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Class of 2012 Abstract / Objectives: To evaluate the literature with respect to drug-drug interactions of the hydroxymethylglutaryl CoA reductase inhibitors atorvastatin, fluvastatin, lovastatin, pitavastitin, pravastatin, simvastatin, and rosuvastatin with warfarin. Methods: This descriptive retrospective study identified articles reporting on each drug-drug interaction from the online databases PubMed (1970 – February 2012) and the drug compendia Micromedex and Facts & Comparisons. The studies included in this investigation were primary literature reports, written in English with human subjects. All studies included were evaluated using the van Roon 5-point quality of evidence scale developed in the Netherlands to assess drug-drug interactions. This scale rates the study type from lowest to highest quality, from zero to four. Case-reports were evaluated using the Drug Interaction Probability Scale (DIPS). The DIPS tool uses 10 questions to evaluate the probability that an adverse event is caused by a drug-drug interaction. Results: Twenty studies met the inclusion criteria. One study involved atorvastatin, four for fluvastatin, three for lovastatin, 2 for pitavastatin, 1 for pravastatin, 5 for rosuvastatin, and 6 for simvastatin. The mean van Roon quality of evidence score was 2.1+/- 0.74, the mean score for atorvastatin, pitavastatin, and pravastatin was 3, with the mean score of fluvastatin, lovastatin, rosuvastatin, and simvastatin was 2. 70% of the literature reviewed were case-reports or letters. Conclusions: The studies and reports supporting HMG-CoA reductase inhibitors and warfarin drug-drug interactions are most commonly case-reports and are of low quality and quantity.

Class of 2013 Abstract / Specific Aims: The purpose of this study is to identify a postoperative warfarin re-initiation protocol used most commonly by certified anticoagulation providers. Our main hypothesis is that certified Anticoagulation providers use a postoperative warfarin re-initiation strategy based upon clinical experience/knowledge as opposed to a guideline-based approach. Methods: The Anticoagulation Forum website will be used to select the anticoagulation providers to interview via telephone. The selection process will be as follows: an excel spreadsheet will be created separating every clinic listed on the website by region, then fifty anticoagulation providers will be randomly selected by utilizing a random number generator function in excel for each region. Anticoagulation providers are listed on the website by region, and then further broken down by states in that region. The intention of separating regions is to attain equal representation of anticoagulation providers across the United States that are listed on the Anticoagulation Forum website. Anticoagulation providers will be called during the months of July, August and September 2012. Any anticoagulation provider contacted that is not certified with the National Certification Board for Anticoagulation Providers (NCBAP) as well as services or clinics not listed on the Anticoagulation Forum website will be excluded. An application will be submitted to the University of Arizona Institutional Review Board (IRB) Human Subjects Protection Program for approval of this study. We plan to randomly call 50 anticoagulation providers from each region of the US listed on the Anticoagulation Forum website. Thus, total estimated sample size is approximately 300 providers. The primary dependent variable is the postoperative warfarin re-initiation protocol. Our demographic variables are as follows: # of years in anticoagulation practice, gender of the provider and their credentials. The data extraction form is comprised of 3 parts. Part 1 will focus on questions directly related to the anticoagulation service, part 2 is for describing the patient population served and part 3 will be related to the provider demographic characteristics. Data will be collected by utilizing a telephone interview questionnaire-based approach. Each certified anticoagulation provider randomly selected from the Anticoagulati Main Results: The information about warfarin re-initiation dose and protocol information are shown in Table 2. A majority of certified anticoagulation providers re-initiate warfarin at the same dose (64%) after temporary interruption compared to a relative warfarin dose (36%) following surgery/procedure. Likewise, more certified anticoagulation providers have a protocol in place (59%) compared to no protocol in place (41%). Conclusion: This study displayed strength when certified anticoagulation providers were able to be contacted and take the time to answer the questionnaire. Certified anticoagulation providers utilize a common warfarin re-initiation strategy. Most providers’ re-initiation warfarin at the same dose at which the patient was receiving prior to surgery. However, there are many other factors that may go into making the decision of which warfarin dose to use postoperatively.

Continuing the study of the relationships between fibrin investment of the tumor, vascularity, and tumor growth, we decided to investigate the relationship of warfarin sodium anticoagulation with tumor growth and vascularization. It was reasoned that if the previously observed altered tumor growth was due the heparin’s anticoagulant effect rather than a direct effect upon the tumor, another anticoagulant with a different mechanism of action would have the same tumor growth reducing capabilities. Warfarin sodium produces reduced fibrin polymer formation by a mechanism entirely different from that of heparin. Heparins’ immediate anticoagulant activity results from a blockade of thrombin’s activity results from a blockade of thrombin’s activity on fibrinogen, prevention of prothrombin conversion to thrombin, and a reduction in platelet adhesiveness. Warfarin’s delayed activity, however, is through an inhibition of vitamin K activity leading to reduced synthesis of several clotting factors. With the decision to use warfarin sodium, experiments were designed to test the hypothesis that a reduction of prevention of fibrin formation and thus tumor encasement with this polymer would alter tumor growth. It was also hypothesized that, accompanying the altered tumor growth, several macroscopic factors including tumor vascularization, extent of tumor attachment, vasodilation of host blood vessels in the locale of the implanted tumor, and local edema fluid would be altered. Experiments were conducted to determine the relationship between the dose of warfarin sodium administered and the degree of alteration of tumor growth and the related factors. An inverse dose-response relationship between dose of warfarin and tumor growth and the related parameters was hypothesized.

Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin.

No description available.

Thesis (M.S.)--University of Michigan, 1977.

Thesis (M.S.)--University of Michigan, 1977.

Chan Wai Hung Fredric. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 67-72). / Abstracts in English and Chinese. / Acknowledgement --- p.i / Abstract --- p.ii / 摘要 --- p.iv / Table of contents --- p.vi / Publications --- p.ix / List of figures --- p.x / List of tables --- p.xi / Abbreviations --- p.xii / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Anticoagulation effect of warfarin --- p.2 / Chapter 1.2 --- Indications of warfarin therapy --- p.3 / Chapter 1.3 --- Monitoring systems for anticoagulation therapy --- p.4 / Chapter 1.4 --- Optimum target intensities for anticoagulation therapy --- p.5 / Chapter 1.5 --- Factors affecting anticoagulation effect of warfarin --- p.6 / Chapter 1.5.1 --- Drugs --- p.7 / Chapter 1.5.2 --- Diet --- p.8 / Chapter 1.5.3 --- Health supplements --- p.8 / Chapter 1.5.4 --- Comorbidities --- p.9 / Chapter 1.5.5 --- Genetic factors --- p.10 / Chapter 1.6 --- Management of anticoagulation therapy in Chinese patients --- p.11 / Chapter 1.7 --- Barriers to optimal INR control --- p.13 / Chapter 1.8 --- Two models of care for anticoagulation therapy - routine medical care and co-ordinated anticoagulation service --- p.14 / Chapter 1.9 --- Outcomes of two models of anticoagulation management --- p.14 / Chapter 1.9.1 --- Clinical outcomes --- p.14 / Chapter 1.9.2 --- Economic outcomes --- p.16 / Chapter 1.10 --- Clinical pharmacist involvement in the management of anticoagulation therapy --- p.17 / Chapter 1.11 --- Anticoagulation management in Hong Kong --- p.18 / Chapter 1.12 --- Hypothesis and objectives --- p.19 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Setting and subjects --- p.22 / Chapter 2.2 --- Interventions --- p.23 / Chapter 2.2.1 --- Newly proposed model --- p.23 / Chapter 2.2.1.1 --- Training of clinical pharmacist --- p.23 / Chapter 2.2.1.2 --- Development of management protocol --- p.24 / Chapter 2.2.1.3 --- Treatment algorithm of pharmacist-managed anticoagulation service --- p.25 / Chapter 2.2.1.4 --- Validation of the Coagucheck Pro DM --- p.28 / Chapter 2.2.2 --- Usual practice model --- p.29 / Chapter 2.3 --- Outcome measures --- p.29 / Chapter 2.3.1 --- Primary clinical outcomes --- p.29 / Chapter 2.3.1.1 --- Therapeutic and expanded therapeutic INR ranges --- p.29 / Chapter 2.3.1.2 --- A method to determine the amount of patient-time spent in each INR category --- p.30 / Chapter 2.3.2 --- Secondary clinical outcomes --- p.31 / Chapter 2.3.3 --- Economic outcomes --- p.32 / Chapter 2.3.4 --- Humanistic outcomes --- p.34 / Chapter 2.4 --- Sample size estimation --- p.34 / Chapter 2.5 --- Statistical analysis --- p.35 / Chapter Chapter 3 --- Results / Chapter 3.1. --- Patient demographics and indications --- p.37 / Chapter 3.2. --- Control of INR --- p.42 / Chapter 3.3. --- Incidence of major bleeding and thromboembolism --- p.44 / Chapter 3.4. --- Direct medical cost analysis --- p.46 / Chapter 3.5. --- Patient satisfaction --- p.48 / Chapter Chapter 4 --- Discussion and Conclusion / Chapter 4.1 --- Discussion --- p.51 / Chapter 4.1.1 --- Clinical outcomes of anticoagulation clinic --- p.52 / Chapter 4.1.2 --- Direct medical cost analysis --- p.56 / Chapter 4.1.3 --- Patient satisfaction --- p.59 / Chapter 4.1.4 --- Limitations --- p.62 / Chapter 4.1.5 --- Future studies --- p.63 / Chapter 4.2 --- Conclusion --- p.66 / References --- p.67 / Appendices / Appendix A. Management protocol --- p.73 / Appendix B. Data collection form --- p.96 / Appendix C. PSQ-18 --- p.104

Bakgrund Förmaksflimmer är en arytmi som uppkommer av att sinusknutan slutar styra hjärtrytmen och impulser initieras istället på flera olika ställen i förmaken. Detta orsakar en snabb och oregelbunden kontraktion med försämrad cirkulation som resultat. Förmaksflimmer är den vanligaste orsaken till stroke och en viktig del i behandlingen av förmaksflimmer är därför att förebygga stroke genom antikoagulerande läkemedel. Warfarin har länge varit förstahandsval, men nya läkemedel, så kallade icke vitamin K antagonist oral antikoagulantia (NOAK) har de senaste åren godkänts som förebyggande behandling vid indikationen förmaksflimmer. Syftet med arbetet var att undersöka effekt, blödningsrisk och kostnad av NOAK som förebyggande behandling av stroke och systemisk emboli hos patienter med förmaksflimmer.  Metod och material Arbetet utfördes som en litteraturstudie där fem kliniska studier från databasen PubMed analyserades. I fyra studier jämfördes de tre faktor Xa-hämmarna apixaban, edoxaban och rivaroxaban, samt trombinhämmaren dabigatran med warfarin. I en studie jämfördes apixaban med Aspirin®.  Resultat Alla NOAK visades reducera risken att drabbas av stroke och emboli minst likvärdigt med warfarin. Dabigatran 150 mg och edoxaban 60 mg visades även vara effektivare än warfarin (RR=0,66; P<0,001, respektive RK=0,79; P<0,001). Apixaban reducerade risken för stroke och systemisk emboli med mer än 50 % i jämförelse med Aspirin® (RK= 0,45; P<0,001). Uppkomst av större blödning var likvärdigt förekommande i jämförelse mellan NOAK och warfarin. Dabigatran 110 mg, edoxaban 30 mg, edoxaban 60 mg och apixaban 5 mg visade på lägre risk för större blödning. Apixaban och Aspirin® visades vara likvärdiga avseende uppkomst av större blödning. Slutsats Icke vitamin K antagonist oral antikoagulantia är effektiva som förebyggande behandling av stroke och emboli hos patienter med förmaksflimmer, med lägre blödningsrisk än warfarin, men till en högre kostnad. / Atrial fibrillation is an arrhythmia characterized by rapid and uncontrolled contraction of the atria. The irregular contractions leads to incomplete circulation, accumulation of blood in the atria and increases the risk of stroke and embolism. An important part in the treatment of atrial fibrillation is to prevent the risk of stroke by use of anticoagulants. The first line treatment is the vitamin K antagonist warfarin. The drug has many side effects such as risk of bleeding, difficulties to adjust the dose and interactions with both drugs and food. In recent years, new drugs, called non vitamin K antagonist oral anticoagulants (NOAC), have been approved as preventive treatment of stroke in patients with atrial fibrillation. These include three factor Xa inhibitors: apixaban, rivaroxaban, and edoxaban, and one thrombin inhibitor: dabigatran. In this study, the efficacy, risk of bleeding and cost of NOAK was investigated for the prevention of stroke and systemic embolism in patients with atrial fibrillation. The study was conducted as a literature study where five clinical trials from the database PubMed was analyzed. In four studies, the three factor Xa inhibitors apixaban, edoxaban and rivaroxaban, and the thrombin inhibitor dabigatran were compared with warfarin. In one study apixaban was compared with Aspirin®. In all studies the prevention of stroke and systemic embolism and risk of bleeding was investigated. All NOAC reduced the risk of stroke and embolism at least equal to warfarin. Dabigatran 150 mg and edoxaban 60 mg was also more effective than warfarin. Apixaban reduced the risk of stroke and systemic embolism with more than 50 % compared with aspirin. The occurrence of major bleeding was similar in comparison of Dabigatran 150 mg, respectively rivaroxaban 20 mg and warfarin. Dabigatran 110 mg, edoxaban 30 mg, edoxaban 60 mg and apixaban 5 mg showed a lower risk of major bleeding than warfarin. Apixaban and Aspirin® appeared to be equivalent regarding the occurrence of major bleeding. Non Vitamin K antagonist oral anticoagulants are effective in the prevention of stroke and embolism in patients with atrial fibrillation, with lower risk of bleeding than warfarin, but with a higher cost.