Ifosfamide and etoposide chemotherapy may interact with warfarin, enhancing the warfarininduced anticoagulant response

2016 ◽  
Vol 54 (01) ◽  
pp. 58-61 ◽  
Author(s):  
Naoto Okada ◽  
Hiroyoshi Watanabe ◽  
Shoji Kagami ◽  
Keisuke Ishizawa
Keyword(s):  
Anticoagulant Response

Predicting the Dose of Warfarin for Therapeutic Anticoagulation

1982 ◽  
Vol 47 (03) ◽  
pp. 230-231 ◽  
Author(s):  
N K Sharma ◽  
P A Routledge ◽  
M D Rawlins ◽  
D M Davies
Keyword(s):  
Therapeutic Range ◽  
Significant Relationship ◽  
Maintenance Dose ◽  
Warfarin Dose ◽  
Loading Dose ◽  
Intravenous Injections ◽  
Therapeutic Anticoagulation ◽  
Close Relationship ◽  
The Relationship ◽  
Anticoagulant Response

SummaryThe validity of a previously described technique for predicting warfarin requirements based on the anticoagulant response to a fixed loading dose was assessed prospectively in 57 patients. There was a close relationship between the predicted and initially observed daily warfarin dose required to maintain the patient within the therapeutic range for anticoagulation. The significant relationship between predicted and observed maintenance dose persisted at 4 and 12 weeks although it decreased with increasing time.The relationship between observed and predicted maintenance requirement of warfarin was not affected by the concomitant use of intermittent intravenous injections of heparin when 9 hr was allowed to elapse between the previous dose of heparin and the thrombotest estimation on which the prediction was based.It is concluded that the method is valuable in predicting an individual’s warfarin requirement, although it does not obviate the need for regular monitoring of anticoagulant control.

scholarly journals Dietary vitamin K influences intra-individual variability in anticoagulant response to warfarin

2004 ◽  
Vol 124 (3) ◽  
pp. 348-354 ◽  
Author(s):  
T. Khan ◽  
H. Wynne ◽  
P. Wood ◽  
A. Torrance ◽  
C. Hankey ◽  
...  
Keyword(s):  
Vitamin K ◽  
Individual Variability ◽  
Dietary Vitamin ◽  
Anticoagulant Response

Decreased anticoagulant response to tissue factor pathway inhibitor in patients with venous thromboembolism and otherwise no evidence of hereditary or acquired thrombophilia

2004 ◽  
Vol 91 (01) ◽  
pp. 80-86 ◽  
Author(s):  
Brigitte Piccapietra ◽  
Johanna Boersma ◽  
Joerg Fehr ◽  
Thomas Bombeli
Keyword(s):  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Mean Value ◽  
Healthy Controls ◽  
Crude Odds Ratio ◽  
Sensitivity Ratio ◽  
Increased Risk ◽  
History Of ◽  
Anticoagulant Response ◽  
Acquired Thrombophilia

SummaryNo relevant deficiency of TFPI or genetic polymorphisms could thus far consistently be associated with venous thromboembolism. We hypothesized that the substrates of the TFPI protein, including FVII or FX (rather than the protein itself) could induce a hypercoagulable state. We created a novel TF-based clotting assay that evaluated the anticoagulant response to exogenously added recombinant TFPI. The response to TFPI was expressed as the ratio of the clotting time with and without TFPI. By using 118 healthy controls, we established a reference range between 1.31 and 1.93 (mean value ± 2 standard deviations (SD), 1.62 ± 0.31). We then evaluated samples from 120 patients with a history of venous thromboembolism but no evidence of hereditary and acquired thrombophilia. The range of the patients’ ratios was significantly (P < 0.001) lower, falling between 1.2 and 1.78 (mean value ± 2 SD, 1.49 ± 0.29). Of the 120 patients, 39 (32.5%) had a TFPI sensitivity ratio below the 10th percentile of the controls, compared with 11 (9.3%) of the healthy controls. The crude odds ratio for venous thrombosis for subjects with a TFPI sensitivity ratio below the 10th percentile was 13 (95% CI; range, 3.1 to 54.9) compared with those with a ratio above 1.8 (90th percentile). Patients with idiopathic thromboembolism did not have a decreased TFPI sensitivity ratio more often than patients with thrombosis with a circumstantial risk factor. Based on these results, a reduced response to TFPI may lead to an increased risk of venous thrombosis.

Fenofibrate Potentiates Warfarin Effects

2003 ◽  
Vol 37 (2) ◽  
pp. 212-215 ◽  
Author(s):  
Karissa Y Kim ◽  
Michael A Mancano
Keyword(s):  
White Woman ◽  
Chart Review ◽  
Warfarin Therapy ◽  
Dosage Reduction ◽  
International Normalized Ratio ◽  
Drug Regimen ◽  
Warfarin Dosage ◽  
Therapeutic Doses ◽  
Anticoagulant Response

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.

The Effect of Furosemide and Bumetanide on Warfarin Metabolism and Anticoagulant Response

1978 ◽  
Vol 18 (2-3) ◽  
pp. 91-94 ◽  
Author(s):  
CLAES M. NILSSON ◽  
EDWARD S. HORTON ◽  
DONALD S. ROBINSON
Keyword(s):  
Anticoagulant Response

scholarly journals New Oral Anticoagulants in the Treatment of Pulmonary Embolism: Efficacy, Bleeding Risk, and Monitoring

Thrombosis ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Kelly M. Rudd ◽  
Elizabeth (Lisa) M. Phillips
Keyword(s):  
Pulmonary Embolism ◽  
Oral Anticoagulants ◽  
Anticoagulation Therapy ◽  
Bleeding Risk ◽  
Vitamin K Antagonist ◽  
New Oral Anticoagulants ◽  
Antagonist Therapy ◽  
Advantages And Disadvantages ◽  
Significant Interest ◽  
Anticoagulant Response

Anticoagulation therapy is mandatory in patients with pulmonary embolism to prevent significant morbidity and mortality. The mainstay of therapy has been vitamin-K antagonist therapy bridged with parenteral anticoagulants. The recent approval of new oral anticoagulants (NOACs: apixaban, dabigatran, and rivaroxaban) has generated significant interest in their role in managing venous thromboembolism, especially pulmonary embolism due to their improved pharmacokinetic and pharmacodynamic profiles, predictable anticoagulant response, and lack of required efficacy monitoring. This paper addresses the available literature, on-going clinical trials, highlights critical points, and discusses potential advantages and disadvantages of the new oral anticoagulants in patients with pulmonary embolism.

Anticoagulant response to activated protein c: Method validation and assay comparison

1995 ◽  
Vol 9 (6) ◽  
pp. 418-423
Author(s):  
Tom Calkins ◽  
Judy Greengard ◽  
John H. Griffin ◽  
David Bylund
Keyword(s):  
Method Validation ◽  
Protein C ◽  
Activated Protein C ◽  
Anticoagulant Response

Enhancement of the anticoagulant response to warfarin in mercuric chloride-treated rats

1978 ◽  
Vol 2 (2) ◽  
pp. 85-89 ◽  
Author(s):  
Marc Baril ◽  
Saroj K. Chakrabarti ◽  
Jules Brodeur
Keyword(s):  
Mercuric Chloride ◽  
Anticoagulant Response
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