Academic literature on the topic 'Heparin Therapeutic use'
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Journal articles on the topic "Heparin Therapeutic use"
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Banik, Nipa, Seong-Bin Yang, Tae-Bong Kang, Ji-Hong Lim, and Jooho Park. "Heparin and Its Derivatives: Challenges and Advances in Therapeutic Biomolecules." International Journal of Molecular Sciences 22, no. 19 (September 29, 2021): 10524. http://dx.doi.org/10.3390/ijms221910524.
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Heparin has been extensively studied as a safe medicine and biomolecule over the past few decades. Heparin derivatives, including low-molecular-weight heparins (LMWH) and heparin pentasaccharide, are effective anticoagulants currently used in clinical settings. They have also been studied as functional biomolecules or biomaterials for various therapeutic uses to treat diseases. Heparin, which has a similar molecular structure to heparan sulfate, can be used as a remarkable biomedicine due to its uniquely high safety and biocompatibility. In particular, it has recently drawn attention for use in drug-delivery systems, biomaterial-based tissue engineering, nanoformulations, and new drug-development systems through molecular formulas. A variety of new heparin-based biomolecules and conjugates have been developed in recent years and are currently being evaluated for use in clinical applications. This article reviews heparin derivatives recently studied in the field of drug development for the treatment of various diseases.
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Mycroft-West, Courtney J., Lynsay C. Cooper, Anthony J. Devlin, Patricia Procter, Scott E. Guimond, Marco Guerrini, David G. Fernig, Marcelo A. Lima, Edwin A. Yates, and Mark A. Skidmore. "A Glycosaminoglycan Extract from Portunus pelagicus Inhibits BACE1, the β Secretase Implicated in Alzheimer’s Disease." Marine Drugs 17, no. 5 (May 16, 2019): 293. http://dx.doi.org/10.3390/md17050293.
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Therapeutic options for Alzheimer’s disease, the most common form of dementia, are currently restricted to palliative treatments. The glycosaminoglycan heparin, widely used as a clinical anticoagulant, has previously been shown to inhibit the Alzheimer’s disease-relevant β-secretase 1 (BACE1). Despite this, the deployment of pharmaceutical heparin for the treatment of Alzheimer’s disease is largely precluded by its potent anticoagulant activity. Furthermore, ongoing concerns regarding the use of mammalian-sourced heparins, primarily due to prion diseases and religious beliefs hinder the deployment of alternative heparin-based therapeutics. A marine-derived, heparan sulphate-containing glycosaminoglycan extract, isolated from the crab Portunus pelagicus, was identified to inhibit human BACE1 with comparable bioactivity to that of mammalian heparin (IC50 = 1.85 μg mL−1 (R2 = 0.94) and 2.43 μg mL−1 (R2 = 0.93), respectively), while possessing highly attenuated anticoagulant activities. The results from several structural techniques suggest that the interactions between BACE1 and the extract from P. pelagicus are complex and distinct from those of heparin.
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Beurskens, Danielle M. H., Joram P. Huckriede, Roy Schrijver, H. Coenraad Hemker, Chris P. Reutelingsperger, and Gerry A. F. Nicolaes. "The Anticoagulant and Nonanticoagulant Properties of Heparin." Thrombosis and Haemostasis 120, no. 10 (August 20, 2020): 1371–83. http://dx.doi.org/10.1055/s-0040-1715460.
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AbstractHeparins represent one of the most frequently used pharmacotherapeutics. Discovered around 1926, routine clinical anticoagulant use of heparin was initiated only after the publication of several seminal papers in the early 1970s by the group of Kakkar. It was shown that heparin prevents venous thromboembolism and mortality from pulmonary embolism in patients after surgery. With the subsequent development of low-molecular-weight heparins and synthetic heparin derivatives, a family of related drugs was created that continues to prove its clinical value in thromboprophylaxis and in prevention of clotting in extracorporeal devices. Fundamental and applied research has revealed a complex pharmacodynamic profile of heparins that goes beyond its anticoagulant use. Recognition of the complex multifaceted beneficial effects of heparin underscores its therapeutic potential in various clinical situations. In this review we focus on the anticoagulant and nonanticoagulant activities of heparin and, where possible, discuss the underlying molecular mechanisms that explain the diversity of heparin's biological actions.
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Ludwig, Ralf. "Therapeutic Use of Heparin beyond Anticoagulation." Current Drug Discovery Technologies 6, no. 4 (December 1, 2009): 281–89. http://dx.doi.org/10.2174/157016309789869001.
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Kutzner, H., and G. Hesse. "Therapeutic use of lowmolecular weight heparin for capillaritis alba." Phlebologie 37, no. 05 (2008): 259–65. http://dx.doi.org/10.1055/s-0037-1622240.
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SummaryThe reason of the so called ulcerated capillaritis alba or idiopathic atrophie blanche is vasculopathy caused by severe venous hypertension. Thrombosed and rarificated vessels worsen the oxygenation, increase permanent inflammation and impede the necessary compression therapy. The anti-inflammatory effects of heparin alleviate pain and being independent from the antithrombotic ones it needs much lower doses for treatment. This anti-inflammatory effect is now becoming more important in clinical phlebology. Case studies of more than 50 patients and one prospective randomized study of 87 patients clearly demonstrate the ameliorated healing of ulcerated atrophie blanche. In our office we could document this positive effect with 22 patients. We present the pathophysiology of low molecular heparins for ulcerated capillaritis alba and our own experiences with it.
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Shaughnessy, SG, E. Young, P. Deschamps, and J. Hirsh. "The effects of low molecular weight and standard heparin on calcium loss from fetal rat calvaria." Blood 86, no. 4 (August 15, 1995): 1368–73. http://dx.doi.org/10.1182/blood.v86.4.1368.bloodjournal8641368.
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Osteoporosis is a well-recognized complication of long-term heparin use. However, the mechanisms by which heparin can influence bone metabolism are unclear. We report here that unfractionated heparin stimulates the process of bone resorption and that the low molecular weight heparins (LMWHs), enoxaparin, fragmin, logiparin, and ardeparin produce significantly less calcium loss than unfractionated heparin. To assess calcium loss from bone, we quantified the release of 45Ca into the culture medium of fetal rat calvaria. 45Ca release was increased in a dose-dependent manner by the addition of either unfractionated heparin or the LMWHs; but more than 50-fold higher LMWH concentrations were required to obtain an equivalent effect to unfractionated heparin. Thus, at concentration > or = 2 micrograms/mL (0.35 anti-Xa units/mL), unfractionated heparin stimulated 45Ca release 1.53 +/- 0.06 fold. 45Ca release was increased to a similar extent by the addition of either 10(- 7) mol/L parathyroid hormone (PTH) or 10(-6) mol/L 1,25 dihydroxyvitamin D3 (1,25 Vit D3). In contrast to unfractionated heparin, LMWH concentrations > or = 100 micrograms/mL (> or = 14.0 anti- Xa units/mL) were required before maximum isotope release was observed. At concentrations well above therapeutic levels, the LMWHs stimulated 45Ca release by only 1.25 /+- 0.01-fold. Heparins with high and low antithrombin III affinities stimulated 45Ca release equally well. Both size and sulfation were found to be major determinants of heparin's ability to promote isotope release. Thus, the ability of defined heparin fragments to stimulate 45Ca release correlated with their molecular weight, and after N-desulfation the ability of heparin to induce isotope release was greatly diminished. Dermatan sulfate had no effect on 45Ca release. We conclude that size and sulfation are major determinants of heparin's ability to promote bone resorption and that the risk of heparin-induced osteoporosis may be reduced by the use of LMWH preparations.
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Hoffman, Nannette B., and David J. Frohnapple. "Heparin Dosing Order Form Use in an Academic-Affiliated Veterans Affairs Medical Center." Journal of Pharmacy Technology 12, no. 6 (November 1996): 276–79. http://dx.doi.org/10.1177/875512259601200609.
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Objective: Because a drug utilization evaluation (DUE) showed poor intravenous heparin prescribing practice in our medical center, we developed a preprinted intravenous heparin order form for use by physicians to improve heparin administration. Methods: Two DUEs were performed, one prior to use of a weight-based heparin dosing order form and another after the introduction of the form. Indicators that were evaluated included dosing, laboratory monitoring, and intramuscular injections. DUE results before and after introduction of the order form were statistically compared using Fisher's exact text. Results: The initial DUE showed that only 3% of patients who were administered intravenous heparin received appropriate dosing, and only 60% had a therapeutic activated partial thromboplastin time (aPTT) ratio within the first 24 hours. Blood samples for the aPTTs were drawn at incorrect × in 27% of patients, and 9% of patients received intramuscular injections of other drugs. After implementation of the preprinted intravenous heparin order form, 73% of the patients received appropriate heparin dosing (p < 0.00001), and 79% of the patients had a therapeutic aPTT ratio within the first 24 hours (p = 0.08). The aPTTs were drawn at incorrect × in 12% of patients, and 3% of patients received intramuscular injections (NS for both). All patients receiving appropriate heparin dosing achieved a therapeutic aPTT ratio within the first 24 hours, whereas only 29% of patients on the acute wards and 50% of those in the intensive care units achieved a therapeutic ratio when dosing was inappropriate (p < 0.0001). Conclusions: We improved the intravenous heparin prescribing practice in an academic-affiliated tertiary Veteran's Affairs Medical Center using a preprinted intravenous heparin order form for physician use. The form was also effective in achieving the desired aPTT ratio within 24 hours.
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Bitsadze, V. O., E. V. Slukhanchuk, J. Kh Khizroeva, M. V. Tretyakova, N. V. Pyatigorskaya, S. V. Akinshina, N. A. Makatsariya, et al. "Anticoagulant, anti-inflammatory, antiviral and antitumor properties of heparins." Obstetrics, Gynecology and Reproduction 15, no. 3 (July 9, 2021): 295–312. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2021.216.
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Our knowledge regarding chemical structure and properties of heparin and its derivatives, including biological properties in blood plasma, on the cell surface and while interacting with receptors, has been progressively growing. New insights are followed by the expansion of therapeutic opportunities and indications for the use of heparins. There are prerequisites for the creation of new generation drugs with modified properties that reduce a bleeding risk while applied for a non-anticoagulant goal. The non-anticoagulant heparin properties allow to consider it as a candidate for pathogenetic treatment of patients with COVID-19. This review focuses on the anticoagulant and non-anticoagulant heparin properties as well as the underlying molecular mechanisms.
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Sung, Michelle, Jeanine Walenga, Walter Jeske, Omer Iqbal, and Mamdouh Bakhos. "Comparing a New Bovine Source Heparin to the Clinically Used Porcine Heparin for Platelet Function Effects and Heparin-Induced Thrombocytopenia Potential." Blood 132, Supplement 1 (November 29, 2018): 2540. http://dx.doi.org/10.1182/blood-2018-99-118781.
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Abstract Background Heparin is a sulfated polysaccharide obtained from intestinal mucosa with anticoagulant properties that is widely used as a standard clinical therapeutic agent to treat and prevent thrombosis. Heparin is known to affect platelet function, and among its side effects is heparin-induced thrombocytopenia (HIT) that can occur in about 1% of patients exposed to heparin. Presently, only porcine source heparin is approved for use in the United States. The aims of this study were to determine if platelet activation by physiological agonists and platelet aggregation induced by HIT antibodies would be equivalent in the presence of bovine source heparin and porcine source heparin. Materials and Methods Seven lots of bovine heparin from Eurofarma and 3 lots of commercial clinical grade porcine heparin (Pfizer/Hospira) were evaluated. The USP Reference Standard for porcine heparin was used to determine anti-Xa and anti-IIa potencies of the bovine heparins. For each study, blood was collected from healthy volunteers (n=5 per test group), anticoagulated with sodium citrate, and centrifuged to obtain platelet rich plasma (PRP). Platelet aggregation responses were assessed using the BioData PAP-8 platelet aggregometer. For the first aim to evaluate platelet function, PRP was combined with heparin at final concentrations of 10.0, 1.0, and 0.1 µg/mL, covering both therapeutic and prophylactic ranges. Platelet agonists included adenosine diphosphate (ADP), collagen, epinephrine, arachidonic acid, and thrombin receptor agonist peptide (TRAP). The aggregation response was quantitated in terms of primary slope (PS), area under the curve (AUC), maximum aggregation (MA), and final aggregation (FA). For the second aim to evaluate the HIT potential, antibodies to the complex of heparin-platelet factor 4 (H-PF4) from banked HIT patient apheresis fluid were combined with donor PRP and heparin. Heparins were tested at final concentrations of 0.1, 0.4, 0.8, 1, and 100 U/mL. PS and FA results were recorded. For all data, comparisons were analyzed with 2-Way ANOVA using SigmaPlot software. Results In the presence of either bovine (BMH) or porcine heparin (PMH), the normal platelet aggregation response of all donors was not altered from that obtained with saline (see representative aggregation tracing in the image below). All heparin concentrations produced the same response. There were no significant differences between the bovine and porcine heparins for each of the 4 platelet aggregation parameters for ADP, arachidonic acid, collagen, epinephrine, and TRAP. Variation in the PS for arachidonic acid and collagen need to be assessed in a larger pool of donors to assure the lack of significant difference. Platelet activation to H-PF4 antibodies was strong at 0.1 to 1 U/mL concentrations with the expected inhibition observed when using 100 U/mL heparin. The HIT potential between bovine heparin and porcine heparin demonstrated no significant difference between the heparins (see MA responses in the image below). There were no lot to lot differences for the bovine heparins or the porcine heparins in either the platelet aggregation studies or the assessment for HIT. Conclusion In these studies of platelet function, the bovine and porcine source heparins were comparable with regards to their effects on platelet aggregation induced by multiple different agonists and their HIT potential. Figure. Figure. Disclosures Walenga: Eurofarma: Research Funding.
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Oliynyk, Oleksandr, Wojciech Barg, Anna Slifirczyk, Yanina Oliynyk, Serhij Dubrov, Vitaliy Gurianov, and Marta Rorat. "Comparison of the Effect of Unfractionated Heparin and Enoxaparin Sodium at Different Doses on the Course of COVID-19-Associated Coagulopathy." Life 11, no. 10 (September 30, 2021): 1032. http://dx.doi.org/10.3390/life11101032.
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Background: COVID-19-associated coagulopathy (CAC) exacerbates the course of coronavirus infection and contributes to increased mortality. Current recommendations for CAC treatment include the use of low-molecular weight heparins (LMWH) at prophylactic or therapeutic doses, as well as the use of unfractionated heparin (UFH). Methods: A randomised, controlled trial enrolled 126 patients hospitalised in the intensive care unit with severe COVID-19 complicated by CAC. The effects of LMWH at preventive and therapeutic doses and UFH at therapeutic doses on mortality and intubation rates were compared. Results: The number of intubations and deaths showed no significant difference depending on the anticoagulant therapy used. However, multivariate logistic regression models revealed an increased risk of intubation (p = 0.026, odds ratio (OR) = 3.33, 95% confidence interval (CI) 1.15–9.59), and an increased risk of death (p = 0.046, OR = 3.01, 95% CI 1.02–8.90), for patients treated with LMWH at a prophylactic dose but not at a therapeutic dose as compared to patients treated with UFH when controlling for other risk factors. Conclusions: The use of unfractionated heparin in the treatment of COVID-19-associated coagulopathy seems to be more effective at reducing the risk of intubation and death than enoxaparin at prophylactic doses.
Dissertations / Theses on the topic "Heparin Therapeutic use"
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Lim, Rebecca. "Role of interferon α and γ in the hepatic progenitor (oval) cell response." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0081.
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[Truncated abstract] Hepatic progenitor cells (HPC) are becoming increasingly recognized as facultative stem cells capable of regenerating the liver during chronic liver injury and also as targets of malignant transformation. Similar markers are expressed by hepatocellular carcinoma (HCC) and HPC, and a precursor-product relationship is well established. This thesis focuses on the ways in which the HPC population can be controlled under circumstances of chronic liver injury, and in this manner, reduce the risk of progression to HCC reduced. The major aim of Chapters 3 to 5 was to elucidate the effect of interferon α (IFNα) therapy on HPC. Chronic hepatitis C affects approximately 250 million individuals world wide. Approximately 80% of infections progress to chronicity, which places the individuals at greater risk of developing HCC. The gold standard of treatment of chronic hepatitis C is a combination of pegylated IFNα and ribavirin. ...The results were surprising. While IFNγ exerted a pro-apoptotic and antiproliferative effect on HPC in vitro, administration of IFNγ to CDE-fed mice for 14 days increased fibrosis, enhanced inflammatory infiltration and exacerbated the HPC response, with concurrent hepatocyte cell death. In addition, increased morbidity and mortality were observed in the IFNγ-treated mice compared to control. IFNγ treatment was found to prime the liver for the HPC response by recruiting inflammatory cells and altering the hepatic cytokine profile, both of which may facilitate an increased HPC response. Numbers of activated HSC were also increased in the IFNγ-treated, CDE-fed mice, correlating with the increased fibrosis seen in these animals. This data contradicts the current experimental use of IFNγ for treatment of fibrosis. Based on our results, we suggest that IFNγ promotes HPC proliferation in the CDE model, by encouraging inflammatory infiltration and hepatocyte damage and this initiates pro-fibrotic events. Concurrent proliferation of HPC and activated HSC further supports the view that there is a close relationship between the two cell types, and thus, a link between the HPC response and fibrosis. In conclusion, findings documented in this thesis suggest that administration of IFNα and IFNγ can contribute to shaping the HPC response. IFNα therapy may reduce HCC risk in chronic hepatitis C patients by bringing the HPC population under control. In contrast, IFNγ treatment can exacerbate the HPC response, liver fibrosis and parenchymal damage, illustrating the need to approach this method of fibrosis treatment with caution.
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Davies, Richard. "Effect of selective COX-2 inhibitors on hepatic progenitor cells and the pathologies of experimental hepatocarcinogenesis." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0190.
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[Truncated abstract] Hepatocellular carcinoma (HCC) is the major malignancy complicating chronic liver disease. New therapies for the prevention of HCC are required due to the limited success and high tumour recurrence rates of existing treatments. Emerging evidence suggests that HCC arise from the transformation of adult liver progenitor cells (LPCs), which have the capacity to differentiate into hepatocytes and biliary cells during liver regeneration. LPC activation precedes neoplasia in experimental hepatocarcinogenesis. LPCs share antigenic epitopes with HCCs, including α-fetoprotein (AFP) and M2- pyruvate kinase (M2PK). In animal models of hepatocarcinogenesis, attenuation of the LPC response reduces the incidence of HCC following prolonged liver injury via a tumour necrosis factor (TNF) dependent mechanism. As TNF is a pro-inflammatory cytokine, these data suggest that anti-inflammatory agents may be effective in inhibiting LPC activation and hepatocarcinogenesis. Cyclo-oxygenase-2 (COX-2) is an inducible enzyme that mediates the production of many prostaglandins during inflammation and carcinogenesis. Recent investigations show that the administration of selective COX-2 inhibitors (SC2Is) may reduce the incidence of a variety of tumours including breast, colon and skin. The broad aim of this thesis was to conduct a series of detailed studies on the effects of a SC2I on LPC activation and the hepatic pathologies associated with hepatocarcinogenesis in order to test the hypothesis that S2CIs may be a beneficial therapy that can reduce liver injury and pre-neoplastic changes in the choline-deficient, ethionine supplemented (CDE) murine model of hepatocarcinogenesis. Administration of a SC2I (SC-236) significantly inhibited a variety of hepatic cell populations that expand during the first month of the CDE mouse model of hepatocarcinogenesis (a choline deficient, ethionine supplemented diet). Numbers of M2PK-positive LPCs (which are more hepatocytic in morphology and are also COX-2 positive) and inflammatory cells were all significantly reduced by SC-236. In contrast, numbers of A6-positive LPCs (which are more biliary cell-like in morphology and do not express COX-2) were unchanged. ... In summary, these data suggest that COX-2 inhibitors such as SC-236 inhibit LPC activation and a variety of pre-neoplastic liver pathologies as a result of COX-2 dependent and independent mechanisms that may be mediated through inhibition of Akt phosphorylation and induction of apoptosis. Moreover, SC2Is may be useful as preventative treatment strategies for HCC in patients with chronic liver disease.
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Filho, Joel Avancini Rocha. ""Efeitos da solução salina hipertônica na reperfusão hepática em pacientes submetidos ao transplante do fígado"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-22032006-202604/.
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INTRODUÇÃO: No transplante do fígado a reperfusão do enxerto é um momento crítico onde as alterações hemodinâmicas ocorrem com maior freqüência e intensidade podendo se associar a mortalidade intra-operatória, à falência de múltiplos órgãos e sistemas, e ao aumento da incidência de não funcionamento do enxerto. Neste estudo testamos a hipótese de que os efeitos benéficos decorrentes da administração da solução salina hipertônica na ressuscitação do choque hemorrágico, considerado fenômeno de isquemia e reperfusão generalizado, possam atenuar os fenômenos hemodinâmicos que sucedem a reperfusão hepática no transplante do fígado. MÉTODOS: 30 pacientes adultos submetidos ao transplante hepático na Disciplina de Transplante e Cirurgia do Fígado do HC-FMUSP foram divididos em 2 grupos: Grupo-1 (n =15) recebeu solução salina hipertônica (NaCl a 7,5%), na dose de 4 mL/kg, na velocidade de 20 mL/min em veia central no início da anastomose de veia porta e Grupo- 2 (n =15) recebeu solução salina isotônica nas mesmas condições citadas. As variáveis utilizadas para a análise da hemodinâmica sistêmica foram: pressão arterial média, pressão venosa central e pressão de artéria pulmonar ocluída, índice cardíaco e índice de resistência vascular sistêmica. A análise da pressão intracraniana foi incluída no estudo dos pacientes com hipertensão intracraniana secundária a hepatite fulminante. Os dados foram coletados em 6 tempos: no término da fase de dissecção, no início da fase anepática, após a administração da solução teste, e no 1o, 5o e 30o minutos após a reperfusão. A síndrome pós-reperfusão foi determinada por três métodos: pela ocorrência de pressão arterial média inferior a 60 mmHg no 1o ou no 5o minuto da reperfusão ou queda maior que 30% do valor pré-reperfusão nos primeiros 5 minutos da reperfusão. RESULTADOS: 1) A pressão arterial média no 1o e no 5o minuto da reperfusão no Grupo 1 (84,9 ± 12,33 e 77,4 ± 4,58 mmHg) foi significativamente maior que no Grupo 2 (62,9 ± 5,22 e 73,9 ± 3,47 mmHg), p < 0,001 e p = 0,046 respectivamente. 2) A incidência de síndrome pós-reperfusão no Grupo 1 (0.0%) foi significativamente menor que no Grupo 2 (33,33%), p = 0,021. 3) O aumento do índice cardíaco imediatamente após o término de infusão da solução teste no Grupo 1 (31,27%) foi significativamente maior que no Grupo 2 (7,54%), p < 0,001. 4) O aumento do índice cardíaco após a reperfusão no Grupo 1 (70,42%) foi significativamente menor que no Grupo 2 (125,91%), p < 0,001. 5) O índice cardíaco no 5o e no 30o minuto da reperfusão no Grupo 1 (6,51 ± 0,81 e 5,56 ± 0,86 L.min-1.m-2) foi significativamente menor que no Grupo 2 (7,41 ± 0,87 e 6,34 ± 0,93 L.min-1.m-2), p= 0,007 e p = 0,024 respectivamente. 6) O índice cardíaco no 5o e no 30ominuto da reperfusão quando comparados aos momentos basais (início da cirurgia) apresentou aumentos no Grupo 1 (26,16% e 7,75%) significativamente menores que no Grupo 2 (45,57% e 24,80%), p= 0,019 e p= 0,021 respectivamente. 7) O índice de resistência vascular sistêmica imediatamente após o término de infusão da solução teste no Grupo 1 apresentou queda de 18,83% enquanto no Grupo 2 foi registrado aumento de 9,21%, p < 0.001. 8) A diminuição do índice de resistência vascular sistêmica após a reperfusão no Grupo 1 (44,52%) foi significativamente menor que no Grupo 2 (61,80%), p < 0,001. 9) O índice de resistência vascular sistêmica no 5o e no 30o minuto após a reperfusão no Grupo 1 (799,35 ± 131,51 e 963,10 ± 171,33 dyn.s.cm-5.m-2) foi significativamente maior que no Grupo 2 (652,14 ± 115,47 e 831,47 ± 113,84 dyn.s.cm-5.m-2), p = 0,003 e p = 0,020 respectivamente. 10) A infusão de líquidos após a reperfusão no Grupo 1 (12,80 ± 1,47 mL/kg/h) foi significativamente menor que no Grupo 2 (15,47 ± 2,23 mL/kg/h), p = 0,001. 11) A natremia média imediatamente após a infusão da solução teste e ao final da cirurgia no Grupo 1 (152,66 ± 4,45 e 148,92 ± 3,60 mEq/L) foi significativamente maior que no Grupo 2 (143,59 ± 3,92 e 142,76 ± 3,17 mEq/L), p < 0,001. 12) A cloremia média imediatamente após a infusão da solução teste e ao final da cirurgia no Grupo 1 (124,03 ± 4,01 e 119,41 ± 3,04 mEq/L) foi significativamente maior que no Grupo 2 (111,20 ± 3,80 e 111,93 ± 6,26 mEq/L), p < 0,001. 13) O pH sangüíneo imediatamente após a infusão da solução teste no Grupo 1 (7,29 ± 0,05) foi significativamente menor que no Grupo 2 (7,34 ± 0,06), p = 0,039. 14) A pressão intracraniana diminuiu 48,77% nos pacientes com hipertensão intracraniana após a administração da solução salina hipertônica, efeito que se sustentou até o final da cirurgia. CONCLUSÕES: A administração da solução salina hipertônica no transplante do fígado aboliu a síndrome pós-reperfusão, atenuou as alterações hemodinâmicas secundárias a reperfusão hepática e reduziu a necessidade de reposição volêmica.INTRODUCTION: The reperfusion phase during orthotopic liver transplantation is a critical event which sometimes promoves profound hemodynamic and cardiac changes that may be responsible for intraoperative death, multiple organ dysfunction syndrome and early graft loss. In the present study we hypothesized that the beneficial effects of hypertonic saline solution infusion during hemorrhagic shock resuscitation, considered as an ischemia and reperfusion phenomenon of the entire organism, may attenuate the hemodynamic instability that follows graft reperfusion during liver transplantation. METHODS: Thirty adult patients presenting for liver transplantation in Hospital das Clínicas of University of São Paulo Medical School were divided in two groups: Group 1 received hypertonic (7.5%) saline solution (4 mL/kg) at a rate of 20mL/min through a central line at the beginning of portal vein anastomosis; Group 2 received normal saline solution under the same conditions. Hemodynamic profiles were evaluated using mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index and systemic vascular resistance index. Intracranial pressure study was included for those patients presenting intracranial hypertension. Data were collected at six different times: at the end of the dissection phase, at the beginning of the anhepatic phase, after the end of test solution infusion, and at 1, 5, and 30 minutes after reperfusion. Postreperfusion syndrome was defined by the occurrence of mean arterial pressure lower than 60mmHg at 1 or 5 minutes after reperfusion, and by a decrease in mean arterial pressure of more than 30% of the baseline values within the first 5 minutes after reperfusion. RESULTS: 1) Mean arterial pressure at 1 and 5 minutes after reperfusion were significantly higher in Group 1 (84.9 ± 12,33 and 77.4 ± 4.58 mmHg) than in Group 2 (62.9 ± 5.22 and 73.9 ± 3.47 mmHg), p< 0.001 and p= 0.046 respectively. 2) Postreperfusion syndrome was absent in Group 1, but present in 33.33% of patients in Group 2, p= 0.021. 3) The cardiac index increase immediately after the test solution infusion was significantly higher in Group 1 (31.27%) than in Group 2 (7.54%), p< 0.001. 4) The rise in cardiac index after reperfusion was significantly lower in Group 1 (70.42%) than in Group 2 (125.91%), p< 0.001. 5) Cardiac index at 5 and 30 minutes after reperfusion was significantly lower in Group 1 (6.51 ± 0.81 and 5.56 ± 0.86 L.min-1.m-2) than in Group 2 (7.41 ± 0.87 and 6.34 ± 0.93 L.min-1.m-2), p= 0.007 and p= 0.024 respectively. 6) When compared to their baseline moments, beginning of surgery, cardiac index at 5 and 30 minutes after reperfusion presented significantly lower increases in Group 1 (26.16% and 7.75%) than in Group 2 (45.57% and 24.80%), p = 0.019 and p = 0.021 respectively. 7) Systemic vascular resistance index immediately after the test solution infusion dropped by 18.83% in Group 1 while it increased by 9.29% in Group 2, p < 0.001. 8) The decrease in systemic vascular resistance index immediately after reperfusion was significantly lower in Group 1 (44.52%) than in Group 2 (61.80%), p < 0.001. 9) Systemic vascular resistance index at 5 and 30 minutes after reperfusion were significantly higher in Group 1 (799.35 ± 131.51 and 963.10 ± 171.33 dyn.s.cm-5.m-2) than in Group 2 (652.14 ± 115.47 and 831.47 ± 113.84 dyn.s.cm-5.m-2), p= 0.003 and p= 0.020 respectively. 10) Fluid requirements after reperfusion were significantly lower in Group 1 (12.80 ± 1.47 mL/kg/h) compared to Group 2 (15.47 ± 2.23 mL/kg/h), p= 0.001. 11) Serum sodium after the test solution infusion and at the end of surgery was significantly higher in Group 1 (152.66 ± 4.45 and 148.92 ± 3.60 mEq/L) than in Group 2 (143.59 ± 3.92 and 142.76 ± 3.17 mEq/L), p< 0.001. 12) Serum chloride after the test solution infusion and at the end of surgery was significantly higher in Group 1 (124.03 ± 4.01 and 119.41 ± 3.04 mEq/L) than in Group 2 (111.20 ± 3.80 and 111.93 ± 6.26 mEq/L), p< 0.001. 13) Blood pH immediately after the test solution infusion was significantly lower in Group 1 (7.29 ± 0.05) than in Group 2 (7.34 ± 0.06), p < 0.039. 14) In those patients with intracranial hypertension, the intracranial pressure decreased 48.77% immediately after hypertonic saline solution infusion, an effect that was sustained throughout graft reperfusion to the end of the surgical procedure. CONCLUSIONS: Hypertonic saline solution infusion during orthotopic liver transplantation abolished the postreperfusion syndrome, attenuated the hemodynamic changes secondary to graft reperfusion and lowered fluid requirements.
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"Hepatic arterial embolization with A lipiodol-ethanol mixture in the cirrhotic liver: an experimental trial in an animal model." 2003. http://library.cuhk.edu.hk/record=b5891589.
Full textAbstract:
Chan Tai-po.Thesis (M.Phil.)--Chinese University of Hong Kong, 2003.
Includes bibliographical references (leaves 94-101).
Abstracts in English and Chinese.
Chapter 1 --- INTRODUCTION --- p.1
Chapter 2 --- HYPOTHESIS --- p.3
Chapter 3 --- OBJECTIVE --- p.4
Chapter 4 --- CLINICAL IMPLICATIONS --- p.5
Chapter 5 --- METHODOLOGY --- p.6
Chapter 5.1 --- Materials --- p.8
Chapter 5.2 --- Study method --- p.13
Chapter 5.3 --- Venues of the research --- p.22
Chapter 5.4 --- Data acquisition --- p.23
Chapter 5.5 --- Data management and analysis --- p.24
Chapter 5.6 --- Ethical considerations --- p.25
Chapter 5.7 --- Participations of persons in the research --- p.28
Chapter 6 --- RESULTS --- p.34
Chapter 6.1 --- Problems and fate of rats in the model development group --- p.34
Chapter 6.2 --- Morbidity and mortality after LEM administration --- p.38
Chapter 6.3 --- Results of radiological findings --- p.39
Chapter 6.4 --- Results of liver function tests --- p.48
Chapter 6.5 --- Results of liver morphology --- p.52
Chapter 6.6 --- Histological results --- p.53
Chapter 7 --- DISCUSSION --- p.69
Chapter 7.1 --- Problems encountered in the development group --- p.69
Chapter 7.2 --- The pilot study group --- p.71
Chapter 7.3 --- The need for the present study --- p.74
Chapter 7.4 --- LEM in cirrhotic rat compared with the normal liver rat --- p.75
Chapter 7.5 --- Liver function markers in cirrhotic liver --- p.76
Chapter 7.6 --- Discussion on the assumptions of the research --- p.80
Chapter 7.7 --- Assessment on measurement error --- p.82
Chapter 7.8 --- Errors in the pilot study --- p.83
Chapter 8 --- CONCLUSIONS --- p.84
Chapter 9 --- Future experiments that may be performed using this model --- p.85
Chapter 10 --- APPENDICES --- p.86
Chapter 10.1 --- Appendix 1: Copy on the letter of ethics approval from the Animal Research Ethics Committee of the Chinese University of Hong Kong --- p.86
Chapter 10.2 --- Appendix 2: Copy on the licences issued by the Department of Health of Hong Kong --- p.88
Chapter 11 --- REFERENCES --- p.94
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Naidoo, Nalini. "A homoeopathic drug proving of Carcharhinus leucas 30CH and a subsequent comparison with that of Galeocerdo cuvier hepar 30CH." Thesis, 2018. http://hdl.handle.net/10321/3083.
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Submitted in partial compliance with the requirements of the Master’s Degree in Technology: Homoeopathy, Durban University of Technology, Durban, South Africa, 2018.Introduction The aim of this study was to conduct a homoeopathic proving of Carcharhinus leucas in the thirtieth centesimal potency (30CH) and to subsequently establish and describe the symptomatology in standard materia medica format and then compare this symptomatology to Galeocerdo cuvier hepar 30CH. Methodology The homoeopathic proving of Carcharhinus leucas 30CH was conducted at the Durban University of Technology and was accomplished by means of a randomised, double blind, placebo controlled trial. Carcharhinus leucas 30CH was manufactured by the researchers according to Method 6, Method 8a and 10 of the German Homoeopathic Pharmacopoeia (Benyunes, 2005: 36-39). The homoeopathic proving was conducted in the form of a double blind placebo controlled study of Carcharhinus leucas 30CH with a total of 30 healthy provers. The prover sample was divided into two groups by a process of randomisation. Twenty four provers (80%) comprised the verum group and the remaining 6 provers (20%) comprised the placebo group. The identity of the proving substance and the potency used was not disclosed to provers. Provers documented their physical, mental and emotional status for one week preceding the administration of the proving remedy. A comprehensive physical examination and case history of every prover was taken before and after the proving period. Provers were instructed to ingest one powder three times a day for two days but were told to discontinue the powders once symptoms arose. The duration of the proving spanned 6 weeks and throughout the proving process, researchers were in constant communication with all the participants. Upon completion of the proving process, journals were collected and the information therein was translated into materia medica and repertory format. This was done in order to acquire the remedy picture of Carcharhinus leucas 30CH. Thereafter, the symptomatology of Carcharhinus leucas 30CH was compared to the symptomatology of Galeocerdo cuvier hepar 30CH. Results The proving of Carcharhinus leucas 30CH produced a total of 590 already existing rubrics and 43 new rubrics. The majority of these rubrics were located in the MIND (127), GENERALS (64), HEAD (55), EXTREMITIES (50), and EYE (34). In regard to the mind, prominent features were apparent such as anger, anxiety, cheerfulness, an aversion or amelioration within company, difficulty concentrating or increased focus, varying delusions and fears and irritability. Pertaining to the head, headaches were evident with varying concomitants and modalities, with headaches predominantly affecting the forehead and sides. Sensations included dryness, heat, heaviness, perspiration and shaking. The extremities displayed symptoms primarily in the forearms, legs and thighs and sensations included paralysis, shaking, swelling and weakness. In regard to the eye, eye pain with multiple modalities were apparent, with symptoms related to the canthi and eyelids. Sensations included heat, heaviness, inflammation, itching and photophobia as well as a visible discolouration of the eye. Analysis of the results presented an understanding of the similarities and differences between Carcharhinus leucas 30CH and Galeocerdo cuvier hepar 30CH. Conclusion As hypothesised, it was evident that administering Carcharhinus leucas 30CH to healthy individuals did yield observable symptomatology. Additionally, it was apparent that various correlations between Carcharhinus leucas 30CH and Galeocerdo cuvier hepar 30CH existed
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Books on the topic "Heparin Therapeutic use"
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Barrowcliffe, Trevor W. Low molecular weight heparin. Chichester, West Sussex, England: Wiley, 1992.
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Kovaliv, Bohdan. Heparyn i heparynoïdy y klinichniĭ praktyt͡s︡i. Lʹviv: Lʹvivsʹkyĭ derz͡h︡avnyĭ medychnyĭ universytet im. Danyla Halyt͡s︡koho, 2003.
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Warkentin, Theodore E., and Andreas Greinacher. Heparin-induced thrombocytopenia. 4th ed. New York: Informa Healthcare, 2007.
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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 4th ed. New York: Informa Healthcare USA, 2007.
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Khaliq, Yasmin. Clinical significance of the nitroglycerin-heparin interaction. [Ottawa, Ont.?: s.n.], 1991.
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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 2nd ed. New York: Dekker, 2001.
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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 3rd ed. New York: Marcel Dekker, 2004.
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Thromoprophylaxis with low-molecular-weight heparins. London: Current Medicine Group, 2006.
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1940-, Kher André, Sarret Monique 1938-, and Toulemonde Francis 1926-, eds. Low molecular weight heparin therapy: An evaluation of clinical trials evidence. New York: Marcel Dekker, 1999.
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Heparin and the prevention of atherosclerosis: Basic research and clinical application. New York: Wiley-Liss, 1990.
Find full textBook chapters on the topic "Heparin Therapeutic use"
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Keeling, David. "Therapeutic anticoagulation." In Oxford Textbook of Medicine, 3018–22. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.161602_update_002.
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Low molecular weight heparins (LMWH) have largely replaced unfractionated heparin. Their much more predictable anticoagulant response combined with high bioavailability after subcutaneous injection means that the dose can be calculated by body weight and given subcutaneously without any monitoring or dose adjustment. Their widespread use resulted in most patients with deep vein thrombosis being managed as outpatients, and this is also increasingly the case for uncomplicated pulmonary embolism....
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Guedeney, Paul, Mathieu Kerneis, Johanne Silvain, Gilles Montalescot, and Jean-Philippe Collet. "Low-molecular-weight heparin." In ESC CardioMed, edited by Raffaele DeCaterina, 250–53. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0050.
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Low-molecular-weight heparins (LMWHs) are an therapeutic alternative to unfractionated heparin (UFH) for parenteral anticoagulation, with more reliable pharmacological properties and also an easier practical use. LMWHs are recommended for acute coronary syndrome and thromboembolic diseases.
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Keeling, David. "Therapeutic anticoagulation." In Oxford Textbook of Medicine, edited by Jeremy Dwight, 3729–34. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0376.
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The main indications for therapeutic anticoagulation are venous thromboembolism, deep vein thrombosis, and pulmonary embolism, and the prevention of stroke in patients with atrial fibrillation or mechanical heart valves. Low-molecular-weight heparins have largely replaced unfractionated heparin in its treatment. Their much more predictable anticoagulant response combined with high bioavailability after subcutaneous injection means that the dose can be calculated by body weight and given subcutaneously without any monitoring or dose adjustment. Their widespread use resulted in most patients with deep vein thrombosis being managed as outpatients, and this is also increasingly the case for uncomplicated pulmonary embolism. Oral direct inhibitors of anticoagulation that specifically target thrombin or factor Xa are increasingly used to treat acute venous thromboembolism and for stroke prevention in atrial fibrillation.
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Chan, Wee, and Jeffrey Ginsberg. "Low-Molecular-Weight Heparin Use in Pregnancy." In New Therapeutic Agents In Thrombosis And Thrombolysis, Revised And Expanded. Informa Healthcare, 2002. http://dx.doi.org/10.1201/9780203909317.ch6.
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"Low-Molecular-Weight Heparin Use in Pregnancy." In New Therapeutic Agents In Thrombosis And Thrombolysis, Revised And Expanded, 108–19. CRC Press, 2002. http://dx.doi.org/10.3109/9780203909317-9.
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Mendoza-Torres, Evelyn, Franklin Torres, Wendy Rosales-Rada, Liliana Encinales, Lil Avendaño, María Fernanda Pérez, Ivana Terán, et al. "COVID-19 Transmission in Children: Implications for Schools." In Primary Health Care. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.99418.
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The COVID-19 pandemic poses multiple issues of importance to child health including threats to physical health and disruption of in-school learning. This chapter reviews what is currently known about COVID-19 epidemiology, presentation, pathophysiology, case definitions, therapies, and in-school transmission in children. COVID-19 has some unique characteristics in children including the rare yet severe Multisystem Inflammatory Syndrome in Children (MIS-C) that may be related to acquired immune responses. There are limited studies to date to define therapeutic guidelines in children, however consensus recommendations from multiple organizations are summarized including the use of immunomodulatory therapies (intravenous immunoglobulin, steroids, anakinra and tocilizumab), antiplatelet (aspirin) and anti-coagulant (low molecular weight heparin) therapies. Finally, considerations for safe return to the classroom are discussed including strategies for optimized student to teacher ratios, hand washing, social distancing, sibling pairing and staged re-opening strategies.
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van Mens, Thijs E., and Saskia Middeldorp. "Management of pulmonary embolism in pregnancy." In ESC CardioMed, 2786–90. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0665.
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Pulmonary embolism, although rare, is a leading cause of maternal mortality. There is no strong evidence base for the diagnosis and management of pregnancy-related pulmonary embolism, hampering firm recommendations. In women with a suspicion of pulmonary embolism, the diagnosis is confirmed in 1 in 25–30 women only. However, imaging is always necessary to exclude pulmonary embolism, as no clinical decision rules or D-dimer-based strategies have been validated in pregnancy. Computed tomography pulmonary angiography and pulmonary scintigraphy are both suitable modalities, unless deep vein thrombosis is confirmed by compression ultrasonography of lower limb veins. Low-molecular-weight heparin (LMWH) in therapeutic doses is the treatment of choice during pregnancy, and anticoagulation should be continued until 6 weeks after delivery with a minimum total duration of 3 months. Use of LMWH or vitamin K antagonists does not preclude breastfeeding. Whether dosing should be based on weight or anti-Xa levels is unknown, and practices differ between centres. Management of delivery, including the type of anaesthesia if deemed necessary, requires a multidisciplinary approach, and several options are possible, depending on local preferences and patient-specific conditions. Prevention of pulmonary embolism with LMWH is indicated in all postpartum women with a history of venous thromboembolism, and in most women also during pregnancy.
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Verheugt, Freek W. A. "Unfractionated heparin." In ESC CardioMed, edited by Raffaele DeCaterina, 248–50. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0049.
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Unfractionated heparin is a very widely used and inexpensive parenteral anticoagulant with a narrow therapeutic window, which makes careful monitoring necessary. Common indications are acute coronary syndromes with or without ST-segment elevation, percutaneous coronary intervention, early treatment of venous thromboembolism, and bridging therapy for interrupted oral anticoagulation. Bleeding is its most common side effect followed by thrombocytopenia and osteoporosis, the latter of which is only seen with longer periods of treatment.
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Capodanno, Davide. "Bivalirudin and argatroban." In ESC CardioMed, edited by Raffaele DeCaterina, 255–59. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0052_update_001.
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The central role of thrombin in the process of clot formation makes it an important therapeutic target. Heparin is a potent anticoagulant, but has a number of limitations, in that—for example—it does not bind clot-bound thrombin, activates platelets, and may determine heparin-induced thrombocytopenia (HIT). Bivalirudin and argatroban, which belong to the class of intravenous direct thrombin inhibitors, potentially overcome many of the limitations of heparin. Bivalirudin is currently indicated as an alternative to unfractionated heparin for selected patients with non-ST-segment elevation acute coronary syndromes undergoing percutaneous coronary intervention, and patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Both argatroban and bivalirudin can be used as an alternative to heparin in patients with HIT and HIT-thrombosis syndrome. This chapter describes the current clinical applications of bivalirudin and argatroban.
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Aronson, J. K. "General principles of drug therapy in psychiatry." In New Oxford Textbook of Psychiatry, 1168–77. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0151.
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The successful use of psychotropic drugs demands an understanding of their pharmaceutical, pharmacokinetic, and pharmacodynamic properties. ♦ Pharmaceutical properties: Pharmaceutical formulations can be manipulated to produce different durations of action, for example the use of oily emulsions of antipsychotic drugs in depot formulations. ♦ Pharmacokinetic properties: Pharmacokinetics is the mathe-matical description of the disposition of drugs in the body by absorption, distribution (to plasma proteins and tissues), and elimination (usually by hepatic metabolism and renal excretion). Differences in drug disposition determine differences in dosage regimens and are important for drug interactions. ♦ Pharmacodynamic properties: Pharmacodynamics is the study of the pharmacological actions of drugs and how actions at the molecular level are translated, via actions at cellular, tissue, and organ levels, into therapeutic or adverse effects. The known pharmacological actions of psychotropic drugs are not necessarily the actions that produce their therapeutic or adverse effects.
Conference papers on the topic "Heparin Therapeutic use"
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Eldor, A., M. Bar-Ner, L. Wasserman, Y. matzner, Z. Fuks, and I. Viodavsky. "HEPARIN AND NON-ANTICOAGULANT HEPARINS INHIBIT HEPARANASE ACTIVITY IN NORMAL AND MALIGNANT CELLS:POSSIBLE THERAPEUTIC USE IN PREVENTION OF EXTRAVASATION AND DISSEMINATION OF BLOOD BORNE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643664.
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Degradation of vascular subendothelium occurs in_vivo during the process of inflammation and tumor invasion. Various observations suggest that the capacity of some blood-borne cells to extravasate may depend in part on their ability to express hepara-nase activity. Incubation of human platelets, human nc-utrophils, or highly metastatic mouse lymphoma cells with sulfate-labeled extracellular matrix (ECM) results in heparanase mediated release of labeled heparan sulfate cleavage fragments (0.5<Kav<0.85 on Sepharose 5B) (J. Clin.Invest. 74: 1842 and 76: 1306; Cancer Res. 43: 2704). The present study was undertaken to test the heparanase inhibitory effect of heparin and non-anticoagulant species of heparin that might havea potential therapeutic use in preventing heparanase mediated extravasation ofblood-borne cells. We prepared totallyor N-desulfated heparins which were either left with their N-position exposed or were subsequently N-acetylated or N-resulfated. These heparins exhibited less than 5% of the anticoagulant activityof native heparin. It was found that total desulfation of heparin abolished its heparanase inhibitory activity whether desulfation was followed by N-acetylation or not. Inhibitory effect was restored by resulfation of the N-position. When only the N-sulfate group was desulfated, inhibitory activity was lost but could be restored by acetylation of the N-position. These results indicate that N-sulfate groups of heparin are necessary for its heparanase inhibitory activity but can be substituted by an acetyl group provided that the 0-sulfate groups are retained. Low Mr heparins (main Mr species of 2500 and 4500 daltons) and heparin fragments as small as the tetrasaccharide inhibited degradation of heparan sulfate in the ECM, albeit to a lower extent than native heparin. Similar effects of the different heparins were observed with heparanase activities from platelets, neutrophils and lymphoma cells. Preliminary in vivo experiments suggest that non-anticoagulant heparins interfere with tumor metastasis and experimental autoimmune diseases (some heparins were kindly provided by Inst. Choay, Paris and Kabi Vitrum, Stockholm).
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Porta, R., R. Pescador, R. Niada, M. Mantovani, and G. Prino. "FIBRINOLYTIC POTENCY OF NON ANTICOAGULANT, OXI-EEDUCED SLOW AND FAST MOVING HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644180.
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It is well known that heparin is able to induce an increase of fibrinolytic activity when i.v. administered in man and in several animal species. Nevertheless, its anticoagulant properties can cause serious problems of bleeding and this restricts the therapeutic use of heparin. An oxi-reductive process applied to heparin leads to a conpound with reduced anticoagulant activity. Moreover, heparin can be separated into slow moving (SM) and fast moving (FM) components on the basis of electrcphoretic properties. The SM and FM components display quantitatively different biological activities. The aim of this paper was to verify if the oxi-reduction could affect or not the fibrinolytic activities of SM and FM. SM and FM, prepared by ethanolic precipitation from parent heparin, were oxidized by periodate and stabilized by reduction (RO-SM and RO-FM). The USP, APTT and anti Xa titres were determined in vitro using sheep plasma and kits from Boehrirger Biochemia (APTT) and Sigpia (Anti Xa). Fibrinolytic activities were assessed ex vivo after i.v. injection into rabbits at different doses to find out the effective dose hundred (ED100). The euglobulin fraction obtained from plasma was applied on human fibrin plates and the lysis areas were measured. The Table gives the resultsThe oxi-reduction decreased dramatically the anticoagulant activities of SM and FM heparins while their fibrinolytic activities were practically unaffected. Tne oxi-reduced heparins could be helpful therapeutic agents in pathological conditions characterized by a diminished fibrinolytic activity. They could represent an effective alternative to heparin; the very lew anticoagulant activities reduce the risk of bleeding, specially in the high risk patients, while the good fibrinolytic activity, comparable to heparin, could allow the dissolution of fibrin clots.
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Meschengieser, S. S., A. I. Woods, and M. Z. Lazzari. "ANTICOAGULATION IN PREGNANCY IN PATIENTS WITH CARDIAC VALVE PROSTHESIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643266.
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The use of oral anticoagulation in pregnancy is controversial due to the risk of embryopathy (1° trimester), intracerebral hemorrhages (2° trimester) and the use of heparin is associated with a high morbidity due to abortion and prematurity. The outcome of 50 pregnancies in 30 patients with heart prosthesis was evaluated. Acenocoumarol and aspirin 500 mg/daily were given in all the patients since their surgery. Anticoagulant doses were controlled with prothrombin time (PT) performed with human brain thromboplastin and APTT. The therapeutic range for the PT was the International Calibrated Ratio (ICR) 2.5 to 3.5. In 12 pregnancies, oral anticoagulation was replaced by subcutaneous heparin in the first trimester; the same policy was followed before delivery except in 4 cases. The foetal loss was 34% with equal distribution along the three trimesters and no correlation with excess of anticoagulation. The incidence of hemorrhage was 6% and the rate of cerebral embolism was also 6% (3 on to 50). Two of the three episodes of embolism appeared while patients were on heparin. A total of 33 normal babies were born (66%). No typical warfarin embryopathy was found and no perinatal mortality was observed. A slight reduction in the anticoagulant doses was necessary in almost half of the cases.As the rate of foetal loss with heparin is not better than with oral anticoagulants and the incidence of embolism is higher, we are doubtful about the indication of subcutaneous heparin in the first trimester considering our absence of malformations with the acenocoumarin.
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Schoch, U., E. Zanetti, and A. von Felten. "PROPHYLAXIS OF THROMBOEMBOLISM DURING PREGNANCY IN THREE SISTERS WITH CONGENITAL ANTITHROMBIN III (AT m) DEFICIENCY COMBINED WITH REDUCED INDUCIBLE FIBRINOLYTIC ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644363.
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AT III deficiency is associated with a high risk of venous thromboembolism, particularly in pregnancy. As prophylactic treatment it has been recommended to normalize plasma levels of AT in by use of AT III concentrates, besides giving heparin.We report on the prophylactic treatment of three sisters (age 21, 25, 32 years) with congenital AT in deficiency (38-53%, normal: 80-120%) as well as a reduced inducible fibrinolytic activity (1.2, 5.8, 7.9%, normal: >8.5%), who already had suffered from severe thromboembolism. During pregnancy prophylactic measures were taken individually, depending on the plasma level of 3-throm-boglobulin (BTG) determined every 2-3 weeks. At the time of the first increase of BTG (around 10th week of gestation) prophylaxis with s. c.heparin 2x7'500IU/d was started, leading to normalization of BTG. When BTG was again elevated, the dose of heparin was successively increased up to 2x15'000IU/d; thereby, functional AT IH levels remained in the range of 28-50%. Two patients received only heparin throughout the pregnancy. However, in one patient BTG levels could not be normalized by heparin alone (60-130ng/ml, normal: <43ng/ml). Injections of AT in concentrate, 11000IU, led to reduction of BTG within 2 hrs (60 → 42, 220 → 61 ng/ml). Therefore, AT m was given from the 25th week of gestation in increasing amounts up to 5'000IU/week (funct. AT m in plasma: 51 -72%) in addition to heparin (2x12'500IU/d), resulting in BTG levels of 33-51 ng/ml. From the onset of labour, all patients received AT IU concentrates (two patients l'OOOIU every second day, one patient 1'0001U daily) together with i. v. heparin 20'000-27'500IU/d, until the oral anticoagulant treatment started after delivery had reached therapeutic levels. The amount of AT m concentrate totally administered was 5'000IU in two patients and 66'000IU in one patient. None of the patients showed ever signs of venous thrombosis.Our observations demonstrate that instead of an AT in substitution with the aim to normalize its plasma level, an effective thrombosis prophylaxis - monitored by plasma levels of BTG - may be achieved with heparin alone or combined with low amounts of AT in concentrate.
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Roberts, H. R. "PREVENTION OF DEEP VENOUS THROMBOSIS: CONCLUSIONS OF A CONSENSUS DEVELOPMENT CONFERENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642966.
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Deep venous thrombosis (DVT) and pulmonary embolism (PE) are major health problems that lead to significant morbidity and mortality. In the United States, it is estimated that these two problems result in over 300,000 hospitalizations annually and available data indicate that 50,000 to 100,000 patients per year die of pulmonary embolism.The advent of several diagnostic tests has permitted the identification of groups of patients at high risk for development of deep venous thrombosis and subsequent pulmonary embolism. Identification of these patient groups has led to therapeutic measures designed to prevent both deep venous thrombosis and subsequent embolic episodes. However, the efficacy of these preventive measures have not been widely adopted and reservations have been expressed regarding use of low dose anticoagulant drugs for prevention of DVT and PE, especially in surgical patients. Because of the apparent reluctance to adopt putative preventive measures for DVT and PE, the National Heart, Lung and Blood Institute convened a Consensus Development Conference on the issue of prevention in 1986. Experts from North America, Europe, and South Africa presented data, both pro and con, on prevention of DVT and PE, using one or more therapeutic regimens. An impartial Panel was then asked to arrive at a consensus statement on the following questions: 1) the level of risk of DVT and PE in different patient groups; 2) the efficacy and safety of prophylactic measures in these groups; 3) the recommended prophylactic regimens for different patient groups, and 4) remaining questions related to prevention of DVT and PE. Recommendations for prevention were based on the assumption that reduction in DVT would also result in reduction of pulmonary embolism. Furthermore, the consensus was based, at least in part, upon data combined from multiple clinical trials. Thus, combined data on 12,000 individuals in randomized clinical trials indicated that in appropriate patient groups, treated with low dose heparin, there was a 68 percent reduction in DVT, as measured by the 125I-fibrinogen uptake test and venography, and that there was a reduction of 49% in pulmonary embolism and a significant decrease in overall mortality resulting from pulmonary embolism.Prophylactic measures for the following different patient groups were assessed: 1) general surgery; 2) orthopedic surgery; 3) urology; 4) gynecology-obstetrics; 4) neurosurgery and neurology; 5) trauma; and 6) medical conditions.Basically, the following prophylactic regimens were considered: 1) low dose heparin; 2) low dose dihydroergotamine heparin; 3) dextran; 4) low dose warfarin; and 5) external pneumatic compression. In general terms, low dose heparin appears to be one of the more effective prophylactic regimens in certain groups of high risk patients. This regimen is not useful in orthopedic or certain neurosurgical procedures where heparin has been shown to be of little value or hazardous. In these cases, dextran, warfarin, or external pnuematic compression may be more beneficial. In some groups of high risk patients, combination of mechanical measures with anticoagulant agents appear to be of value in prevention of DVT and PE.The recommendations of the Consensus Panel for Prevention of DVT and PE for each patient group will be assessed.
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Broekmans, A. W., F. J. M. der Meer, and K. Briët. "TREATMENT OF CONGENITAL THROMBOTIC SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643718.
Full textAbstract:
Hereditary antithrombin III deficiency,protein C deficiency, and protein S deficiency predispose to the occurrence of venous thrombotic disease at a relatively youngage and often without an apparent cause. These disorders inherit as an autosomal dominant trait. Heterozygotes are at risk fosuperficial thrombophlebitis, thrombosis atnearly every venous site, and pulmonary embolism. Homozygous protein C deficiency may present itself with a purpura fulminans syndrome shortly after birth.In the acute phase of venous thromboembolism heparin is effective for preventing extension of the thrombotic process, and pulmonary embolism. In patients with antithrombin III deficiency the concomittant useof antithrombin III concentrate is controversial, although some patients may requirehigher doses of heparin.Substitution therapy is only indicated in homozygous protein C deficient patientswith purpura fulminans. Fresh frozen plasma i.v. is the treatment of choice, in a dosage of 10 ml/kg once or twice daily. The current prothrombin complex concentrates may induce new skin lesions and disseminated intravascular coagulation. After the lesions have been healed(mostly in 4 to6 weeks)coumarin therapy may effectively prevent new episodes of purpura fulminans, provided the prothrombin time is kept within 2,5 - 4,0 INR. Heparin is ineffective for preventing purpura fulminans due to homozygous protein C deficiency.The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. This is supported by the observation that patients may remain free of thrombosis during long-term treatment and may have recurrences shortly after the withdrawal of the coumarin drug. The therapeutic range for the prothrombin time should be within 2,0 - 4,0 INR, target value 3,0 INR. In the initial phase of oral anticoagulant therapy protein C deficient patients are prone to the development of coumarin induced hemorrhagic skin (tissue) necrosis.In the patients studied in Leiden, it occurred in about 3% of the treated patients. Heparin appears to be ineffective for the prevention of coumarin-induced skin necrosis; high loading doses of coumarin should be avoided and the prothrombin timeshouldbe checked dialy during the initial phase of oral anticoagulant treatment. Tissue necrosis may contribute to bleeding complications after fibrinolytic therapy, ashas been observed in two protein C deficient patients.In clinical situations with an increased risk for thrombosis such as surgery and pregnancy, heparin (in-low-doses) alone orin combination with coumarins have been used succesfully for the prevention of thrombosis. The need for antithrombin III concentrates in patients with hereditary antithrombin III deficiency in such situations is not substantiated.Although anabolic steroids are capable to increase the plasma concentrations of antithrombin III and of protein C in the respective deficiency states, its efficacy in preventing thrombotic episodes remains to be established.An optimal strategy for preventing thrombosis in congenital thrombotic syndromes is to identify still asymptomatic patients. In case of antithrombin III, protein C, and protein S deficiency this search is feasible. During risk situations for thrombosis patients are to be protected against the development of thrombosis.In Leiden pregnant women with one of the deficiencies are treated from the 14th week of pregnancy, initially with a shortacting coumarin drug, after the 34th week withheparin s.c. b.i.d. at therapeutic dosages,and after delivery coumarin therapy is reTnstituted during 6 weeks. The use of oralcontraceptives should be avoided, unlesspatients are under coumarin treatment. As long as deficient patients remain asymptomatic no antithrombotic treatment is indicated. After the first documented thromboticincident patients are treated indefinitelywith oral anticoagulants.
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Bartl, K., H. Lill, and A. Dessauer. "APPLICATION OF THE ROUTINE PHOTOMETRIC COAGULATION ASSAYS PT, APTT AND FIBRINOGEN TO A CENTRIFUGAL ANALYZER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643257.
Full textAbstract:
The vast majority of coagulation tests in the routine laboratory are the global assays PT, APTT and the single factor determination of fibrinogen. We developed a convenient ilystem consisting of these photometric assays and the Cobas® Bio equipped with an external calculator. By use of this system all three determinations are possible from the same sample cup. For a profile of all 3 parameters, a sample through-put of about 60 per hours is possible. For PT and APTT determinations, the photometric assays on basis of chromogenic substrates are used. The time is measured, until defined amounts of p-nitroani1ine are split off from the substrate by the thrombin formed. Fibrinogen is measured in a kinetic turbidimetric reaction during fibrin formation by batroxobin. The performance data are as follows: The coefficients of variation for the PT assay (25 μl of sample and 225 μl of reagent) are 0.5-1 % (X = 31,9 sec or 115,0 sec respectively, n = 20). The normal range is 70-120 %, the therapeutic range 12-27 %. The assay is extremely sensitive for the factors VII, V, X and II. It is both suited for the control of oral anticoagulant therapy and the screening of factor deficiencies. The CV values for the APTT assay (20 μl of sample, 200 μl of reagent and 20 μl of starting reagent) are 0,5-1,3 % for normal plasma samples. The normal value ranges from 36-58 sec. Plasma with 0.3 USP units heparin/ml yields 80 sec (ratio = 1,6). Factor VIII and IX levels of 50 % prolong the APTT ratio for about 1,3 or 1,2 respectively. The data of the clinical evaluation proved the assay suitable for the control of the heparin therapy and the screening of the endogeneous coagulation system. The fibrinogen assay (20 μl of undiluted sample and 300 μl of reagent) shows a linear relationship between measuring signal and concentration from 50-800 mg/dl. The correlation with the functional clotting assay to Clauss is rather good (r = 0,98). There is only a slight interference due to fibrin(ogen) degradation products compared to the clotting test. The performance data and the clinical data make the system Cobas® Bio and the sensitive photometric assays an interesting alternative to the conventional clotting tests in the routine laboratory.
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Ferreira, Hanna dos Santos, Agata Layanne Soares da Silva, and João Lucas de Sousa Peres. "Fibrinolytic therapy in the treatment of pediatric ischemic stroke." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.033.
Full textAbstract:
Introduction: Pediatric stroke is a disorder that can result in morbidity and mortality. The ischemic type is the most common and has thrombolytics as the preferred therapy. Objective: To evaluate the therapeutic management and efficacy of fibrinolytics in pediatric patients with ischemic stroke. Methodology: The literature review was carried out in PUBMED, MEDLINE, Embase databases, with the descriptors “Fibrinolytic Agents”, “Thrombolytic Therapy”, “Ischemic Stroke”, “Stroke”, “Pediatrics” and “Treatment”. Included were clinical trials, randomized controlled trials, cohort, case- control, and case series in English or Portuguese published in the last 5 years. It gathered 8 articles. Results: Treatment in the acute phase and for secondary prevention in the chronic phase of pediatric stroke are antithrombotic therapies and platelet antiaggregants, commonly aspirin. Comparing the latter and low molecular weight heparin, neither has shown superiority in preventing stroke recurrence. Without good evidence, however, aspirin is indicated for idiopathic stroke and anticoagulants in cardioembolic stroke by some guidelines. In recombinant tissue plasminogen activator therapy in one paper it was suggested there is more risk for conversion to hemorrhagic events compared to untreated, but in another paper hemorrhage was not seen. There was high mortality with this therapy and higher chances of being discharged to short term hospital, skilled nursing facility or intermediate care facility. In endovascular therapy, delay in diagnosis limits its use and stroke complications did not differ between patients who did or did not undergo this therapy. Conclusion: Further studies are needed to evaluate the efficacy of fibrinolytics.
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Brien, W., M. Inwood, and K. Dillon. "QUALITY ASSURANCE OF THERAPEUTIC HEPARIN/ORAL ANTICOAGULANT THERAPY IN A GENERAL TEACHING HOSPITAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644170.
Full textAbstract:
In preparation for the development of a standard anticoagulation protocol and as part of a quality assurance programme, a retrospective analysis of anticoagulation therapy in a teaching hospital was undertaken. The results of this audit were compared to the results of other workers who have previously emphasized controversial areas of anticoagulation therapy and potential benefits of a standard anticoagulation protocol.Charts from seventy-nine patients with a diagnosis of venous thrombosis were analyzed. Fifty-five percent of the patients were at increased risk of bleeding and forty-five percent had an extensive proximal vein thrombosis, but not apparent consideration of a heparin dose adjustment was noted. Patients received heparin for an average 9.7 days, with concomitant coumadin therapy for an average 4.8 days. Patients on heparin were over/ or undercoagulated on average 5.4 days and ninety-four percent of patients on coumadin had a PT (rabbit brain) greater than 18 seconds for at least one day. Sixty percent of patients had their dose changes noted in a tabular form for easy reference. Less than fifty percent had their hemoglobin or platelet counts followed while on heparin. The APTT and TCT are used to follow heparin therapy and discrepant results were noted in thirty-three percent. All patients' discrepancies were investigated automatically by the coagulation laboratory. Less than thirty percent of patients received formal teaching from the clinical pharmacist concerning coumadin therapy.We feel that these results show a need for a standard protocol for heparin coumadin therapy. It has been shown that a standard protocol favourable chemical, financial and therapeutic benefits
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Fears, R. "THE EFFECT OF HEPARIN AND FIBRIN ON THE ENZYMATIC EFFICIENCIES OF THROMBOLYTICS IN_ VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643032.
Full textAbstract:
Selective fibrinolysis may be achieved physiologically by the binding of both endogenous plasminogen activator (t-PA) and plasminogen to fibrin. It has been suggested that t-PA may also exhibit fibrin-selectivity when used at therapeutic doses for acute myocardial infarction whereas the other principal thrombo-lytics, urokinase (UK) and streptokinase (SK).plasminogen, are not bound. However, in the present kinetic studies it was found that plasminogen activation by SK.lys-plasminogen was enhanced by soluble fibrin (the effect mainly on Km), the affinity of binding to fibrin was similar to t-PA (dissociation constant approx. 100 nM) and the reaction mechanism appeared similar (Rapid Equilibrium Ordered Bireactant). When evaluating the in vivo significance of fibrin-enhancement, variation in the form of the substrate (i.e., glu1- or lys77-forms) and the contribution of heparin must also be considered. Both t-PA and UK activities were potentiated by heparin (the effect mainly on Km) but in the presence of fibrin the effect of heparin on t-PA was attenuated; SK.plasminogen enzymatic activity was unaffected by heparin. Thus, in the presence of heparin, in vivo, there may be an exacerbation of the systemic action of t-PA. As differences in fibrin binding and enhancement between t-PA and intact SK.plasminogen - the activator that is produced from APSAC (Eminase) - are relative rather than absolute, therapeutic activity will be influenced more by the dosage regimen and the clearance rate.