Journal articles: 'Warfarin dosage'

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Lala, Mallika, Gilbert J. Burckart, Cheryl M. Takao, Vera Pravica, Jeremiah D. Momper, and Jogarao V. S. Gobburu. "Genetics-Based Pediatric Warfarin Dosage Regimen Derived Using Pharmacometric Bridging." Journal of Pediatric Pharmacology and Therapeutics 18, no. 3 (September 1, 2013): 209–19. http://dx.doi.org/10.5863/1551-6776-18.3.209.

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BACKGROUND Warfarin dosage regimens using CYP2C9 and VKORC1 polymorphisms have been extensively studied in adults and is included in US Food and Drug Administration-approved warfarin labeling. However, no dosage algorithm is available for pediatric patients. OBJECTIVE To derive a genetics-based pediatric dosge regimen for warfarin, including starting dose and titration scheme. METHODS A model-based approach was developed based on a previously validated warfarin dosage model in adults, with subsequent comparison to pediatric data from pediatric warfarin dose, genotyping, and international normalized ratio (INR) results. The adult model was based on a previously established model from the CROWN (CReating an Optimal Warfarin dosing Nomogram) trial. Pediatric warfarin data were obtained from a study conducted at the Children’s Hospital of Los Angeles with 26 subjects. Variant alleles of CYP2C9 (rs1799853 or *2, and rs1057910 or *3) and the VKORC1 single nucleotide polymorphism (SNP) rs9923231 (−1639 G>A) were assessed, where the rs numbers are reference SNP identification tags assigned by the National Center for Biotechnology Information. RESULTS A pediatric warfarin model was derived using the previously validated model and clinical pharmacology considerations. The model was validated, and clinical trial simulation and stochastic modeling were used to optimize pediatric dosage and titration. The final dosage regimen was optimized based on simulations targeting a high (≥60%) proportion of INRs within the therapeutic range by week 2 of warfarin therapy while minimizing INRs >3.5 or <2. CONCLUSIONS The proposed pediatric warfarin dosage scheme based on individual CYP2C9 (alleles *1,*2,*3) and VKORC1 rs9923231 (-1639 G>A) genotypes may offer improved dosage compared to current treatment strategies, especially in patients with variant CYP2C9 and VKORC1 alleles. This pilot study provides the foundation for a larger prospective evaluation of genetics-based warfarin dosage in pediatric patients.

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Recker, Mark W., and Karen L. Kier. "Potential Interaction between Clarithromycin and Warfarin." Annals of Pharmacotherapy 31, no. 9 (September 1997): 996–98. http://dx.doi.org/10.1177/106002809703100907.

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Objective To report a possible drug interaction between clarithromycin and warfarin in a patient with chronic atrial fibrillation. Case Summary A patient with chronic atrial fibrillation was placed on warfarin therapy. International normalized ratios (INRs) ranged from 1.61 to 3.99 while the dosage was being adjusted during the first 5 months of warfarin therapy. The dosage was titrated to 20 mg/wk; laboratory tests obtained 2 weeks after this dosage was started indicated an INR of 2.1. The same dosage was continued. Clarithromycin 500 mg bid was started for an acute exacerbation of bronchitis 10 days after the last INR was obtained and was continued for 14 days of therapy. An INR obtained 3 days after completion of the clarithromycin therapy was 16.8. The warfarin was withheld and vitamin K 20 mg im was administered. The INR obtained the next day was 1.52. The warfarin was restarted and the dosage was titrated to between 22.5 and 25 mg/wk, with INRs ranging from 0.85 to 3.14. Discussion Many factors influence the metabolism of warfarin, including disease states, medications, age, and diet. Data collected in this case suggested clarithromycin may have contributed to the increase in the effect of warfarin. Inhibition of the cytochrome P450 oxidizing system appears to be the reason for the increase. Numerous drugs and disease states affect the rate at which this system metabolizes drugs. Conclusions The potential interaction between clarithromycin and warfarin warrants prudent monitoring of the INR during concurrent administration of these drugs. Warfarin dosages may need to be reduced during concurrent clarithromycin therapy to prevent bleeding complications. Further controlled clinical trials are needed to substantiate the interaction between clarithromycin and warfarin.

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Zatuchni, Jacob. "Guidelines for Warfarin Dosage." Drug Intelligence & Clinical Pharmacy 22, no. 10 (October 1988): 825–26. http://dx.doi.org/10.1177/106002808802201022.

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Liu, Hong-Qiang, Chang-Po Zhang, Chang-Zhen Zhang, Xiang-Chen Liu, and Zun-Jing Liu. "Influence of Two Common Polymorphisms in theEPHX1Gene on Warfarin Maintenance Dosage: A Meta-Analysis." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/564149.

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We conducted a meta-analysis to investigate the influence of two common single nucleotide polymorphisms (SNPs) (rs2292566 G>A and rs4653436 A>G) in theEPHX1gene on warfarin maintenance dosages. Relevant literatures were searched using thePubMed, Embase, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, CBM, andCNKIdatabases without any language restrictions. STATA Version 12.0 software (Stata Corporation, College Station, TX, USA) was used for this meta-analysis. Standard mean difference and its corresponding 95% confidence interval (95% CI) were calculated. Seven studies met the inclusion criteria, including 2,063 warfarin-treated patients. Meta-analysis results illustrated thatEPHX1rs2292566 G>A polymorphism might be strongly correlated with a higher maintenance dose of warfarin. However, no interaction ofEPHX1rs4653436 A>G polymorphism with warfarin maintenance dosage was detected. A further subgroup analysis based on stratification by ethnicity indicated thatEPHX1rs2292566 G>A polymorphism was positively correlated with warfarin maintenance dosage among Caucasians, but not Asians. No associations were observed betweenEPHX1rs4653436 A>G polymorphism warfarin maintenance dosage among both Caucasians and Asians. Our meta-analysis provides robust and unambiguous evidence thatEPHX1rs2292566 polymorphism may affect the maintenance dose of warfarin in Caucasians.

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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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Dang, Mai-Trang N., Julie Hambleton, and Steven R. Kayser. "The Influence of Ethnicity on Warfarin Dosage Requirement." Annals of Pharmacotherapy 39, no. 6 (June 2005): 1008–12. http://dx.doi.org/10.1345/aph.1e566.

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BACKGROUND: The optimal dose of warfarin varies among individuals, and the prediction of a maintenance dose is difficult. Ethnicity has been reported to influence warfarin dosing. OBJECTIVE: To quantitate the influence of ethnicity on warfarin dose requirement. METHODS: We conducted a retrospective cohort study at a university anticoagulation clinic to evaluate the influence of ethnicity on warfarin dose. Inclusion criteria included age ⩾18 years, target international normalized ratio (INR) 2–3, and warfarin management within the clinic for ⩾3 months with a minimum of 5 clinic visits. We collected clinical and demographic data including age, gender, weight, ethnicity, disease states, concomitant medications, indication, weekly warfarin dosage, and INR. To assess potential confounders, multivariate, repeated-measures regression analysis was used to identify and adjust for variables that may influence the maintenance dose of warfarin. RESULTS: Of the 345 patients who met the inclusion criteria, 27% were Asian American, 6% Hispanic, 54% white, and 14% African American. The adjusted mean (95% CI) weekly warfarin doses for patients with an INR goal of 2 to 3 were Asian Americans 24 mg (21 to 27), Hispanics 31 mg (25 to 37), whites 36 mg (34 to 39), and African Americans 43 mg (39 to 47) (p < 0.001). Additional factors found to influence warfarin dose requirement included age, weight, concomitant use of amiodarone, and diagnosis of venous thromboembolism. CONCLUSIONS: Warfarin dose requirements vary across ethnic groups even when adjusted for confounding factors, suggesting that genetic variation contributes to interpatient variability.

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Müller, C. R., S. Rost, M. Watzka, C. G. Bevans, and J. Oldenburg. "Comparative genetics of warfarin resistance." Hämostaseologie 34, no. 02 (2014): 143–59. http://dx.doi.org/10.5482/hamo-13-09-0047.

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SummaryWarfarin and other 4-hydroxycoumarinbased oral anticoagulants targeting vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1) are administered to humans, mice and rats with different purposes in mind – to act as pesticides in high-dosage baits for killing rodents, but also to save lives when administered in low dosages as antithrombotic drugs in humans. However, high-dosage warfarin used to control rodent populations has resulted in numerous mutations causing warfarin resistance. Currently, six single missense mutations in mice, 12 distinct missense mutations in rats, as well as compound heterozygous or homozygous mutations with up to six distinct missense mutations per Vkorc1 allele have been described. Warfarin resistance missense mutations for human VKORC1 have also been found world-wide, but differ characteristically from those in rodents. In humans, 26 distinct mutations have been characterized, but occur only rarely either in heterozygous or, even rarer, in homozygous form.In this review, we summarize the known VKORC1 missense mutations causing warfarin and other 4-hydroxycoumarin drug resistance, identify genomics databases as new sources of data, explore possible underlying genetic mechanisms, and summarize similarities and differences between warfarin resistant VKORC1 variants in humans and rodents.

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Absher, Randall K., M. Elisabeth Moore, and Mary H. Parker. "Patient-Specific Factors Predictive of Warfarin Dosage Requirements." Annals of Pharmacotherapy 36, no. 10 (October 2002): 1512–17. http://dx.doi.org/10.1345/aph.1c025.

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OBJECTIVE: To identify patient-specific factors predictive of maintenance warfarin dosage requirements >5 mg/d. METHODS: One hundred forty-six adults taking warfarin were identified from a community hospital and an outpatient anticoagulation clinic. Patient demographics and data on warfarin doses, laboratory results, and medication use were obtained by abstracting patient records. Estimates of vitamin K intake were obtained using a questionnaire and structured interview. Multiple logistic regression was used to identify patient characteristics independently predictive of warfarin maintenance requirements >5 mg/d. An assessment tool for estimating an individual patient's likelihood of requiring warfarin maintenance doses >5 mg/d was derived from the logistic regression model and was assessed in both the study cohort and a separate historical validation cohort of 125 patients. RESULTS: Five factors were independently associated with warfarin requirements >5 mg/d: age <55 years, male gender, African American ethnicity, vitamin K intake >400 μg/d, and body weight ≥91 kg. The assessment tool derived from these factors correctly classified semiquantitative warfarin requirements as non—high-dose in 84 of 93 study cohort patients and 71 of 78 validation cohort patients, and correctly classified requirements as high-dose in 10 of 13 study cohort patients and 11 of 15 validation cohort patients. CONCLUSIONS: African American ethnicity is a newly identified predictor of warfarin requirements >5 mg/d and is independent of dietary vitamin K intake. An assessment tool incorporating this and other predictors can estimate a patient's likelihood of requiring such dosages.

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Zhu, Yusheng, Michael Shennan, Kristen K. Reynolds, Nancy A. Johnson, Matthew R. Herrnberger, Roland Valdes, and Mark W. Linder. "Estimation of Warfarin Maintenance Dose Based on VKORC1 (−1639 G>A) and CYP2C9 Genotypes." Clinical Chemistry 53, no. 7 (July 1, 2007): 1199–205. http://dx.doi.org/10.1373/clinchem.2006.078139.

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Abstract Background: CYP2C9 polymorphisms are associated with decreased S-warfarin clearance and lower maintenance dosage. Decreased expression of VKORC1 resulting from the −1639G>A substitution has also been implicated in lower warfarin dose requirements. We investigated the additional contribution of this polymorphism to the variance in warfarin dose. Methods: Sixty-five patients with stable anticoagulation were genotyped for CYP2C9 and VKORC1 with Tag-It™ allele-specific primer extension technology. Plasma S-warfarin concentrations and warfarin maintenance dose were compared among patients on the basis of the VKORC1 −1639G>A genotype. Results: Eighty percent of CYP2C9*1/*1 patients stabilized on <4.0 mg/day warfarin had at least 1 VKORC1 −1639A allele. Mean warfarin doses (SD) were 6.7 (3.3), 4.3 (2.2), and 2.7 (1.2) mg/day for patients with the VKORC1 −1639GG, GA, and AA genotypes, respectively. Steady-state plasma concentrations of S-warfarin were lowest in patients with the VKORC1 −1639AA genotype and demonstrated a positive association with the VKORC1 −1639G allele copy number (trend P = 0.012). A model including VKORC1 and CYP2C9 genotypes, age, sex, and body weight accounted for 61% of the variance in warfarin daily maintenance dose. Conclusions: The VKORC1 −1639A allele accounts for low dosage requirements of most patients without a CYP2C9 variant. Higher plasma S-warfarin concentrations corresponding to increased warfarin maintenance dosages support a hypothesis for increased expression of the VKORC1 −1639G allele. VKORC1 and CYP2C9 genotypes, age, sex, and body weight account for the majority of variance in warfarin dose among our study population.

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Edwards, Clive, Timothy Butler, Hilary Wynne, and Farhad Kamali. "The Influence of (R)- and (S)-Warfarin, Vitamin K and Vitamin K Epoxide upon Warfarin Anticoagulation." Thrombosis and Haemostasis 84, no. 07 (2000): 39–42. http://dx.doi.org/10.1055/s-0037-1613964.

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SummaryThe contribution of (R)and (S)-warfarin enantiomers, vitamin K and vitamin K epoxide and patient factors to inter-individual variability in daily warfarin requirements were examined in a group of 73 patients. Simple correlation analysis showed a significant positive relationship between INR values and plasma (S)-warfarin concentrations (r = 0.25; p = 0.038). Multivariate analysis for relationships with INR demonstrated a highly significant positive relationship between INR and (S)- warfarin (p = 0.004) and plasma vitamin K epoxide concentrations (p = 0.028), and a significant negative relationship between INR and plasma vitamin K concentrations (p = 0.034). Twenty five percent of variation in INR could be explained by these variables (adjusted R2 = 0.25). Correlation analysis of data showed that warfarin dosage was significantly and negatively correlated with patient age (r = −0.42; p <0.0001). Patient age accounted for 25% of variation in warfarin dosage requirements (R2 = 0.25). The combined effects of age and vitamin K appear to account for much of the inter-individual variability in warfarin dosage requirements.

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박선미, 인용원, 이영미, and 민경아. "Proposal for Warfarin Dosage Guideline during Warfarin-Propafenone Combination Therapy." Journal of Korean Society of Health-System Pharmacists 30, no. 1 (February 2013): 52–63. http://dx.doi.org/10.32429/jkshp.2013.30.1.005.

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Li, Shuang, Shixuan Liu, Xiaoran Roger Liu, Mengru Mira Zhang, and Weikai Li. "Competitive tight-binding inhibition of VKORC1 underlies warfarin dosage variation and antidotal efficacy." Blood Advances 4, no. 10 (May 20, 2020): 2202–12. http://dx.doi.org/10.1182/bloodadvances.2020001750.

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Abstract Dose control of warfarin is a major complication in anticoagulation therapy and overdose is reversed by the vitamin K antidote. Improving the dosage management and antidotal efficacy requires mechanistic understanding. Here we find that effects of the major predictor of warfarin dosage, SNP −1639 G>A, follow a general correlation that warfarin 50% inhibitory concentration decreases with cellular level of vitamin K epoxide reductase (VKORC1), suggesting stoichiometric inhibition. Characterization of the inhibition kinetics required the use of microsomal VKORC1 with a native reductant, glutathione, that enables effective warfarin inhibition in vitro. The kinetics data can be fitted with the Morrison equation, giving a nanomolar inhibition constant and demonstrating that warfarin is a tight-binding inhibitor. However, warfarin is released from purified VKORC1-warfarin complex with increasing amount of vitamin K, indicating competitive inhibition. The competition occurs also in cells, resulting in rescued VKORC1 activity that augments the antidotal effects of vitamin K. Taken together, warfarin is a competitive inhibitor that binds VKORC1 tightly and inhibits at a stoichiometric (1:1) concentration, whereas exceeding the VKORC1 level results in warfarin overdose. Thus, warfarin dosage control should use VKORC1 level as a major indicator, and improved antidotes may be designed based on their competition with warfarin.

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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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Trilli, Lauren E., Catherine L. Kelley, Sherrie L. Aspinall, and Beverly A. Kroner. "Potential Interaction between Warfarin and Fluvastatin." Annals of Pharmacotherapy 30, no. 12 (December 1996): 1399–402. http://dx.doi.org/10.1177/106002809603001207.

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OBJECTIVE: To report three cases of a suspected interaction between warfarin and fluvastatin. CASE SUMMARIES: Three patients receiving stable warfarin dosages with therapeutic international normalized ratios (INRs) exhibited increased INRs when fluvastatin was added to their maintenance regimens. While none of the patients experienced a bleeding episode, they did require a reduction in their weekly warfarin dosage to achieve an appropriate level of anticoagulation. DISCUSSION: Reports of an interaction between warfarin and lovastatin have been described previously; however, to our knowledge, this is the first published report of a possible interaction between warfarin and fluvastatin. These cases were chosen because other factors that could potentially increase the INR were ruled out as significant contributors. CONCLUSIONS: The exact mechanism for the potential interaction between warfarin and fluvastatin is unknown. Until more is known, it is advisable to monitor patients more frequently when fluvastatin is initiated, discontinued, or adjusted in patients taking warfarin.

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Murphey, Lisa M., and Elizabeth H. Hood. "Bosentan and Warfarin Interaction." Annals of Pharmacotherapy 37, no. 7-8 (July 2003): 1028–31. http://dx.doi.org/10.1345/aph.1c398.

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OBJECTIVE: To report a case of decreased international normalized ratio (INR) in a patient receiving warfarin and bosentan. CASE SUMMARY: A 35-year-old African American woman with a history of primary pulmonary hypertension managed with warfarin, diltiazem, and hydrochlorothiazide was initiated on bosentan therapy. The patient's INR had been stable and within therapeutic range (goal 2.0–3.0) for the previous 3 months with warfarin 27.5 mg/wk, but became subtherapeutic after 10 days of bosentan therapy. Addition of over-the-counter medications, herbal products, vitamins, or dietary changes was denied. The INR remained subtherapeutic for 5 weeks despite weekly warfarin dose increases. After these 5 weeks of dosage increases, the INR became supratherapeutic for 3 weeks, resulting in a subsequent dosage decrease. The resultant warfarin dose required to maintain a therapeutic INR was 45 mg/wk, a 63.6% dosage increase after the initiation of bosentan. DISCUSSION: This case shows that a clinically significant interaction between bosentan and warfarin may exist. An objective causality assessment revealed that the interaction was probable. Although the possibility of this interaction has been noted, no previously documented occurrence of this interaction has been identified. CONCLUSIONS: Bosentan may significantly decrease the anticoagulant properties of warfarin. The INR should be monitored more frequently when bosentan is initiated, adjusted, or discontinued in patients taking warfarin.

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Dalere, Gloriann M., Robert W. Coleman, and Bert L. Lum. "A Graphic Nomogram for Warfarin Dosage Adjustment." Pharmacotherapy 19, no. 4 (April 1999): 461–67. http://dx.doi.org/10.1592/phco.19.6.461.31038.

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Cheng, Tsung O. "Chinese patients require lower dosage of warfarin." International Journal of Cardiology 139, no. 1 (February 2010): 1. http://dx.doi.org/10.1016/j.ijcard.2009.06.056.

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Streif, W., M. Andrew, V. Marzinotto, P. Massicotte, A. K. C. Chan, J. A. Julian, and L. Mitchell. "Analysis of Warfarin Therapy in Pediatric Patients: A Prospective Cohort Study of 319 Patients." Blood 94, no. 9 (November 1, 1999): 3007–14. http://dx.doi.org/10.1182/blood.v94.9.3007.

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Abstract This study details warfarin use in a large pediatric population followed in a central anticoagulation clinic. A prospective, consecutive cohort of nonselected children were studied. Patients were divided into groups by age, target international normalized ratio (INR) range, disease, medications, and vitamin K supplemented enteral nutrition use. Groups were analyzed on multiple aspects of warfarin therapy using multivariate methods. A total of 319 patients received 352 warfarin courses representing 391 treatment years. Age independently influenced all aspects of therapy. When compared with all older children, the ≤1 year of age group required increased warfarin doses, longer overlap with heparin, longer time to achieve target INR ranges, more frequent INR testing and dose adjustments, and fewer INR values in the target range. Although significantly different than children ≤1 year, children 1 to 6 years of age showed the same findings when compared with 7- to 18-year-olds. Fontan patients required 25% decreased dosage as compared with other congenital heart disease patients. Children on corticosteroids had less INRs in the target range and children on phenobarbital/carbamazepine required increased maintenance dosages of warfarin. Also, patients receiving enteral nutrition required increased dosages of warfarin. Serious bleeding occurred in 2 children (0.5% per patient year). Recurrent thromboembolic events (TEs) occurred in 8 children. Two children had recurrences while receiving warfarin (1.3% per patient year). This study outlines the profound effect of age and relative complexity of clinical management of warfarin therapy in children.

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Streif, W., M. Andrew, V. Marzinotto, P. Massicotte, A. K. C. Chan, J. A. Julian, and L. Mitchell. "Analysis of Warfarin Therapy in Pediatric Patients: A Prospective Cohort Study of 319 Patients." Blood 94, no. 9 (November 1, 1999): 3007–14. http://dx.doi.org/10.1182/blood.v94.9.3007.421k09_3007_3014.

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This study details warfarin use in a large pediatric population followed in a central anticoagulation clinic. A prospective, consecutive cohort of nonselected children were studied. Patients were divided into groups by age, target international normalized ratio (INR) range, disease, medications, and vitamin K supplemented enteral nutrition use. Groups were analyzed on multiple aspects of warfarin therapy using multivariate methods. A total of 319 patients received 352 warfarin courses representing 391 treatment years. Age independently influenced all aspects of therapy. When compared with all older children, the ≤1 year of age group required increased warfarin doses, longer overlap with heparin, longer time to achieve target INR ranges, more frequent INR testing and dose adjustments, and fewer INR values in the target range. Although significantly different than children ≤1 year, children 1 to 6 years of age showed the same findings when compared with 7- to 18-year-olds. Fontan patients required 25% decreased dosage as compared with other congenital heart disease patients. Children on corticosteroids had less INRs in the target range and children on phenobarbital/carbamazepine required increased maintenance dosages of warfarin. Also, patients receiving enteral nutrition required increased dosages of warfarin. Serious bleeding occurred in 2 children (0.5% per patient year). Recurrent thromboembolic events (TEs) occurred in 8 children. Two children had recurrences while receiving warfarin (1.3% per patient year). This study outlines the profound effect of age and relative complexity of clinical management of warfarin therapy in children.

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Zhao, Li, Jin Wang, Shaoxin Shi, Yuan Wu, Jumei Liu, Shiwei He, Yue Zou, Huabin Xie, Shengxiang Ge, and Huiming Ye. "Plasma miRNA profiles associated with stable warfarin dosage in Chinese patients." PeerJ 8 (October 13, 2020): e9995. http://dx.doi.org/10.7717/peerj.9995.

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Background We used bioinformatic analysis and quantitative reverse transcription polymerase chain reaction (RT-qPCR) assays to investigate the association between plasma microRNAs (miRNAs) and stable warfarin dosage in a Chinese Han population. Methods Bioinformatics analysis was used to screen out potential warfarin dose-associated miRNAs. Three plasma miRNAs were validated in 99 samples by RT-qPCR. Kruskal–Wallis test and multivariate logistic regression were used to compare differences in plasma miRNAs expression levels between three warfarin dosage groups. Results There were significant between-group differences among the three dose groups for hsa-miR-133b expression (p = 0.005), but we observed an “n-shaped” dose-dependent curve rather than a linear relationship. Expression levels of hsa-miR-24-3p (p = 0.475) and hsa-miR-1276 (p = 0.558) were not significantly different in the multivariate logistic regression. Conclusion miRNAs have received extensive attention as ideal biomarkers and possible therapeutic targets for various diseases. However, they are not yet widely used in precision medicine. Our results indicate that hsa-miR-133b may be a possible reference factor for the warfarin dosage algorithm. These findings emphasize the importance of a comprehensive evaluation of complex relationships in warfarin dose prediction models and provide new avenues for future pharmacogenomics studies.

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Jackevicius, Cynthia A., and Mannhu N. Ton. "Enhanced Interaction between Warfarin and High-Dose Ketoconazole: A Case Report." Case Reports in Medicine 2009 (2009): 1–3. http://dx.doi.org/10.1155/2009/315687.

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This case describes the increased anticoagulation effect associated with the use of high-dose ketoconazole. A 59-year-old man treated with warfarin for aortic valve replacement was prescribed high-dose ketoconazole and hydrocortisone for the treatment of prostate cancer. Despite lowering the warfarin dosage by 35% during the start of high dose ketoconazole, an additional dose reduction was required subsequently when the INR rose from 2.62 to 3.82 within nine days. After a total dose reduction of 43%, the INR returned to therapeutic range within two weeks. The Naranjo probability scale revealed a probable adverse reaction of increased anticoagulant effect associated with high dose ketoconazole. Due to the inhibition of warfarin metabolism by ketoconazole, patients taking high dose ketoconazole concomitantly with warfarin may need their warfarin dosage reduced by more than is currently recommended, as well as receive more frequent INR monitoring to avoid over anticoagulation.

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Mason, Barb J. "Anticoagulant Clinic Warfarin Adherence Rates and Assessment." Journal of Pharmacy Technology 12, no. 3 (May 1996): 97–101. http://dx.doi.org/10.1177/875512259601200307.

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Objective: To identify warfarin medication-taking patterns and the relationship between adherence and international normalized ratio (INR). Design: Two-month, single-blind, observational cohort. Setting: Veterans Affairs Medical Center ambulatory care clinics. Patients: Twenty-three veteran outpatients followed in a nurse-managed anticoagulation clinic were enrolled by consecutive sample. Patients were excluded if they used a medication reminder device, were scheduled to have warfarin discontinued within the next 2 months, or had been receiving warfarin less than 1 month. Twenty patients were evaluable. Intervention: All study patients received warfarin in a vial with an electronic medication-event monitoring system (MEMS) device. Patients were not told that adherence was being monitored. Main Outcome Measure: Mean and preclinic warfarin adherence, dosage changes, and INR values were tabulated. Results: Thirty-five percent of the patients were nonadherent with warfarin therapy. Mean and preclinic warfarin adherence rates were 86% and 90%, respectively. Medication-taking behavior was underestimated in 75% of patients. Dosage changes were more common in nonadherent patients. There was not a significant correlation between INR and adherence. Conclusions: MEMS adherence data could have changed pharmacologic management in select patients.

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최슬기, kieho sohn, 인용원, 민경아, and 전명훈. "Proposal for Warfarin Dosage Guideline during Capecitabine Therapy." Journal of Korean Society of Health-System Pharmacists 27, no. 3 (September 2010): 293–304. http://dx.doi.org/10.32429/jkshp.2010.27.3.003.

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Carter, Barry L., William Barr, William Rock, and Jerry W. Taylor. "Warfarin Dosage Predictions Assisted by the Analog Computer." Therapeutic Drug Monitoring 10, no. 1 (March 1988): 69–73. http://dx.doi.org/10.1097/00007691-198801000-00012.

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Carter, Barry L., William Barr, William Rock, and Jerry W. Taylor. "Warfarin Dosage Predictions Assisted by the Analog Computer." Therapeutic Drug Monitoring 10, no. 1 (1988): 69–73. http://dx.doi.org/10.1097/00007691-198810010-00012.

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Hirsh, J. "Inadequate monitoring of warfarin dosage [letter] [see comments]." Blood 80, no. 2 (July 15, 1992): 562–63. http://dx.doi.org/10.1182/blood.v80.2.562.562.

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Hirsh, J. "Inadequate monitoring of warfarin dosage [letter] [see comments]." Blood 80, no. 2 (July 15, 1992): 562–63. http://dx.doi.org/10.1182/blood.v80.2.562.bloodjournal802562.

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Chen, Jin-Jer. "S28-4 WARFARIN DOSAGE REQUIREMENT BASED ON PHARMACOGENETICS." International Journal of Cardiology 122 (December 2007): S23. http://dx.doi.org/10.1016/s0167-5273(08)70381-4.

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Saleh, Mohammad I., and Sameh Alzubiedi. "Dosage Individualization of Warfarin Using Artificial Neural Networks." Molecular Diagnosis & Therapy 18, no. 3 (February 27, 2014): 371–79. http://dx.doi.org/10.1007/s40291-014-0090-7.

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Li, Siyue, Yuangao Zou, Xia Wang, Xunbei Huang, Yong Sun, Yuqing Wang, Li Dong, and Hong Jiang. "Warfarin Dosage Response Related Pharmacogenetics in Chinese Population." PLOS ONE 10, no. 1 (January 16, 2015): e0116463. http://dx.doi.org/10.1371/journal.pone.0116463.

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Lastória, Sidnei, Arcangelo T. Fortes Jr, Francisco H. Abreu Maffei, Marcone Lima Sobreira, Hamilton A. Rollo, Regina Moura, and Winston Bonetti Yoshida. "Comparison of initial loading doses of 5 mg and 10 mg for warfarin therapy." Jornal Vascular Brasileiro 13, no. 1 (March 2014): 12–17. http://dx.doi.org/10.1590/jvb.2014.004.

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CONTEXT: The question of what is the best loading dosage of warfarin when starting anticoagulant treatment has been under discussion for ten years. We were unable to find any comparative studies of these characteristics conducted here in Brazil. OBJECTIVE: To compare the safety and efficacy of two initial warfarin dosage regimens for anticoagulant treatment. METHODS: One-hundred and ten consecutive patients of both sexes, with indications for anticoagulation because of venous or arterial thromboembolism, were analyzed prospectively. During the first 3 days of treatment, these patients were given adequate heparin to keep aPTT (activated partial thromboplastin time) between 1.5 and 2.5, plus 5 mg of warfarin. From the fourth day onwards, their warfarin doses were adjusted using International Normalized Ratios (INR; target range: 2 to 3). This prospective cohort was compared with a historical series of 110 patients had been given 10 mg of warfarin on the first 2 days and 5 mg on the third day with adjustments based on INR thereafter. Outcomes analyzed were as follows: recurrence of thromboembolism, bleeding events and time taken to enter the therapeutic range. RESULTS: Efficacy, safety and length of hospital stay were similar in both samples. The sample that were given 10 mg entered the therapeutic range earlier (means: 4.5 days vs. 5.8 days), were on lower doses at discharge and had better therapeutic indicators at the first return appointment. CONCLUSIONS: The 10 mg dosage regimen took less time to attain the therapeutic range and was associated with lower warfarin doses at discharge and better INR at first out-patients follow-up visit.

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Tian, Lihong, Pingping Xiao, Bingrong Zhou, Yishan Chen, Lijuan Kang, Qingqing Wang, Jianfeng Lin, Min Son, and Qingxiu Wu. "Influence of NQO1 Polymorphisms on Warfarin Maintenance Dose: A Systematic Review and Meta-Analysis (rs1800566 and rs10517)." Cardiovascular Therapeutics 2021 (August 12, 2021): 1–9. http://dx.doi.org/10.1155/2021/5534946.

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This meta-analysis was conducted to analyze the effect of NQO1 polymorphism on the warfarin maintenance dosage. Using strict inclusion and exclusion criteria, we searched PubMed, EMBASE, and the Cochrane Library for eligible studies published prior to July 7, 2021. The required data were extracted, and experts were consulted when necessary. Review Manager Version 5.4 software was used to analyze the relationship between NQO1 polymorphisms and the warfarin maintenance dosage. Four articles involving 757 patients were included in the meta-analysis. Patients who were NQO1 rs10517 G carriers (AG carriers or GG carriers) required a 48% higher warfarin maintenance dose than those who were AA carriers. Patients with NQO1 rs1800566 CT carriers required a 13% higher warfarin dose than those who were CC carriers, with no associations observed with the other comparisons of the NQO1 rs1800566 genotypes. However, the results obtained by comparing the NQO1 rs1800566 genotypes require confirmation, as significant changes in the results were found in sensitivity analyses. Our meta-analysis suggests that the NQO1 rs10517and NQO1 rs1800566 variant statuses affect the required warfarin maintenance dose.

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Yoshida, Winston Bonetti, Regina Paolucci El Dib, Ricardo de Alvarenga Yoshida, and Francisco Humberto de Abreu Maffei. "Ximelagatran versus warfarin for prophylaxis of venous thromboembolism in major orthopedic surgery: systematic review of randomized controlled trials." Sao Paulo Medical Journal 124, no. 6 (November 2006): 355–61. http://dx.doi.org/10.1590/s1516-31802006000600012.

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BACKGROUND: Ximelagatran has been recently studied for prophylaxis in surgical orthopedic cases. PURPOSE: We proposed to establish whether interventions involving ximelagatran, as compared with warfarin, would increase thromboembolic prophylaxis in patients undergoing major orthopedic knee surgery. DATA SOURCE: Studies with random assignment were identified by an electronic search of the medical literature up to 2006. Data were double-entered into the Review Manager software, version 4.2.5. DATA SYNTHESIS: We included three well-conducted clinical trials involving 4,914 participants. Sub-groups with two dosages of ximelagatran (24 mg and 36 mg, b.i.d.), were defined. Ximelagatran showed significantly lower frequency of total venous thromboembolism (VTE) than warfarin, but only with the 36-mg dosage (risk relative, RR: 0.72; 95% confidence interval, CI: 0.64-0.81; p < 0.00001). For the 24-mg subgroup, total VTE frequency was similar (RR: 0.86; 95% CI: 0.73-1.01; p = 0.06). No significant differences were shown with either ximelagatran dosage for deep vein thrombosis (DVT), pulmonary embolism, any bleeding or severe bleeding. At the end of the treatment, alanine aminotransferase (ALT) elevation was less frequent in the 24-mg ximelagatran sub-group (RR: 0.33; 95% CI: 0.12-0.91; p = 0.03], but during the follow-up period, the ALT elevation rate was greater in the 36-mg ximelagatran group (RR: 6.97; 95% CI: 1.26-38.50; p = 0.03]. CONCLUSIONS: Ximelagatran appears to be more effective than warfarin when used in higher dosages (36 mg b.i.d.), but at the expense of increased frequency of ALT elevation during the follow-up period.

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He, Shiwei, Yuan Wu, Shuidi Yan, Jumei Liu, Li Zhao, Huabin Xie, Shengxiang Ge, and Huiming Ye. "Methylation of CYP1A1 and VKORC1 promoter associated with stable dosage of warfarin in Chinese patients." PeerJ 9 (June 22, 2021): e11549. http://dx.doi.org/10.7717/peerj.11549.

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Objective To investigate the association between DNA methylation and the stable warfarin dose through genome-wide DNA methylation analysis and pyrosequencing assay. Method This study included 161 patients and genome-wide DNA methylation analysis was used to screen potential warfarin dose-associated CpGs through Illumina Infinium HumanMethylation 450 K BeadChip; then, the pyrosequencing assay was used to further validate the association between the stable warfarin dose and alterations in the methylation of the screened CpGs. GenomeStudio Software and R were used to analyze the differentially methylated CpGs. Results The methylation levels of CpGs surrounding the xenobiotic response element (XRE) within the CYP1A1 promoter, differed significantly between the different dose groups (P < 0.05), and these CpGs presented a positive correlation (r> 0, P < 0.05) with an increase in the stable dose of warfarin. At the VKORC1 promoter, two CpGs methylation levels were significantly different between the differential dose groups (P < 0.05), and one CpG (Chr16: 31106793) presented a significant negative correlation (r < 0, P < 0.05) among different dose (low, medium, and high) groups. Conclusion This is a novel report of the methylation levels of six CpGs surrounding the XRE within the CYP1A1 promoter and one differential CpG at the VKORC1 promoter associated with stable warfarin dosage; these methylation levels might be applied as molecular signatures for warfarin.

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Soma-Pillay, P., Z. Nene, T. M. Mathivha, and A. P. Macdonald. "The effect of warfarin dosage on maternal and fetal outcomes in pregnant women with prosthetic heart valves." Obstetric Medicine 4, no. 1 (March 2011): 24–27. http://dx.doi.org/10.1258/om.2010.100067.

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There are several challenges in the management of pregnant women with mechanical heart valves. Pregnancy increases the risk of thromboembolism and there is currently no consensus on the safest anticoagulation method during pregnancy. The objective of the study was to determine the correlation between the warfarin dose and pregnancy outcome in pregnant women with prosthetic heart valves. Warfarin in pregnancy was associated with a low risk of valve thrombosis or maternal death. The risk for fetal abnormalities was not related to the maternal warfarin dosage. However, the risk for stillbirth was significantly increased with increasing doses of warfarin.

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Shen, Guomin, Hao Zhang, Weidong Cui, Evan Sadler, Michael Gross, and Weikai Li. "Warfarin Inhibits Vitamin K Epoxide Reductase By Specifically Blocking at a Conformational and Redox State." Blood 124, no. 21 (December 6, 2014): 4214. http://dx.doi.org/10.1182/blood.v124.21.4214.4214.

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Abstract Warfarin targets vitamin K epoxide reductase (VKOR) to interfere with blood coagulation in humans. Warfarin is the most widely used oral anticoagulant, but its inhibition mechanism remains largely unknown. Here we use quantitative mass spectrometry to show that warfarin changes the intracellular redox state of human VKOR. Warfarin induces this redox shift at a physiological dosage that correlates well with warfarin-inhibited VKOR activity. The warfarin-induced redox change is prevented by the mutation of two critical cysteines, suggesting that they form a disulfide bond essential for warfarin binding. We also mapped warfarin binding through its interaction with warfarin resistant mutations located at different structural regions of human VKOR. Modeling of these interactions suggests how warfarin binds to a VKOR conformation that is stabilized by the essential disulfide bond. Thus, after sixty years of clinical use of warfarin, we now have a good mechanistic understanding that this drug blocks human VKOR at a specific conformational and redox state. Disclosures No relevant conflicts of interest to declare.

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Parrett, J. L., A. B. Reaves, T. H. Self, and R. E. Owens. "Enzalutamide‐warfarin interaction necessitating warfarin dosage adjustment: A case report of successful clinical management." Journal of Clinical Pharmacy and Therapeutics 43, no. 2 (September 12, 2017): 276–79. http://dx.doi.org/10.1111/jcpt.12612.

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Zotova, I. V., A. G. Nikitin, E. N. Fattakhova, A. N. Brovkin, D. S. Khodyrev, E. Y. Lavrikova, M. Y. Isaeva, A. S. Kosukhina, V. V. Nosikov, and D. A. Zateyshchikov. "THE AFFECT OF INFLUENCE OF GENES' POLYMORPHISMS CYP2C9 AND VKORC1ON THE SAFETY OF THE THERAPY BY WARFARIN." Journal of Clinical Practice 4, no. 4 (December 15, 2013): 3–10. http://dx.doi.org/10.17816/clinpract443-10.

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To study the distribution of alleles and genotypes of polymorphic markers of genes CYP2C9 and VKORC1 of Russian patients who live in Moscow, and in order to assess the influence of genetic factors on warfarin therapy 400 patients have been genotyped. The dosage of warfarin which is required for achievement of INR target values has been different among owners of different geno- types of polymorphic markers of genes CYP2C9 . Meanwhile the highest average dose has been required for genotype *1/*1 and the lowest – for owners of alleles *2 and *3 . For polymorphism G(- 1639)A of the gene VKORC1 the dosage of warfarin which is required for achievement of the INR target values, has been different among owners of different genotypes. The highest average dose has been required for genotype GG, and the lowest – for genotype AA. The results will allow to work out more accurate algorithm of choosing of the initial dose of warfarin depending on the genotypes of polymorphic markers of genes CYP2C9 and VKORC1.

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Burkova, T. V., and I. A. Goncharova. "GENETIC FACTORS INFLUENCING THE EFFECTIVENESS AND SAFETY OF LONG-TERM ANTICOAGULANT THERAPY." Cardiovascular Therapy and Prevention 12, no. 3 (June 20, 2013): 89–94. http://dx.doi.org/10.15829/1728-8800-2013-3-89-94.

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Late postoperative thrombotic and haemorrhagic complications in anticoagulant-treated patients remain one of the key problems of the modern clinical medicine. At present, the most widely used anticoagulant is warfarin, a vitamin K antagonist. One of the reasons for a pathological reaction to the therapeutic concentration of warfarin could be individual features of warfarin metabolism, determined by relevant genes. The literature data suggest that protein-coding CYP2C9 and VKORC1 genes play an important role in the development of postoperative complications. However, the individual warfarin dosage can be influenced by a wide range of other genetic polymorphisms.

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John, Sumi Elsa, Dinu Antony, Muthukrishnan Eaaswarkhanth, Prashantha Hebbar, Fadi Alkayal, Jaakko Tuomilehto, Osama Alsmadi, and Thangavel Alphonse Thanaraj. "Genetic variants associated with warfarin dosage in Kuwaiti population." Pharmacogenomics 18, no. 8 (June 2017): 757–64. http://dx.doi.org/10.2217/pgs-2017-0020.

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Lindh, Jonatan D. "Comment: Patient-Specific Factors Predictive of Warfarin Dosage Requirements." Annals of Pharmacotherapy 37, no. 3 (March 2003): 454. http://dx.doi.org/10.1345/aph.1c025a.

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REDWOOD, M., CLARE TAYLOR, BARBARA J. BAIN, and J. H. MATTHEWS. "The Association of Age with Dosage Requirement for Warfarin." Age and Ageing 20, no. 3 (1991): 217–20. http://dx.doi.org/10.1093/ageing/20.3.217.

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Brooks, Cath, Jane M. Rutherford, Jane Gould, Margaret M. Ramsay, and David K. James. "Warfarin dosage in postpartum women: a case-control study." BJOG: An International Journal of Obstetrics and Gynaecology 109, no. 2 (February 2002): 187–90. http://dx.doi.org/10.1111/j.1471-0528.2002.00490.x.

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Brooks, C. "Warfarin dosage in postpartum women: a case–control study." BJOG: An International Journal of Obstetrics and Gynaecology 109, no. 2 (February 2002): 187–90. http://dx.doi.org/10.1016/s1470-0328(02)00490-1.

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Dimberg, Ivar, Bartosz Grzymala-Lubanski, Anette Hägerfelth, Mårten Rosenqvist, Peter Svensson, and Anders Själander. "Computerised assistance for warfarin dosage — Effects on treatment quality." European Journal of Internal Medicine 23, no. 8 (December 2012): 742–44. http://dx.doi.org/10.1016/j.ejim.2012.07.011.

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Brooks, Cath, Jane M. Rutherford, Jane Gould, Margaret M. Ramsay, and David K. James. "Warfarin Dosage in Postpartum Women: A Case-Control Study." Obstetrical & Gynecological Survey 57, no. 8 (August 2002): 491–92. http://dx.doi.org/10.1097/00006254-200208000-00007.

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Rumyantsev, N. A., D. A. Sychev, V. G. Kukes, R. E. Kazakov, A. A. Rumyantsev, and T. V. Taratuta. "Experience of individualization of oral anticoagulants use and dosage in personalized medicine centre conditions." Kazan medical journal 96, no. 6 (December 15, 2015): 1065–68. http://dx.doi.org/10.17750/kmj2015-1065.

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The application of pharmacogenetic testing was analyzed in patients treated at the center of personalized medicine, in order to analyze gene polymorphism frequency - response predictors to indirect anticoagulants therapy, estimation of the warfarin dose selection time, the hospitalization duration. The presence of VKORC1 and CYP2C9 polymorphisms or homozygous polymorphisms combinations is quite common in the Russian population: CYP2C9*2 polymorphism (15.3%) was observed in 8 patients, CYP2C9*3 (9.6%) in 5 patients. VKORC1 gene A allele was detected in 18 patients, accounting for 34.6% of the whole group. In patients with this polymorphism warfarin administration according to the traditional algorithm often leads to excessive anticoagulation and bleeding. Initiation of warfarin therapy according to the scheme taking into account genotyping significantly increases the treatment safety and reduces the adverse events incidence in this group of patients.

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Davis, David A., and Susan E. Fugate. "Increasing Warfarin Dosage Reductions Associated with Concurrent Warfarin and Repeated Cycles of 5-Fluorouracil Therapy." Pharmacotherapy 25, no. 3 (March 2005): 442–47. http://dx.doi.org/10.1592/phco.25.3.442.61598.

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Piovella, Franco, Marisa Barone, Chiara Beltrametti, Chiara Piovella, Andrea M. D’Armini, Federico Capra Marzani, Vittorio Arici, et al. "Efficacy of Fondaparinux in the Treatment of Heparin-Induced Thrombocytopenia with Venous Thromboembolism: Reduction of Thromboembolic Burden, Normalization of Platelet Count and Disappearance of Anti-Platelet Factor 4/Heparin Antibodies." Blood 108, no. 11 (November 16, 2006): 575. http://dx.doi.org/10.1182/blood.v108.11.575.575.

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Abstract Heparin-induced thrombocytopenia (HIT) and heparin-induced thrombocytopenia with thrombosis (HITT) may develop during anticoagulant treatment in patients submitted to various regimens of unfractionated or low-molecular weight heparins. Several molecules have been studied as alternative anticoagulants in patients with HIT or HITT, including danaparoid, argatroban, lepirudin. Lepirudin requires dosage adjustments in patients with renal insufficiency and has potential for antibody formation. Argatroban requires dosage adjustments in patients with hepatic insufficiency. Argatroban increases the International Normalized Ratio (INR) when co-administered with warfarin, leading to dosage difficulties when transitioning to warfarin therapy. Anticoagulation of patients with HIT or HITT may be limited by antibodies cross-reactivity with danaparoid and by new generation of antibodies with lepirudin. Fondaparinux is the first of a new class of synthetic antithrombotics: the selective inhibitors of coagulation factor Xa. It is the most advanced competitor of low molecular weight heparins, which are the reference drugs in prophylaxis and treatment of venous thromboembolism. Fondaparinux does not bind to platelet factor 4 (PF4) and does not react with anti-PF4/heparin antibodies in in vitro testing. We treated 20 patients who develop HIT (3 patients) or HITT (17 patients, of whom 4 had both DVT and PE). Nine patients were previously submitted to extracorporeal circulation with unfractionated heparin (UFH) followed by low-molecular weight heparin (LMWH) for major cardiac surgery. The remaining patients had been previously treated with either UHF or LMWH at therapeutic or prophylactic dosage in internal medicine or surgery wards. In the 17 patients who developed HITT, we applied therapeutic dosages of fondaparinux, i.e. 7.5 mg QD or lower, accordingly with their bleeding risk. To the remaining patients with HIT we gave prophylactic dosages of fondaparinux, i.e. 2.5 mg QD. Patients with HITT were treated for 4 to 25 days before starting warfarin. Fondaparinux was stopped when INR of 2.0 or more was reached. All patients showed a significant reduction of their thromboembolic burden. One episode of major bleeding was recorded in a post-surgical patient. All patients but one showed sustained normalization of the platelet number. In the remaining patient platelet count remained unchanged. Treatment was switched from fondaparinux to lepirudin and after few days her platelets reverted to close-to-normal levels. In seven patients, submitted to therapeutic dosages of fondaparinux, anti-PF4/heparin antibody titers were determined using a PF4/heparin enzyme-linked immunosorbent assay (ELISA): in all cases antibody levels progressively decreased close to disappearance by 30–45 days. This series of cases provides further evidence for the safety and efficacy of fondaparinux in the treatment of both HIT or HITT.

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Diener, H. C., and S. H. Hohnloser. "Dabigatran for stroke prevention in atrial fibrillation." Hämostaseologie 32, no. 03 (2012): 216–20. http://dx.doi.org/10.5482/ha-1196.

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SummaryDabigatran is a novel direct thrombin inhibitor that has recently been approved for primary and secondary stroke prevention and prevention of systemic embolism in patients with atrial fibrillation. In the pivotal RE-LY study, dabigatran 110 mg BID was demonstrated to be associated with a stroke rate similar to that observed with warfarin (INR target 2.0 to 3.0), but with a lower rate of major haemorrhage. Dabigatran administered at a dose of 150 mg BID was significantly more effective in stroke prevention than warfarin and showed a similar rate of major hemorrhages. Of note, both dosages resulted in an approximately 60–70% relative risk reduction of haemorrhagic stroke. The dosage of 110 mg BID should be preferably used in patients aged 75–80 years or older as the rate of extracranial bleeding events tends to increase with dabigatran 150 mg BID above this age limit. In RE-LY, myocardial infarcts occurred at a very low incidence. There were numerically more myocardial infarcts in dabigatran-treated patients than in warfarin patients; however, other myocardial ischaemic events were similar in the three treatment arms.

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Journal articles on the topic 'Warfarin dosage'

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