)Ag levels correspond nicely with the procoagulant activity of the concerning proteins. These data provide indirect evidence for the existence of abnormal (non and/or subcarboxylated) forms of the vitamin K-dependent proteins during oral anticoagulant treatment.Genetic variants with a mutation in one of the sites involved in the formation of the Ca(II)-s tab i1ized structure could be detected for factor IX, factor VII and factor II. However, the extent of reduction of the ratio Ca(II)Ag/-NonCa(II)Ag differed considerably in those variants.
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Borowska, A., D. Lauri, A. Maggi, E. Dejana, G. de Gaetano, and J. Pangrazzi. "IMPAIREMENT OF PRIMARY HAEMOSTASIS BY LMW-HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643172.
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Low molecular weight (LMW) heparlns have been developed with the aim of reducing anticoagulant activity thereby minimizing the bleeding complications of conventional heparin. Unexpectedly, bleeding events were reported during treatment with some LMW-heparins, in clinical and experimental studies. We studied the effect of four different LMW-heparlns on primary haemostasis In male rats (CD COBS, Charles River) after l.v. administration of 0.75 mg/kg b.w. of the drugs. LMW heparin A was devoid of any activity on an experimental model of “template” bleeding time in rats (110.6±5.9 sec versus 108.7±4.1 control values) whereas LMW-heparins B, C and D prolonged the bleeding time to a different extent (228.7±19.9, 161.5±6.4 and 161.7±8.6 respectively). Pretreatment of animals with aspirin (100 mg/kg b.w. per o.s). resulted In a significant potentiation of the “template” bleeding time. In vitro platelet aggregation Induced by collagen (20 μg/ml) or by collagen in combination with ADP (5-10 μM) was strongly inhibited by LMW-heparln B, while LMW-heparln A showed no effect. LMW-heparins C and D exerted an Intermediate level of Inhibition of platelet aggregation. The same pattern of aggregating response was found when LMW-heparins A and B were given i.v. to rats (0.75 mg/kg b.w.) and platelet aggregation was studied “ex vivo” 15 min after drug administration.These data may help explain the impairment of primary haemostasis associated with some LMW-heparin preparations.
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Roth, A., G. I. Barbash, H. I. Miller, G. Keren, S. Laniado, and U. Seligsohn. "BLEEDING COMPLICATIONS DURING RT-PA THROMBOLYSIS RELATED TO USE OF ANTI-INFLAMMATORY DRUGS PRIOR TO ACUTE MYOCARDIAL INFARCTION ADMISSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642977.
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Of 57 patients with acute myocardial infarction (AMI) treated with rt-PA, we observed 2 major bleeding complications, both in patients who had been treated with anti-inflammatory drugs prior to admission. The thrombolytic protocol included: lOmg rt-PA in bolus and continuous infusion of 110 mg over 6 hr 5,000 iu heparin in bolus and continuous infusion of 25,000 iu/ 24hr, and aspirin 250 mg/24hr. The first patient, a 64 year old woman had been taking indomethacin 25 mg × 3 daily, during 3 weeks prior to the AMI. Rt-PA protocol was initiated with relief of chest pain and disappearance of ST elevation, but at 2 hr rt, sciatic pain developed. Treatment was continued accor ding to protocol in spite of the pain, but on the 3rd day hemoglobin decreased to 7.8%. Abdominal CT scan disclosed retroperitoneal hemorrhage. All anticoagulant medications were stopped, and 4 units of blood were transfused. The retro-peritoneal mass dissolved gradually. The second patient, a 68 year old male was treated by diclofenac 100 mg for 5 days prior to admission for AMI, and consequently aspirin was removed from the rt-PA protocol. However, 2 hr after completion of the 6 hr rt-PA infusion, gross hematuria and a “coffee ground” vomiting developed. Heparin infusion was discontinued and antacid treatment initiated, resulting in cessation of bleeding within a few hrs. In both patients the anticipated prolongation of APTT (heparin) and about 30% decrease in fibrinogen level were observed as the sole abnormality, and thus we related the bleeding episodes to the anti-aggregating effect of indomethacin and diclofenac respectively. We suggest that the use of anti-inflammatory drugs prior to administration of rt-PA protocol can be hazardous, and that special prudence (possibly protocol modification) is warranted.
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Pérez-Requejo, J. L., J. Aznar, T. Santos, and J. Vallés. "ANTIPLATELET ACTIVITY OF DYPIRIDAMOLE IN HUMAN WHOLE BLOOD WITH PHYSIOLOGICAL LEVELS OF IONIZED CALCIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643421.
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In spite of the windespread use of dypiridanole (DP) as an anti thrombotic drug, its usefullnes has not been generally proved. The clinical trials have been somewhat inconclusive or challenge and most of the studies were not able to snow a clear inhibitory action of DP on platelet aggregation. Using the impedance aggre gometer it has been shewn that the antiplatelet action of DP can be demonstrated in whole blood (WB) ex vivo an it was suggested that this was due to the inhibition of adenosin reuptake by the red cells. We have recently described (Thrombos & Haerostas 54: 799, 1985) a method, that detects the early platelet-collagen interaction in whole blood, which has been called BASIC wave. Using slight modifications of the BASIC wave method, we were able to study the platelet-collagen interactions in native WB with physio logical levels of calcium and its inhibition by DP ex vivo. We performed the BASIC wave in 25 human healthy volunteers in WB without sodium citrate, WB with citrate and citrated platelet rich plasma (PRP) before and 2 hours after the oral administration of DP 3mg/kg. We observed that in WB with citrate, DP produced a 66% inhibition of the BASIC wave (p<0.005) in PRP the inhibition was 40.7% (p< 0.005) but it was a non-significant 21.7% in WB without citrate. Using hirudin 40U/ml as anticoagulant, the inhi bition was the same as in WB without citrate. There were no correlation between the oral dose and the DP plasma levels or with the observed inhibition of the BASIC wave. We postulate that the antiplatelet action of DP is only demonstrable in citrated samples, beer negligible in native blood with physiological levels of calcium. The present report could explain the lack of firm da ta supporting the antithrombotic action of DP in clinical trials. Furthermore, the method here presented allows the study of anti -thrombotic drugs ex vivo in whole blood in its normal calcium environement.
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Lefrere, J. J., D. Vittecoq, D. Gozin, and J. Modai. "CIRCULATING ANTICOAGULANT IN AIDS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644859.
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The frequency of a circulating anticoagulant has been reported to be high in AIDS, in particular in case of Pneumocystic carinii pneumonia (Pep). Twenty-five non-hemophiliac patients (23 homosexual males,1 drug addict, 1 tranfused) with AIDS were followed over a six month period. Mean age was 32 (21-42). All patients had a markedly decreased T4/T8 ratio (mean 0.12), a low absolute T4 level (mean : 155/mm3), an elevated total serum immunoglobulins level.Activated partial thromboplastin time (APTT), prothrombintime and thrombin time were measured once a week during hospitalisation. A prolonged APTT (more than 10 seconds as compared to controls) with normal prothrombin time and thrombin time was found only once in 11patients and in two or more occasions in two others.No specific factor level of intrinsic pathway wasfound low enough to explain a prolonged APTT.Evidenceofcirculating anticoagulant (failure to correct aprolonged APTT by equal mixure of normal plasma and patient plasma) was found in all these 13 patients.Nothrombotic or haemorraghic manifestations occured.AIDS manifestations were 2 Pep.1 cytomegalovirus retinitis. 2 Kaposi's sarcomas, 1 Hodgkin's disease, 2 mycobacterium avium intracellulare pulmonary infection, 4 central nervous system toxoplasmosis, 1 Cryptococcus meningitis. Amongst the 12 patients with normal APTT,3_Pcp, 2 cytomegalovirus retinitis. 2 Kaposi's sarcomas, 2 central nervous system toxoplasmosis, 1 unexplained fever, and 2 oesophagus candidiasis were diagnosed. A transiently prolonged APTT associated to a circulating inhibitor seems to be common in AIDS. Weobserved this anomaly in 52 % (13/25). In our five cases of Pcp, 3 had normal APTT. During other opportunistic infections, the circulating inhibitor was found.The similar complications seen in two groups suggest that a circulating anticoagulant is not specifically associated to any opportunistic infection and any malignancybut appearr independently from these circumstances.