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Journal articles on the topic 'Warfarin'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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9

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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10

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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11

Fang, Margaret C., and Daniel E. Singer. "Warfarin or Not Warfarin?" Annals of Internal Medicine 142, no. 8 (April 19, 2005): 676. http://dx.doi.org/10.7326/0003-4819-142-8-200504190-00021.

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12

King, Cynthia A., Kathleen M. Babcock, Rhianna J. Godios, and Benjamin S. King. "Significant drug–drug interaction between warfarin and nafcillin." Therapeutic Advances in Drug Safety 9, no. 11 (August 31, 2018): 667–71. http://dx.doi.org/10.1177/2042098618796186.

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Nafcillin, a beta-lactam semisynthetic penicillin, is highly resistant to penicillinase and is similar to other penicillins except that it is primarily metabolized in the liver. It is believed that nafcillin causes CYP3A4 enzyme induction which decreases warfarin’s half-life. The onset of CYP3A4 induction by nafcillin occurs within the first 7 days, but maximal effects may take up to 2 weeks. Once nafcillin is discontinued, the effects persist for several weeks. A 79-year-old male with a history of atrial fibrillation and a 53-year-old male with a history of recurrent venous thromboembolism required significantly higher weekly warfarin doses during courses of nafcillin therapy. Both patients required a 2.5–3.5-fold increase from their baseline weekly warfarin dose to achieve therapeutic international normalized ratios (INRs) while on nafcillin. Traditional protocol-driven warfarin management can result in suboptimal anticoagulation in patients on warfarin and nafcillin.

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13

Ahmad, Yousif, and Gregory Y. H. Lip. "Stroke Prevention in Atrial Fibrillation: Where are We Now?" Clinical Medicine Insights: Cardiology 6 (January 2012): CMC.S8976. http://dx.doi.org/10.4137/cmc.s8976.

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Atrial fibrillation is the commonest arrhythmia worldwide and is a growing problem. AF is responsible for 25% of all strokes, and these patients suffer greater mortality and disability. Warfarin has traditionally been the only successful therapy for stroke prevention, but its limitations have resulted in underutilisation. Major progress has been made in AF research, leading to improved management strategies. Better risk stratification permits identification of truly low-risk patients who do not require anticoagulation and we are able to simplify ourevaluation of a patient's bleeding risk. The advent of novel anticoagulants means warfarin is no longer the only choice for stroke prophylaxis. These drugs circumvent many of warfarin's inconveniences, but only long-term study and use will conclusively demonstrate how they compare to warfarin. The landscape of stroke prevention in AF has changed with effective alternatives to warfarin available for the first time in 60 years—but each new option brings new considerations.

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14

Park, Soohyun, and Insil Jang. "Factors Affecting Medication Adherence in Patients with Mechanical Heart Valves Taking Warfarin: The Role of Knowledge on Warfarin, Medication Belief, Depression, and Self-Efficacy." International Journal of Environmental Research and Public Health 18, no. 10 (May 14, 2021): 5214. http://dx.doi.org/10.3390/ijerph18105214.

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Non-adherence is highlighted as one of the main contributors to the occurrence of adverse events and negative clinical outcomes in patients treated with warfarin. The aim was to examine knowledge on warfarin, medication belief, depression, and self-efficacy as factors influencing medication adherence for anticoagulation control. This was a cross-sectional study. The participants in this study were patients who visited an outpatient clinic of cardiovascular surgery to administer anticoagulants after mechanical valve replacement surgery at a tertiary hospital in Seoul. Responses of 154 participants on questionnaires were analyzed from 10 September to 26 December 2020. Multiple regression analyses were performed to assess the factors influencing medication adherence among the patients with anticoagulation control. Factors influencing medication adherence were consuming warfarin for 3 to 5 years, awareness of target prothrombin time international normalized ratio, knowledge of warfarin, and depression. Medication beliefs and self-efficacy had no significant influence on medication adherence. The most important factors associated with medication adherence in patients with mechanical heart valves were knowledge about warfarin and depression. In the control of oral anticoagulants that require continuous management, education and providing accurate guidance is more important than personal preferences. Clinical nurses should facilitate educational programs tailored to the characteristics of the patient, including their purpose and method of taking warfarin, specific diets, their knowledge on warfarin’s interaction with other drugs, symptoms of adverse events, and self-management. In addition, healthcare providers should check whether warfarin therapy is being controlled by evaluating medication adherence and depression levels among patients.

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15

Sahinkus, Salih. "In-Hospital Clinical Ooutcomes of COVID-19 Patients Treated with Oral Anticoagulants." Angiology & Vascular Surgery 7, no. 2 (November 8, 2022): 1–4. http://dx.doi.org/10.24966/avs-7397/100094.

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Objective: We aimed to investigate the effects of warfar in and new-generation oral anticoagulants on the prognosis of patients diagnosed with Corona Virus Disease 2019 (COVID-19). Materials and Methods: Patients diagnosed with COVID-19 were divided into two groups depending on whether they were using warfarin or a new-generation oral anticoagulant. The types of chronic diseases, drugs used, haematological and biochemical parameters and prognoses in each group were statistically analysed. Results: Twenty-three patients (37.1%) using warfarin and 39 (62.9%) patients using new-generation oral anticoagulants were included in the study. There was no significant difference between the two groups in terms of demographic characteristics and laboratory data. The mortality rates for the warfarin and new-generation anticoagulant groups were similar (39.1% vs. 43.6%, respectively; p = 0.731). Conclusion: There was no difference in the effects of warfarin and new-generation oral anticoagulants on mortality among the patients with COVID-19.

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16

&NA;. "Warfarin." Reactions Weekly &NA;, no. 1376 (November 2011): 30. http://dx.doi.org/10.2165/00128415-201113760-00102.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1377 (November 2011): 37–38. http://dx.doi.org/10.2165/00128415-201113770-00129.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1377 (November 2011): 38. http://dx.doi.org/10.2165/00128415-201113770-00133.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1377 (November 2011): 38. http://dx.doi.org/10.2165/00128415-201113770-00134.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1379 (November 2011): 37. http://dx.doi.org/10.2165/00128415-201113790-00141.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1382 (December 2011): 35. http://dx.doi.org/10.2165/00128415-201113820-00128.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1382 (December 2011): 35. http://dx.doi.org/10.2165/00128415-201113820-00129.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1383 (January 2012): 37. http://dx.doi.org/10.2165/00128415-201213830-00127.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1385 (January 2012): 45–46. http://dx.doi.org/10.2165/00128415-201213850-00167.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1390 (February 2012): 42. http://dx.doi.org/10.2165/00128415-201213900-00162.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1391 (March 2012): 41–42. http://dx.doi.org/10.2165/00128415-201213910-00153.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1391 (March 2012): 42. http://dx.doi.org/10.2165/00128415-201213910-00154.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1392 (March 2012): 46. http://dx.doi.org/10.2165/00128415-201213920-00156.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1393 (March 2012): 41. http://dx.doi.org/10.2165/00128415-201213930-00146.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 695 (April 1998): 12. http://dx.doi.org/10.2165/00128415-199806950-00042.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 709 (July 1998): 12. http://dx.doi.org/10.2165/00128415-199807090-00044.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 713 (August 1998): 12. http://dx.doi.org/10.2165/00128415-199807130-00035.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 717 (September 1998): 11–12. http://dx.doi.org/10.2165/00128415-199807170-00036.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 720 (September 1998): 12. http://dx.doi.org/10.2165/00128415-199807200-00033.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 742 (March 1999): 12. http://dx.doi.org/10.2165/00128415-199907420-00035.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 745 (April 1999): 12. http://dx.doi.org/10.2165/00128415-199907450-00041.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1167 (September 2007): 26–27. http://dx.doi.org/10.2165/00128415-200711670-00079.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1169 (September 2007): 27. http://dx.doi.org/10.2165/00128415-200711690-00074.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1172 (October 2007): 27. http://dx.doi.org/10.2165/00128415-200711720-00084.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1175 (October 2007): 27. http://dx.doi.org/10.2165/00128415-200711750-00092.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1179 (November 2007): 34. http://dx.doi.org/10.2165/00128415-200711790-00107.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1179 (November 2007): 35. http://dx.doi.org/10.2165/00128415-200711790-00110.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1180 (December 2007): 38. http://dx.doi.org/10.2165/00128415-200711800-00123.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1183 (January 2008): 30. http://dx.doi.org/10.2165/00128415-200811830-00097.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1188 (February 2008): 23. http://dx.doi.org/10.2165/00128415-200811880-00075.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1191 (March 2008): 25–26. http://dx.doi.org/10.2165/00128415-200811910-00079.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1193 (March 2008): 30. http://dx.doi.org/10.2165/00128415-200811930-00095.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1127 (November 2006): 22. http://dx.doi.org/10.2165/00128415-200611270-00072.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1133 (January 2007): 26. http://dx.doi.org/10.2165/00128415-200711330-00090.

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&NA;. "Warfarin." Reactions Weekly &NA;, no. 1146-1147 (April 2007): 26–27. http://dx.doi.org/10.2165/00128415-200711460-00082.

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