Relevant bibliographies by topics / Warfarin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Warfarin'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Warfarin"

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Alsancak, Yakup, Serkan Sivri, Telat Keleş, Tahir Durmaz, and Engin Bozkurt. "A rare complication of warfarin: late onset warfarin induced skin necrosis." Türk Aile Hekimliği Dergisi 21, no. 1 (March 15, 2017): 41–43. http://dx.doi.org/10.15511/tahd.17.00141.

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Li, Qiang, Wen-yue Yang, Ling-ling Qu, Huan-Yang Qi, Yun Huang, and Zheng Zhang. "Interaction of Warfarin with Human Serum Albumin and Effect of Ferulic Acid on the Binding." Journal of Spectroscopy 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/834501.

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Angelica sinensis(Oliv.) Diels combined treatment with warfarin would increase the risk of bleeding. Ferulic acid is an abundant hydroxycinnamic acid inA. sinensisand warfarin is the most widely used oral anticoagulant. The studies on supermolecular interaction of warfarin with human serum albumin (HSA) and the influence of ferulic acid on the binding would contribute to the understanding of the metabolic processes of warfarin and the effect of ferulic acid. We focus on investigating the effect of warfarin on fluorescence spectrum of human serum albumin (HSA), fluorescence quenching mechanism, binding constant, Hill coefficient, binding mode, and the effect of different ferulic acid concentrations on the binding. Warfarin quenched the intrinsic fluorescence of HSA mainly by static quenching. Accession of ferulic acid reduced the binding of HSA-warfarin. By decreasing binding constant and the Hill coefficient of warfarin with HSA, ferulic acid could improve the plasma concentration of free warfarin, which would increase the risk of bleeding. Warfarin’s free concentration increased at least 50% under the condition of simulated human body. The results indicated thatA. sinensiscombined treatment with warfarin would increase the risk of bleeding. And the results provide an important theoretical support for warfarin used as oral anticoagulant.
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Thompson, Dennis F., Marsha A. Raebel, Elizabeth K. Hussey, and George E. Dukes. "Do All Histamine2-Antagonists Cause a Warfarin Drug Interaction?" DICP 23, no. 9 (September 1989): 675–79. http://dx.doi.org/10.1177/106002808902300911.

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Cimetidine, the first marketed histamine2-receptor antagonist, has been shown to decrease the clearance of warfarin consistently through inhibition of cytochrome P-450 metabolism. The clinical significance of this drug–drug interaction has been questioned due to: (1) the lowering of the warfarin therapeutic range, (2) the lowering of the total daily therapeutic cimetidine dosage, (3) the advent of once-daily cimetidine dosing, and (4) the demonstration that the clearance of the less active warfarin R-enantiomer is decreased to a greater extent than the more active S-enantiomer. Ranitidine has been implicated in both increasing and decreasing warfarin's hypoprothrombinemic effect (noted in the warfarin package insert), despite the majority of investigations demonstrating no warfarin clearance changes. Careful examination of the implicating data indicates that the majority of the warfarin pharmacodynamic and pharmacokinetic variance that occurs with combined ranitidine-warfarin therapy cannot be attributed to a drug–drug interaction. No data are available to implicate the newer histamine2-antagonists, famotidine and nizatidine, in causing a decrease in warfarin metabolism.
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Jaffer, Amir, Jason Hurbanek, Nariman Morra, and Daniel Brotman. "Warfarin prophylaxis and venous thromboembolism in the first 5 days following hip and knee arthroplasty." Thrombosis and Haemostasis 92, no. 11 (2004): 1012–17. http://dx.doi.org/10.1160/th04-04-0204.

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SummaryMany orthopaedic surgeons use warfarin to prevent venous thromboembolism (VTE) following hip or knee arthroplasty. Since warfarin’s antithrombotic effects are delayed, we hypothesized that early VTE (occurring within 5 days post-operatively) would be more common in arthroplasty patients receiving warfarin monotherapy compared to those receiving enoxaparin. We performed a secondary analysis of a case-control study examining risk factors for post-operative thrombosis in postmenopausal women. We defined cases as patients who were diagnosed with thrombosis within 5 days of surgery. Controls without thrombosis were matched with cases by age, surgeon, year of surgery and surgical joint. 84 women with early post-operative thrombosis (cases) were matched with 206 controls. 18 cases (21.4%) had been prescribed warfarin monotherapy, compared with 7 controls (3.4%). 58 (69.1%) cases and 195 (94.7%) controls had been prescribed subcutaneous enoxaparin 30 mg twice daily, starting 12-24 hours after surgery. The odds ratio for any early thrombosis in patients receiving warfarin as opposed to enoxaparin 30 mg twice daily was 8.6 (p<0.0001). For proximal thrombosis, the odds ratio was 11.3 (p<0.0001). Multivariate analysis did not alter these findings. Warfarin’s delayed antithrombotic effects may not provide adequateVTE prophylaxis in the immediate post-operative setting. We suggest caution in employing warfarin monotherapy following joint arthroplasty.
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Jones, Cade B., and Susan E. Fugate. "Levofloxacin and Warfarin Interaction." Annals of Pharmacotherapy 36, no. 10 (October 2002): 1554–57. http://dx.doi.org/10.1345/aph.1c074.

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OBJECTIVE: To report 4 cases of hypoprothrombotic response resulting from addition of levofloxacin therapy to chronic warfarin therapy and to review related literature to support or refute a warfarin—levofloxacin interaction. CASE SUMMARY: Four patients, 34–81 years old, were prescribed levofloxacin concomitantly with stable warfarin therapy. Three patients had a target international normalized ratio (INR) range of 2.0–3.0 and experienced an increase in INR to 3.5, 8.12, and 11.5 on days 11, 5, and 4 of a 10-day course of levofloxacin, respectively. The fourth patient experienced minor bleeding, with a slightly elevated INR on the second day of levofloxacin therapy that required up to a 19% warfarin dose reduction during levofloxacin treatment. DISCUSSION: An initial premarketing clinical trial concluded that levofloxacin had no effect on warfarin's pharmacokinetics and pharmacodynamic response. Two case reports have since documented an increase in INR in patients taking long-term warfarin on completion of levofloxacin therapy. Our case reports provide further evidence of a significant increase in INR observed during concomitant levofloxacin therapy. The proposed mechanism of this interaction is displacement of warfarin from protein binding sites, reduction in gut flora producing vitamin K, and decreased warfarin metabolism. CONCLUSIONS: Prolonged prothrombin response in patients undergoing chronic warfarin therapy has been well documented with many antibiotics, including fluoroquinolones. Recognition of newer antibiotics' effects on warfarin therapy is important to guide safe use and monitoring of anticoagulation therapy. Our case studies demonstrate significant elevations in INR values during and up to 1 day after levofloxacin therapy in patients undergoing stable warfarin therapy.
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Meeks, Mimi L., Kenneth W. Mahaffey, and Michael D. Katz. "Danazol Increases the Anticoagulant Effect of Warfarin." Annals of Pharmacotherapy 26, no. 5 (May 1992): 641–42. http://dx.doi.org/10.1177/106002809202600506.

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OBJECTIVE: To report two cases demonstrating an interaction between danazol and warfarin, resulting in the potentiation of warfarin's effect and bleeding complications. DATA SOURCES: Case reports, review articles, and studies identified by MEDLINE. STUDY SELECTION: All published English-language reports involving danazol and warfarin interactions were reviewed. DATA SYNTHESIS: Danazol, a synthetic testosterone derivative, is used in the treatment of endometriosis, fibrocystic breast disease, menorrhagia protein C deficiency, and hemophilia. We describe two cases including an interaction between danazol and warfarin, resulting in bleeding complications. There are at least two other reported cases of this interaction. This interaction may be attributable to several mechanisms. Danazol may inhibit the metabolism of warfarin and/or it may have a direct effect on the coagulation and fibrinolytic systems. CONCLUSIONS: Based on this report and other published cases, clinicians must be aware that danazol may increase the anticoagulant effect of warfarin. Patients receiving warfarin who are prescribed danazol must be monitored closely to prevent excessive anticoagulation and subsequent bleeding. Studies are needed to determine the frequency of this interaction and its underlying mechanisms.
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Kim, Karissa Y., and Michael A. Mancano. "Fenofibrate Potentiates Warfarin Effects." Annals of Pharmacotherapy 37, no. 2 (February 2003): 212–15. http://dx.doi.org/10.1177/106002800303700210.

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OBJECTIVE: To describe 2 patients in whom the initiation of fenofibrate potentiated warfarin's anticoagulant effects. CASE SUMMARY: A 71-year-old white woman and an 80-year-old white woman with multiple medical conditions were both stabilized on long-term warfarin therapy. During the course of anticoagulation, both patients were prescribed fenofibrate and experienced threefold and twofold increases in international normalized ratio (INR), respectively, requiring total weekly warfarin dosage reductions of 30–40%. Before starting fenofibrate therapy, both patients' coagulation values were within the therapeutic range. When interviewed, patients and caregivers denied bleeding, bruising, changes in diet, alcohol ingestion, nonadherence with therapy, or changes in drug regimen except for the addition of fenofibrate. Upon chart review, evaluation of potentially contributory parameters, such as other changes in drug therapy, thyroid function, liver function, and drug–disease interactions, showed that these parameters remained stable and were ruled noncontributory. DISCUSSION: The addition of fenofibrate in 2 patients on stable and therapeutic doses of warfarin increased the anticoagulant response to warfarin. A clear temporal relationship with the addition of fenofibrate and the appearance of the interaction was seen. Fenofibrate is highly protein bound, with the potential to displace warfarin from its binding protein, leading to an enhanced hypoprothrombinemic effect. Fenofibrate is also a mild to moderate inhibitor of CYP2C9, the enzyme responsible for warfarin metabolism. The combination of these effects — displacement of warfarin by fenofibrate coupled with decreased metabolism of warfarin — may increase the anticoagulant response to warfarin. Using the Naranjo probability scale, these interactions were designated as probable. CONCLUSIONS: We suggest serial monitoring of INR and consider an empiric 20% reduction in warfarin dosage when fenofibrate is initiated, with the possibility for a greater warfarin dosage reduction based on INR results.
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Milligan, Paul E., Gerald A. Banet, Amy D. Waterman, Susan K. Gatchel, and Brian F. Gage. "Substitution of Generic Warfarin for Coumadin in an HMO Setting." Annals of Pharmacotherapy 36, no. 5 (May 2002): 764–68. http://dx.doi.org/10.1345/aph.1a327.

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BACKGROUND: Substitution of generic warfarin for Coumadin presents safety concerns due to warfarin's narrow therapeutic index and because a prior generic formulation was removed from the US market after it was associated with adverse events. OBJECTIVE: To determine whether a health maintenance organization (HMO) can add generic warfarin to its formulary without adversely affecting warfarin management or increasing adverse events. DESIGN: In a prospective, observational study, an HMO that formerly dispensed only Coumadin added a generic warfarin preparation (Barr Laboratories, Pomona, NY) to its formulary. SETTING: An anticoagulation service (ACS) affiliated with an HMO that was based in St. Louis, MO. PARTICIPANTS: The cohort consisted of 182 enrollees in the ACS as of May 1, 1999. At the start of the study, these participants were taking Coumadin; by October 31, 2000, all had switched to Barr warfarin. MEASUREMENTS AND MAIN RESULTS: We collected data 8 months prior to and 10 months after the introduction of generic warfarin for the following endpoints: international normalized ratio (INR) control, frequency of INR monitoring, number of dose changes, and rate of thrombotic and hemorrhagic events. Statistical process control charts were used to differentiate between random variation in the endpoints and changes due to different warfarin formulations, and we used the Wilcoxon signed-rank test to look for a change in any endpoint after patients changed to generic warfarin. No significant differences were found in any endpoint. CONCLUSIONS: Substitution of Barr warfarin for Coumadin did not significantly affect INR control, warfarin management, or adverse events. Our findings suggest that HMOs can safely substitute at least 1 generic formulation of warfarin without extra monitoring.
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Casserly, Elizabeth A., Sara E. Rogers, and Sidney V. Keisner. "Lack of interaction between enzalutamide and warfarin in a metastatic castration-resistant prostate cancer patient." Journal of Oncology Pharmacy Practice 23, no. 1 (July 9, 2016): 68–70. http://dx.doi.org/10.1177/1078155215609979.

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Enzalutamide is an androgen receptor antagonist used for the treatment of metastatic castration-resistant prostate cancer. Enzalutamide is classified as a strong cytochrome P450 3A4 inducer, a moderate 2C9 and 2C19 inducer, and a time-dependent inducer of 1A2. Warfarin’s more potent enantiomer is primarily metabolized by cytochrome P450 2C9 and has a narrow therapeutic window. Enzalutamide is thought to decrease therapeutic warfarin concentrations per pharmacokinetic studies performed during drug development. This case report describes a 59–year-old man undergoing treatment with enzalutamide for metastatic castration-resistant prostate cancer with a history of femoral vein thrombosis. The patient was receiving a total weekly warfarin dose of 37.5 mg prior to starting enzalutamide. Enzalutamide was initiated and warfarin continued at a constant dose without decrease in the patient’s INR. The patient continued on enzalutamide and warfarin for 1 year without having any documented subtherapeutic INRs. This report illustrates one case in which the interaction between warfarin and enzalutamide was not clinically significant.
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Ruiz-Ruiz, Francisco J. "Warfarin or Not Warfarin?" Annals of Internal Medicine 142, no. 8 (April 19, 2005): 676. http://dx.doi.org/10.7326/0003-4819-142-8-200504190-00020.

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Dissertations / Theses on the topic "Warfarin"

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Zhang, Jieying Eunice. "Pharmacogenetics of warfarin." Thesis, University of Liverpool, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569544.

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Warfarin is one of the most commonly used oral anticoagulants worldwide and is highly efficacious for the treatment and prevention of thromboembolic disorders. However, due to its narrow therapeutic index and large interindividual variability, it remains a challenging drug to prescribe. Genetic factors (CYP2C9 and VKORCI), together with clinical factors (age and body weight), account for up to 60% of warfarin dose variance but the remaining ~40% variability remains unexplained. A polymorphism rs2108622 in CYP4F2, a vitamin K oxidase, has previously been associated with increased warfarin stable dose requirements, accounting for 1-7% dose variability. In our cohort of prospectively recruited patients (n = 311), we were unable to confirm these results. Interestingly, after fine mapping of the CYP4F2 gene region, we found a SNP rs2189784, which is in LD with rs2108622, to be associated with time to therapeutic INR (Pc = 0.03). Further fine mapping of the CYP4F gene cluster together with the utilisation a bank of well characterized Caucasian surgical liver samples (n = 149) and data from a genome-wide association study (n = 714), showed that CYP4F2 rs2108622 and rs2189784 SNPs were found to be associated with increasing CYP4F2 and decreasing CYP4FII or CYP4Fl2 mRNA expression, respectively. Interestingly, a CYP4Fll variant rsl060467 (in LD with rs2108622) was associated with reduced CYP4F2 rnRNA expression. Furthermore, rsl060467 contributes to 2.5% of warfarin dose variability and was associated with reduced warfarin dose requirement (~1 mg/day, Pc = 0.003), an effect in the opposite direction previously reported with CYP4F2 rs2108622 by Caldwell et al. (2008) and other studies. Warfarin-resistant patients have been reported to harbour VKORCI missense mutations. Extended regions of VKORCI were sequenced in our patients (n = 65) with resistance to warfarin, defined by clinical and pharmacodynamic criteria. Seven novel heterozygous mutations were identified and in silica analyses predicted the promoter c.-160G>C mutation creates a putative Spl transcription factor binding site and that the missense mutation c.79C>G to be deleterious. To confirm these predictions, in vitro functional studies were carried out using EMSA, transient transfection assays, and DNA methylation. c.-160G>C was found to create a weak binding site for Spl transcription factor, and caused an increase in promoter activity by ~20% (P = 0.003). The c.79C>G mutation reduced levels of PIVKA-II by ~10%. Associations of VKORCI genotypes with DNA methylation did not remain significant after correction for multiple testing. The effect of warfarin on the rate of decline of vitamin K-dependent clotting factors, and the role of SNPs in the clotting factor genes, is not known. Using a large prospective cohort of patients (n = 619), SNPs in F7 and F 10 genes showed association with variability in factor VII levels. The rate at which the plasma levels of factors II, X and protein C decline affect how patients respond to warfarin, in particular the achievement of warfarin stable dose and time to therapeutic INR. Furthermore, the change in clotting factor X level accounted for 1.4% of warfarin dose variability. In conclusion, the results presented in this thesis demonstrate that multiple genetic, clinical and biochemical factors account for the variability in warfarin response. Further understanding of such complex interactions, along with the advent of genomics technologies and development of new computational and conceptual tools, will yield insights to the accurate prediction of drug efficacy and toxicity, which will hopefully translate into improved outcomes for patients.
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Ab, Ghani Azizah. "Pharmacogenetics in warfarin therapy." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/18317/.

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Warfarin is a challenging drug to dose accurately, especially during the initiation phase because of its narrow therapeutic range and large inter-individual variability. Therefore, the aim of this thesis was to investigate the use of pharmacogenetics and clinical data to improve warfarin therapy. Genetic variants in cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) are known to influence warfarin dose. Therefore we developed a pharmacogenetic dosing algorithm to predict warfarin stable dose prospectively in a British population based on 456 patients who started warfarin in a hospital setting and validated it in 262 retrospectively recruited patients from a primary care setting. The pharmacogenetic algorithm which included CYP2C9*2, CYP2C9*3 and VKORC1-1693 together with body surface area, age and concomitant amiodarone use, explained 43% of warfarin dose variability. The mean absolute error of the dose predicted by the algorithm was 1.08 mg/day (95% CI 0.95-1.20). 49.6% of patients were predicted accurately (predicted dose fell within 20% of the actual dose). The HAS-BLED score, a bleeding risk score has recently been suggested for use in the management of patients with atrial fibrillation. We validated HAS-BLED performance in predicting major bleeding using a prospective cohort with 6 months follow-up (n=482) (c-statistic 0.80 95% CI (0.71-0.90). Factors significantly associated with major bleeding in our cohort (p≤0.1) were concurrent amiodarone use, labile INR, concurrent clopidogrel use, bleeding predisposition, concurrent aspirin use and CYP2C9*3. Adding a genetic covariate (CYP2C9*3) to the HAS-BLED score did not significantly improve its performance in predicting major bleeding. Considering CYP2C9*3 is a rare allele, our study was underpowered and requires further investigation in a larger cohort. A retrospective study of 97 Caucasian children was conducted to gain greater understanding of the factors that affect warfarin anticoagulant control and response in children. Results from multiple regression analysis of genetic and non-genetic factors showed that indication for treatment (Fontan or non-Fontan group), VKORC1 -1693, and INR group explained 20.8% of variability in proportion time in which INR measurements fell within the target range (PTTR); CYP2C9*2 explained 6.8% of the variability in INR exceeding target range within the first week of treatment; CYP2C9*2, VKORC1 -1693, age and INR group explained 41.4% of warfarin dose variability and VKORC1 -1693 explained 8.7% of haemorrhagic events. The contributions of CYP2C9 and VKORC1 polymorphism were small in the above outcomes. We therefore went onto explore other genetic markers using genome-wide scanning. Two SNPs on chromosome 5, rs13167496 and rs6882472 were found to be significantly associated at a genome-wide significance level with PTIR. However, none of SNPs were significantly associated with warfarin stable dose, INR values exceeding the target range within the first week of treatment and bleeding complications. Because of our small sample size, these findings will need to be validated in a replication cohort. Finally, we have validated and evaluated the performance of Genie HyBeacon®, a point of care therapy (POCT) instrument to genotype 135 samples for CYP2C9*2, CYP2C9*3 and VKORC1 -1693. We showed that the instrument accuracy was >98% (agreement with ABI Taqman® genotyping), it was relatively simple to use and had a good turn-around time (1.6 hours) making it suitable for clinical use. In conclusion, the results presented in this thesis demonstrate how knowledge of pharmacogenetics may help in assessing improvement in the quality of care of patients on warfarin. However, for personalized medicine to be widely adopted in clinical practice, payers need evidence of clinical- and cost-effectiveness. How such evidence is produced and evaluated varies in different healthcare settings, which further increases the challenge of implementing personalised medicine into the clinic.
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Choiniere, Jennifer. "Content and Uniformity of Mexican Manufactured Lovastatin and Warfarin Versus American Manufactured Lovastatin and Warfarin." The University of Arizona, 2005. http://hdl.handle.net/10150/624720.

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Class of 2005 Abstract
Objective: To analyze the quantity of active ingredient as well as the content uniformity of lovastatin and warfarin manufactured in Mexico as compared to the lovastatin and warfarin manufactured in the United States. Methods: High-pressure liquid chromatography assays modified from the U.S. Pharmacopoeia will be used to evaluate the amount of active ingredient found in lovastatin and warfarin manufactured in Mexico and America. Area-under-the-curve analysis was done to evaluate relative quantities of the active ingredients. Results: The amount of lovastatin found in the Mexican manufactured product was found to be 64%, and content uniformity was found to be 73%, both values are outside of the acceptable range of 90%-110% set by the USP-NF guidelines. The amount of warfarin found in the Mexican manufactured product was found to be 84% with a content uniformity of 100%. The average content value is outside of the acceptable range of 90%-110% set by the USP-NF guidelines. Conclusion: The results of this study showed that the amounts of active ingredients found in Mexican manufactured lovastatin and warfarin were significantly different from the amounts found in the American manufactured products.
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Ghaswalla, Parinaz K. "Medication-Related Problems in Older Adults: A Focus on Underuse of Warfarin and Warfarin-Antibiotic Interactions." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2631.

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The work presented in this dissertation focuses on two important medication-related problems in older adults, that is, untreated indication and drug-drug interactions, specifically with respect to a high-risk medication such as warfarin. Warfarin is a challenge to use in clinical practice due to its narrow therapeutic index, variability in dose-response and its interactions with numerous foods and drugs. This dissertation presents the research from two projects. In the first project the prevalence and predictors of warfarin use in nursing home (NH) residents with atrial fibrillation (AF), and use of secondary stroke prevention strategies was determined, in order to understand the patterns of anticoagulant use in frail NH residents and to identify patient characteristics associated with warfarin use. In the second project the effect of oral antibiotics on anticoagulation outcomes, when prescribed concomitantly with warfarin, was determined, in order to provide evidence on the clinical significance of warfarin-antibiotic interactions in older adults. In the first project a cross-sectional analysis of the prescription and resident files from the 2004 National Nursing Home Survey was done to determine the prevalence of AF and rates of use of warfarin and other anti-platelet agents, such as aspirin and clopidogrel. A multiple logistic regression model was used to determine factors associated with warfarin use. In this sample of older NH residents, 13% of residents had a diagnosis of AF, with indications for warfarin use and no contraindications to warfarin. From these patients, 30% received anticoagulant therapy with warfarin and 23% of the remaining patients received either aspirin or clopidogrel, suggesting that more than 50% of residents with AF did not receive any form of anticoagulant therapy. Non-white race, history of bleeding, and use of anti-platelet medications were associated with reduced odds of receiving warfarin. The second project was a retrospective medical record review of older patients from an outpatient anticoagulation clinic at a Veterans Affairs medical center. Results of the repeated measures ANOVA suggested a significant increase in post-antibiotic INR values with fluoroquinolones, azithromycin and amoxicillin. In addition, the percentage of patients with warfarin dose adjustments was significantly greater with fluoroquinolones and azithromycin as compared to cephalexin. No bleeding events were reported for any of these patients. In conclusion, the results of the projects suggest that there is underuse of warfarin in NH settings. Furthermore, antibiotics may be safely prescribed with warfarin in older adults as long as the INR is monitored closely.
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Eriksson, Niclas. "On the Prediction of Warfarin Dose." Doctoral thesis, Uppsala universitet, Klinisk farmakologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-172864.

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Warfarin is one of the most widely used anticoagulants in the world. Treatment is complicated by a large inter-individual variation in the dose needed to reach adequate levels of anticoagulation i.e. INR 2.0 – 3.0. The objective of this thesis was to evaluate which factors, mainly genetic but also non-genetic, that affect the response to warfarin in terms of required maintenance dose, efficacy and safety with special focus on warfarin dose prediction. Through candidate gene and genome-wide studies, we have shown that the genes CYP2C9 and VKORC1 are the major determinants of warfarin maintenance dose. By combining the SNPs CYP2C9 *2, CYP2C9 *3 and VKORC1 rs9923231 with the clinical factors age, height, weight, ethnicity, amiodarone and use of inducers (carbamazepine, phenytoin or rifampicin) into a prediction model (the IWPC model) we can explain 43 % to 51 % of the variation in warfarin maintenance dose. Patients requiring doses < 29 mg/week and doses ≥ 49 mg/week benefitted the most from pharmacogenetic dosing. Further, we have shown that the difference across ethnicities in percent variance explained by VKORC1 was largely accounted for by the allele frequency of rs9923231. Other novel genes affecting maintenance dose (NEDD4 and DDHD1), as well as the replicated CYP4F2 gene, have small effects on dose predictions and are not likely to be cost-effective, unless inexpensive genotyping is available. Three types of prediction models for warfarin dosing exist: maintenance dose models, loading dose models and dose revision models. The combination of these three models is currently being used in the warfarin treatment arm of the European Pharmacogenetics of Anticoagulant Therapy (EU-PACT) study. Other clinical trials aiming to prove the clinical validity and utility of pharmacogenetic dosing are also underway. The future of pharmacogenetic warfarin dosing relies on results from these ongoing studies, the availability of inexpensive genotyping and the cost-effectiveness of pharmacogenetic driven warfarin dosing compared with new oral anticoagulant drugs.
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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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Khan, Tayyaba Irfan. "Factors affecting anticoagulation response to Warfarin." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413389.

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Myszka, David Gerard. "Photoaffinity labeling of warfarin binding proteins /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487694702785693.

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Msolli, Ines. "Nanosystèmes polymères pour la libération contrôlé de la Warfarine : conception et évaluation biologique." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD033/document.

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Dans ce travail de thèse, nous avons synthétisé des dérivés de poly(acide (R,S)-3,3-diméthylmalique) (PDMMLA). Les copolymères de PDMMLA sont composésprincipalement de deux monomères: un monomère hydrophobe contenant un groupementhexylique et un monomère hydrophile contenant un groupement acide. Grâce à la proportionde chaque monomère dans le copolymère final, la balance hydrophile/hydrophobe est ajustée.Donc six copolymères ont été obtenus: trois copolymères statistiques PDMMLAHn-co-Hex100-n et trois copolymères à blocs PDMMLAHn-b-Hex100-n. Ces copolymères sont àl’origine de nanoparticules sans et avec un principe actif. La Warfarine a été encapsulée à lafois avec des nanoparticules de PDMMLAHn-co-Hex100-n et de PDMMLAHn-b-Hex100-n.Les nanoparticules formées sont caractérisées afin d'en déterminer la forme, la taille et lacharge de surface. Donc des nanoparticules de forme sphérique, ayant une taille inférieure à100 nm et ayant une charge de surface inférieure à -30 mV ont été obtenues. Lesnanoparticules de PDMMLAH30-co-Hex70, ont été choisies pour étudier la libérationcontrôlée de la warfarine dans des conditions de température et de pH physiologiques. Lesrésultats obtenus montrent une libération lente et progressive de la warfarine à partir dessystèmes nanoparticulaires ainsi conçus et réalisés. De tels systèmes nanoparticulaires à basede dérivés amphiphiles du PDMMLA offriraient ainsi des outils d'intérêt pour l'encapsulationet la libération contrôlée de nombreux principes actifs hydrophobes tels que le dérivécoumarinique inhibiteur de la thrombine (DCBC) dont l'activité antithrombine en systèmepurifié est plus élevée que celle de l'argatroban
In this work we synthesized derivatives of poly((R,S)-3,3-dimethylmalic acid) (PDMMLA).PDMMLA copolymers are mainly composed of two monomers: a hydrophobic monomercontaining a hydroxyl group and a hydrophilic monomer containing an acid group. Due to theproportion of each monomer in the final copolymer, the hydrophilic / hydrophobic balance ismodulated. Thus, six copolymers were obtained: three random copolymers PDMMLAHn-co-Hex100-n and three block copolymers: PDMMLAHn-b-Hex100-n.These copolymers are at the origin of nanoparticles without and with an active principle.Warfarin, which has been successfully encapsulated with both PDMMLAHn-co-Hex100-nand block, copolymer nanoparticles: PDMMLAHn-b-Hex100-n. The formed nanoparticlesshowed fairly high encapsulation efficiency for both types of copolymers.The PDMMLA nanoparticles are characterized in order to determine their shape, size andsurface charge. Thus nanoparticles of spherical shape, having less than 100 nm size andhaving a surface charge of less than -30 mV have been obtained. The PDMMLAH30-co-Hex70nanoparticles were chosen to study the controlled release of warfarin under physiologicaltemperature and pH conditions. Obtained results show a slow and progressive release ofwarfarin. Such nanoparticulate systems based on amphiphilic derivatives of PDMMLA wouldthus offer tools of interest for the encapsulation and controlled release of many hydrophobicactive principles such as the coumarin derivative thrombin inhibitor (DCBC) whoseantithrombin activity in purified system is higher than that of argatroban
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Hickmott, Helen Ruth. "Factors affecting the pharmacological activity of warfarin." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251170.

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Books on the topic "Warfarin"

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Royal College of General Practitioners. and National Patient Safety Agency, eds. Special focus: Warfarin. London: Royal College of General Practitioners, 2004.

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Wessler, Stanford, Carl G. Becker, and Yale Nemerson, eds. The New Dimensions of Warfarin Prophylaxis. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-5985-3.

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1917-, Wessler Stanford, Becker Carl G, and Nemerson Yale, eds. The new dimensions of warfarin prophylaxis. New York: Plenum Press, 1987.

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Lodwick, Al. Warfarin, rat poison to wonder drug: A guide to its use and interactions. Pueblo, Colo: Lodwick Pub., 2002.

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Bowles, Jane Anne. A comparison of different methods of prescribing warfarin. Hamilton: St. Joseph's Hospital, 1991.

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Parker, James N., and Philip M. Parker. Warfarin: A medical dictionary, bibliography, and annotated research guide to Internet references. Edited by NetLibrary Inc. San Diego, CA: ICON Health, 2004.

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Sullivan, Daniel. Acceptance of various rodenticide baits under field conditions by Columbian and Richardson ground squirrels. Helena, Mont: Montana Dept. of Agriculture, Environmental Management Division, Technical Services Bureau, 1985.

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Parker, Philip M., and James N. Parker. Coumadin: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2003.

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Kwan, Debora. The effects of acute and chronic acetaminophen dosing on the pharmacodynamics and pharmacokinetics of the (R)- and (S)- enantiomers of warfarin. Ottawa: National Library of Canada, 1993.

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Warfare. London: Phoenix, 1997.

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Book chapters on the topic "Warfarin"

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Herridge, Margaret S., Jane Batt, and Scott K. Epstein. "Warfarin." In Encyclopedia of Intensive Care Medicine, 2465. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_2432.

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Hadlock, Gregory C., Allison E. Burnett, and Edith A. Nutescu. "Warfarin." In Anticoagulation Therapy, 9–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73709-6_2.

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DeLoughery, Thomas G. "Warfarin." In Hemostasis and Thrombosis, 125–31. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09312-3_25.

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DeLoughery, Thomas G. "Warfarin." In Hemostasis and Thrombosis, 161–68. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19330-0_25.

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Roth, Elliot J. "Warfarin (Coumadin)." In Encyclopedia of Clinical Neuropsychology, 3677. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2214.

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Roth, Elliot J. "Warfarin (Coumadin)." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2214-2.

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Hashim, Jeffrey, Daniel Thomas Ginat, and Juan E. Small. "Warfarin (Coumadin)." In Neuroimaging Pharmacopoeia, 249–56. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12715-6_32.

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Hashim, Jeffrey, Daniel Thomas Ginat, and Juan E. Small. "Warfarin (Coumadin)." In Neuroimaging Pharmacopoeia, 305–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08774-5_43.

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Roth, Elliot J. "Warfarin (Coumadin)." In Encyclopedia of Clinical Neuropsychology, 2670–71. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_2214.

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Rose, Anne E. "Inpatient Warfarin Management." In Anticoagulation Management, 3–26. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22602-6_1.

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Conference papers on the topic "Warfarin"

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Soni, A., A. Muthyala, S. Sasidharan, R. Shrestha, J. Scott, and R. A. Rosiello. "To Warfarin or Not to Warfarin, That Is the Question!" In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1829.

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Powers, P. J., M. Gent, R. Jay, J. Hirsh, M. Levine, and G. Turpie. "DEEP VEIN THROMBOSIS PROPHYLAXIS IN SURGICALLY TREATED FRACTURED HIP PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643692.

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Deep vein thrombosis is a major complication in'patients treated surgically for fractured hip. Methods employed toreduce the risk of thrombosis include dextran, ASA, warfarin, low or adjusted dose heparin and calf compression, but none has widespread acceptance.A randomized trial wascarried out to assess the effectiveness of sodium warfarinand acetyl salicylic acid(aspirin) compared to placebo inthe prevention of venous thrombosis in fractured hip patients. One hundred and ninty four patients were randomizedto receive warfarin (65 patients), ASA (66 patients) or placebo (63 patients).Prophylaxis commenced post operatively and continued for 21 days or until discharge, if earlier.Warfarin patients received 10 mg sodium warfarin orally as soon as possible after surgery. Warfarin was then given daily according to the prothrombin time (PT), to obtain a PT of 16 seconds on the 5th post operative day. The PT was maintain at 16 to 18 seconds until the end of treatment.ASA and placebo patients received enteric coated tablets, 650 mg twice daily, in a double blind fashion beginning as soon as possible post operatively and continuingto the end of treatment. Surveillance testing and I-fibrinogen leg scanning and impedance plethysmography was performed and venography was done if either test suggested thrombus at the popliteal vein or above. Otherwise venography was performed at day 21 or prior to discharge, if earlier. Venous thrombosis occurred in 13 patients (20%) in the warfarin group, 27 patients (^0.9%) in the ASA group, and 29 patients (46%) in the placebo group (P=0.005). Proximal vein thrombosis or pulmonary embolism occurred in 6patients (9.2%) in the warfarin group,7 patients (10.6%) in the ASA and 19 patients (30.2%) in the placebo group (P=0.002). Two major hemorrhages occurred in the warfarin group, none in the ASA group, and 2 in the placebo group.The results of this study show sodium warfarin to be safeand effective in reducing thromboembolic complications infractured hip patients and ASA to be effective in reducing thrombosis involving the proximal deep veins of the lower limbs in these patients.
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McKernan, A., J. M. Thomson, and L. Poller. "A PROSPECTIVE RANDOMISED CONTROLLED STUDY OF MINI-DOSE WARFARIN PROPHYLAXIS OF DEEP VEIN THROMBOSIS IN MAJOR SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643879.

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A prospective randomised study has been undertaken to assess the clinical effectiveness of oral anticoagulation using minidose warfarin (1 mg daily for 2-4 weeks before major gynaecological surgery) compared with conventional oral anticoagulant prophylaxis and an untreated randomised control group. The conventional oral anticoagulant prophylaxis was based on a therapeutic range of 1.5 - 2.0 INR at the time of operation and 2.0 - 3.0 INR post-operatively. Overall the mini-dose warfarin group showed no pre-operative prolongation of the prothrombin time with the Manchester Reagent although a minority of patients showed a 1-2 second prolongation of the prothrombin time before operation. Post operatively the mini-dose warfarin group showed an exaggerated prolongation of the prothrombin time which normally occurs after operation and was observed in the untreated controls. Factor VII assays paralleled these findings. Minidose warfarin, while not prolonging the prothrombin time before operation, resulted in delayed platelet aggregation with the Chandler's tube technique in almost all patients.The incidence of deep vein thrombosis has been reduced in both mini-dose and conventional dose oral anticoagulant series compared with the untreated- group. It appears that the minimal changes in the prothrombin time, factor VII and platelet aggregation tests, observed in the mini-dose warfarin group, may offer sufficient protection against post-operative thrombosis in a moderate risk group undergoing abdominal or pelvic surgery.
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Gerhart, T., H. Yett, A. Donovan, M. A. Lee, M. Smith, and E. W. Salzman. "ORGANON 10172 VS. WARFARINTO PREVENT VENOUS THROMBOSIS AFTER HIP FRACTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643686.

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Deep venous thrombosis (DVT) remains a serious and frequent complication after fracture of the hip, and even the mostefficacious prophylactic agents, e.g., warfarin, may fail to prevent DVT in up to 2056 of cases. There is evidence that low molecular weight heparin or heparin-like agents may have advantages in antithrombotic prophylaxis with reduced hemorrhagic sideeffects in patients at risk of DVT. We are engaged in a randomized prospective trial comparing the antithrombotic effect ofwarfarin (PT 1.5x control)with that of Organon 10172, a mixture ofsulfated low molecular weight glycosamioglycans (750 anti-Xa u b.i.d. sc., begunpreop and continued 9 days, followe by warfarin). Diagnosis is by 125-1 fibrinogen scan and impedence plethysmography with confirmatory phlebography. At present71 patients have been admitted, and patient groups are comparable in age, sex, type of fracture, and all other significant respects. DVT has been diagnosed in 7of 36 patients given warfarin an in 1 of35 patients who received Organon10172. Pulmonary embolism has not beenencountered. GI bleeding has occurred twice on warfarin and once on Organon 10172 There has been no difference in estimated operative blood loss, transfusion requirements, or other major bleeding complications.One patient on warfarin died ofmyocardial infarction and pneumonia. There were no other adverse reactions.The study is still in progress. The present trend in the results suggests that the heparinoid Organon 10172 may be a promising new agent to prevent DVT in high risk patients, such as those with fractures of the hip.
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Chi, Chih-Lin, Xinpeng Shen, Kourosh Ravvaz, John Weissert, and Peter Tonellato. "Personalize Warfarin Trearment by Optimizing Protocol Assignment." In 2018 IEEE International Conference on Healthcare Informatics (ICHI). IEEE, 2018. http://dx.doi.org/10.1109/ichi.2018.00067.

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Zhao, Zhongming, Shivi Kansal, and Bonny L. Bukaveckas. "SmartWarf - A portable automated warfarin dosing tool." In 2009 International Symposium on Collaborative Technologies and Systems. IEEE, 2009. http://dx.doi.org/10.1109/cts.2009.5067500.

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Aydar, S., S. Alataş, L. Numanoğlu, and A. Sönmezdağ. "EFFECT OF ORAL ANTICOAGULANTS ON STABLE ROSETTE FORMATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643271.

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Human peripheral blood T lymphacytes when cultered in the presence of mitogen Phytohemogglutinin (PHA) acquire the capacity to form E rosettes with sheep erythrocytes that are resistant to incubation at 37° C. Whereas human thymus lymphocytes form 37° C stable E rosettes. On the other hand, it is shown that the use of anticoagulants can prevent cancer metastases which brings forth the importance of explaining the relationship between the lymphocyte functions and anticoagulant action mecha-nismus. In order to investigate this relationship, we did a group af experiments with lymphocytes of normal children and of children with severe burn wounds. Peripheral blood lymphocytes were seperated by “Lymphoprep” centrifugation technique. The lymphocytes of normal children and patients with burn were divided in two groups: A-Activated lymphocytes: 1×106 /ml lymphocytes were cultured and activated by PHAfor 48 hours at 37° C in RPMI 1640. B-Non activated lymphocytes were in culture witout PHA. 1×10™6 M/ml warfarin sulfate was added to some of the cultures of each group prior to the culture conditions. At the end of the 48 hour incubation, heat stable rosette formation was determined by the method of Wauve and co-workers. Significantly elevated levels of heat stable rosette forming cells were found in the PHA activated culture treated with warfarin sulfate in normals and patients with burn. Although the blastic transformation of T lymphocytes was found to be depressed, heat stable rosette formation of warfarin sulfate treated lymphocytes abtained from burn patients was observed to be significantly elevated. It is concluded that warfarin sulfate increases the activity of T lymphocytes by interfering with the resynthesis of heai stable E receptors.
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Wang, Zeyuan, Josiah Poon, Jie Yang, and Simon Poon. "Warfarin Dose Estimation on High-dimensional and Incomplete Data." In Hawaii International Conference on System Sciences. Hawaii International Conference on System Sciences, 2021. http://dx.doi.org/10.24251/hicss.2021.419.

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Chi, Chih-Lin, Kourosh Ravvaz, John Weissert, and Peter J. Tonellato. "Optimal decision support rules improve personalize warfarin treatment outcomes." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7591261.

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Crow, M. J., A. B. Latif, A. I. Critchley, C. Stainton, P. Nealon, and S. M. Rajah. "COMPUTER PREDICTION OF ANTICOAGULATION STATUS AND WARFARIN DOSE FOLLOWING CARDIAC SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643275.

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Fluctuations are freguently seen in the anticoagulant status of patients in the immediate post operative period following prosthetic heart valve replacement. These patients are at high risk of haemorrhage or thromboembolism. We have used a pharmokinetic model of warfarin metabolism to develop a computer programme to predict the maintenance dose of warfarin from early prothrombin activity determinations. This will enable controlled anticoagulation to be achieved. The expression for warfarin kinetics employs 4 constants determined by the residual sum of the sguares, which are used immediately to redefine dosage predictions. In a pilot study data obtained from 16 patients post operation 3, 5 and 7 days after commencing treatment, has been used to predict the reguired maintenance dose at 21 days. These predicted doses were then compared with the maintenance dose achieved by clinical practice. The programme was told to optimise its dose to achieve a PT ratio of 3 whereas clinically the ratio was allowed to vary in the therapeutic range of 2 to 4. Predicted doses at 21 days are shown.in the table:Correlation between predicted and clinical maintenance doses after 3 and 5 days treatment was poor but had improved significantly by 7 days, despite similar levels of prothrombin activity. Predicted prothrombin activity never exceeded the upper limit of the therapeutic range, and the predicted dose can be uprated on addition of further data within 2 minutes.After 7 days computer predicted warfarin dose has produced a good correlation with the clinical maintenance dose (the doses of only 3 patients varying by more than 1 mg/day). The significant fluctuations seen in the prothrombin ratio during clinical dosage were not observed with computer dosing and we now feel it is safe to use this programme to anticoagulate patients post operatively.
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Reports on the topic "Warfarin"

1

Purba, Abdul, Saraswati Gumilang, Dhihintia Jiwangga, Nurina Hasanatuludhhiyah, and Maarten Postma. Cost and clinical outcomes in the use of new oral anticoagulants versus warfarin in deep vein thrombosis: A systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0106.

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Review question / Objective: What are the benefits of using new oral anticoagulants compared to warfarin in terms of efficacy, bleeding, and cost among people with deep vein thrombosis? This study aimed to compare the effectiveness, bleeding incidence, and cost between NOAC and warfarin in DVT patients. Condition being studied: The patient confirmed DVT with the results of the Wells' score and D-dimer test stating "possible DVT" and followed by an ultrasound examination which stated "DVT positive". Patients are taking oral anticoagulants to treat DVT or to prevent a recurrence. Oral anticoagulants consist of apixaban, rivaroxaban, edoxaban, dabigatran, and warfarin.
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Oh, SangHyeon, Seoyong Choi, and Jee-Eun Chung. Comparative efficacy and safety of reduced dose of DOACs in patients with atrial fibrillation. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0073.

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Review question / Objective: To compare the risk of stroke/systemic embolism (S/SE), mortality and bleeding in AF patients with reduced-dose DOACs. Rationale: Although each DOAC has its dose reduction criteria, many physicians still prefer to prescribe the reduced-dose DOACs, regardless of label adherence. However, inappropriate administration of DOACs is an important clinical problem because patients may not benefit from the recommended DOAC dose to prevent stroke and systemic embolism. Therefore, this study aims to investigate the risk of stroke/systemic embolism (S/SE) and mortality in AF patients with reduced-dose DOACs. Condition being studied: Adult patients with AF taking DOACs or Warfarin.
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Zhu, He. Postoperative bleeding of therapeutic endoscopy in patients using direct oral anticoagulant or warfarin: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0172.

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Ye, Hao-Zhen, Jia-Jia Gao, He Zhou, Zhi-Wei Li, Hong-Wei Xu, and Ben Wang. The risk of postpolypectomy bleeding in patients receiving direct oral anticoagulants compared to warfarin or non-anticoagulants: a systematic review with meta-analysis of cohort studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0124.

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Vatet, Ian V. Can Network-Centric Warfare Save Undersea Warfare? Fort Belvoir, VA: Defense Technical Information Center, February 2000. http://dx.doi.org/10.21236/ada379174.

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AIR UNIV MAXWELL AFB AL. Electronic Warfare. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada562410.

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Sherman, William C. Air Warfare. Fort Belvoir, VA: Defense Technical Information Center, March 2002. http://dx.doi.org/10.21236/ada421698.

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JOINT CHIEFS OF STAFF WASHINGTON DC. Electronic Warfare. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada464647.

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Van Messel, John A. Unrestricted Warfare: A Chinese Doctrine for Future Warfare? Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada509132.

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Sullivan, Gordon R., and James M. Dubik. Envisioning Future Warfare. Fort Belvoir, VA: Defense Technical Information Center, January 1995. http://dx.doi.org/10.21236/ada450234.

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