In most instances, the interacting drugs either inhibit or induce warfarin metabolism. These types of interactions are easily managed when the medications are for the treatment of chronic diseases. In such circumstances, close INR monitoring is required during the initiation or discontinuation of the medications. Advise patient to limit total acetaminophen dosage to less than 2 g per day; if higher dosages are used, increased monitoring may be necessary. Decreases warfarin metabolism within a week of coadministration; effect may persist for 1 to 3 months after discontinuation of amiodarone May induce hypothyroidism or hyperthyroidism.
A 25 percent reduction in the warfarin dosage is recommended when amiodarone is initiated. Monitor INR closely when amiodarone is added or withdrawn. Fluconazole Diflucan , ketoconazole Nizoral and miconazole Monistat decrease warfarin metabolism. Hyperthyroidism results in metabolism of vitamin K clotting factors and increased sensitivity to oral anticoagulants.
Increase warfarin metabolism and frequently reduce hypoprothrombinemic effect of warfarin. Monitor INR when barbiturates are added or withdrawn; the addition of warfarin in patients stabilized on a chronic barbiturate regimen is of less significance. Use colestipol Colestid , which has a lower potential for interaction, instead of cholestyramine Questran in patients who need a bile sequestrant. Increase warfarin doses when carbamazepine is added, and reduce doses when carbamazepine is discontinued stabilization occurs after 4 to 6 weeks.
Methylthiotetrazole ring in cefoperazone Cefobid , cefamandole Mandol , cefotetan Cefotan and cefmetazole Zefazone inhibits production of vitamin K—dependent clotting factors. Avoid concomitant use of warfarin and cefoperazone, cefamandole, cefotetan or cefmetazole. May increase clotting factor synthesis May inhibit oxidative metabolism. If possible, avoid oral contraceptives because of increased risk of thromboembolism Monitor INR frequently when oral contraceptives are used concurrently with warfarin.
Displaces warfarin from protein binding, inhibits platelet aggregation, causes gastric erosions. Acute ethanol use may inhibit anticoagulant metabolism. Chronic ethanol use induces liver enzymes.
Cirrhosis is associated with reduced warfarin metabolism. Caution patients to drink in moderation and to avoid binge drinking.
Because liver damage results in greater sensitivity to warfarin, use lower starting doses. Note that lovastatin Mevacor is more commonly associated with hypoprothrombinemia. Displaces warfarin from protein-binding sites Inhibits warfarin metabolism. Avoid concomitant administration of warfarin and nalidixic acid.
Monitor INR if concomitant use is necessary. Inhibit platelet aggregation Cause gastric erosions. Consider having patients take misoprostol Cytotec to reduce risk of gastric erosions. Dicloxacillin Pathocil and nafcillin Unipen may enhance warfarin metabolism. Inhibit platelet aggregation Cause gastric erosions In large doses, result in hypoprothrombinemic effect. If aspirin is needed, advise patients to use a small dosage mg or less per day.
If possible, avoid concurrent use of warfarin and trimethoprim-sulfamethoxazole. Interaction is probably dose-related and more likely to occur with vitamin E dosages greater than U per day; monitor INR if larger dosages are taken.
Effects of oral anticoagulants are directly antagonized by the excessive ingestion of foods or dietary supplements containing vitamin K. Advise patients to eat a consistent diet and to avoid taking large doses of vitamin supplements containing a great deal of vitamin K.
In: Pharmacotherapy self assessment program module 1 cardiovascular. Kansas City, Mo. Retrieved September from the World Wide Web at http:www. Additional information derived from Warfarin.
In: Drugdex. Englewood, Colo. Often, the interacting drugs that pose the greatest problem are those used for short-term indications. Antibiotics are a common example. When interactions occur, close monitoring or the use of alternative antimicrobial agents is appropriate. Warfarin is more likely to be used safely by a patient who is aware of the potential for drug interactions, understands the rationale for monitoring and can identify the symptoms of warfarin toxicity early.
Patient instruction booklets in English and other languages are available from several sources. Most local pharmacies supply similar information to patients.
When used appropriately, warfarin is a highly effective and safe medication. To maximize the safety of warfarin therapy, the physician should do the following: Identify the therapeutic goal. Estimate the chronic maintenance dosage based on the presence of factors associated with hyperresponsiveness or hyporesponsiveness, such as concomitant drug use, liver disease and poor nutrition.
Initiate therapy at the patient's anticipated maintenance dosage. Loading doses are not necessary. Make any necessary adjustments by looking at the cumulative weekly dosage and adding or subtracting 10 to 20 percent evenly over the week. Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. He also serves as clinical assistant professor at the University of Maryland School of Pharmacy, Baltimore. Horton graduated from the University of Pittsburgh School of Pharmacy and earned his doctor of pharmacy degree from Duquesne University, Pittsburgh.
Bushwick graduated from the University of Maryland School of Medicine, Baltimore, and completed a family practice residency at York Hospital. Address correspondence to Jon D. Horton, Pharm. George St. Reprints are not available from the authors. Establishing an outpatient anticoagulation clinic in a community hospital. Am J Health Syst Pharm ;—7. Oral anticoagulants: mechanism of action, clinical effectiveness, and optimal therapeutic range.
Chest ; 4 Suppl S—46S. National prescription audit: physician specialty report, dispensed data. Plymouth Meeting, Pa. Retail perspective and provider perspective audit.
Agency for Health Care Policy and Research. Life-saving treatments to prevent stroke underused. Press release, September Antithrombotic therapy in patients with mechanical and biologic prosthetic heart valves. Antithrombotic therapy in valvular heart disease. The duration of oral anticoagulant therapy after a second episode of venous thromboembolism. N Engl J Med. Antithrombotic therapy in atrial fibrillation. Optimal duration of oral anticoagulant therapy: a randomized trial comparing four weeks with three months of warfarin in patients with proximal deep vein thrombosis.
Thromb Haemost. Anticoagulant thrombolytic, and antiplatelet drugs. New York: McGraw-Hill, — Applied pharmacokinetics. Spokane, Wash. Comparison of 5-mg and mg loading doses in initiation of warfarin therapy. Ann Intern Med. Aging and the anticoagulant response to warfarin therapy.
Monitoring effects of oral anticoagulants during treatment with heparin. Br Med J [Clin Res]. Comment While provocative, these findings leave important questions unanswered.
Citation s : Azoulay L et al. October 18, Chief of Internal Medicine Medical Director. Beverly, Massachusetts. Cambridge, Massachusetts. Physician Geriatric Primary Care. Lewistown, Pennsylvania. Lip GY, et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation.
Douketis JD, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. Connolly SJ, et al. J Am Coll Cardiol. Friberg L, et al. Although the development of DVT after giving a higher loading dose in our patient could be a pure coincidence, we felt that the temporal relationship between the onset of the DVT timed with the increase in the warfarin loading dose is compelling.
Also, the paucity of obvious clinical risk factors for a hypercoagulable state increased our suspicion. This case study illustrates the importance of considering DVT as a possible complication of unopposed warfarin therapy. Warfarin-induced skin necrosis is a well-established adverse event of a warfarin loading dose.
This case is the first ever reported case of a possible iatrogenic warfarin-induced DVT. It highlighted the importance of adhering to the lower loading doses specified in protocols. Understanding the pharmacokinetics and pharmacodynamics of warfarin would help ensure safe and effective prescription of the drug. A high index of suspicion may allow for the rapid reversal of the warfarin effect with therapeutic heparinization before the processes of adverse procoagulation begin.
National Center for Biotechnology Information , U. Int Med Case Rep J. Published online Sep 9. Author information Copyright and License information Disclaimer.
Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. This article has been cited by other articles in PMC. Abstract We are presenting a year-old female who was admitted to hospital with deep vein thrombosis DVT. Keywords: warfarin, deep vein thrombosis, slow-start regimen, protein C, protein S, warfarin-induced skin necrosis, stroke prophylaxis.
Video abstract Download video file. Case report A year-old female was admitted to hospital with deep vein thrombosis DVT. Open in a separate window.
0コメント