Carefully monitor PT and INR in patients receiving romidepsin and warfarin concomitantly. Colestipol can bind with vitamin K in the diet, impairing vitamin K absorption, which, in turn, may increase warfarin's hypoprothrombinemic effect. Consider discontinuation of anticoagulants in a patient taking inotersen with a platelet count of less than 50,000 per microliter. The S-enantiomer of warfarin exhibits 2 to 5 times more anticoagulant activity than the R-enantiomer, but the R-enantiomer generally has a slower clearance. However, these dosing regimens have not been validated in randomized clinical trials. Alterations in vitamin K intake influence the response to warfarin. Mean prothrombin times decreased slightly, but only for the first few days of treatment. Clinically important bleeding of this type, however, is relatively rare. Increased INR may occur and the risk of bleeding may be potentiated. The patient involved had familial antithrombin deficiency and was stabilized on warfarin as her only medication. You must declare any conflicts of interest related to your comments and responses. Intramuscular injections of other drugs should be avoided if possible in patients receiving warfarin. Close monitoring of the INR and clinical status of the patient may be prudent if echinacea is used with warfarin until more data are available. Adjust warfarin dosage based on INR and clinical response. Darunavir is a CYP3A4 inhibitor and the R-enantiomer of warfarin is a 3A4 substrate. Physiological changes resulting from smoking cessation, with or without treatment with bupropion, may alter the pharmacokinetics or pharmacodynamics of certain drugs (e.g.,warfarin) for which dosage adjustment may be necessary. (For patients with liver dysfunction, severe renal impairment, post-surgical or coagulopathic reduce this to 0.1mg/kg to a maximum of 5mg, or delay initiation). Per prescribing information for warfarin sodium (Coumadin), however, all HMG-CoA reductase inhibitors (statins), including atorvastatin, have been associated with potentiation of warfarin's clinical effect. Consider alternate therapy for aspirin for analgesic or antipyretic uses. Methohexital: (Moderate) Closely monitor the INR if coadministration of warfarin with barbiturates is necessary as concurrent use may decrease the exposure of warfarin leading to reduced efficacy. The S-enantiomer of warfarin exhibits 2 to 5 times more anticoagulant activity than the R-enantiomer, but the R-enantiomer generally has a slower clearance. Denileukin Diftitox: (Moderate) An additive risk of bleeding may be seen in thrombocytopenic patients receiving antineoplastic agents in combination with anticoagulants. Concomitant administration of zileuton and warfarin resulted in a 15% decrease in the clearance of R-warfarin but no change in the clearance of the more potent S-isomer. After stabilization of his warfarin dose for 3 weeks, fenofibrate was restarted, and the patient was rechallenged on 2 occasions. The INR decreased once the patient decreased her dose of fish oil to 1 gram/day. Systemic hematological effects may also occur with the use of topical NSAIDs. If carbamazepine is discontinued, dosage reductions of warfarin may be necessary. Toremifene is a weak CYP2C9 inhibitor and the S-enantiomer, the active metabolite of warfarin, is a CYP2C9 substrate. Bempedoic Acid; Ezetimibe: (Moderate) Coadministration with ezetimibe has not demonstrated significant effects on the bioavailability or the anticoagulant effects of warfarin when studied in 12 healthy adult males. Patients should be monitored for changes in the INR when either of these drugs is initiated or discontinued, or if the dosage is changed. Dosage adjustments of warfarin may be necessary within 2 weeks of beginning barbiturate treatment, but the effect of the barbiturate on warfarin metabolism may persist for more than a month after discontinuing the barbiturate. Concurrent use may increase the INR and the risk of bleeding. The impact of Echinacea on the safety and efficacy of warfarin therapy are unknown, but studies suggest an interaction is possible. Single doses or short (i.e., several days) courses of treatment with acetaminophen are probably safe in most patients taking warfarin. Cisapride: (Moderate) Data indicate that administration of cisapride to patients receiving oral anticoagulants (e.g., warfarin) may cause a prolongation in the prothrombin time and increase the INR. Medical products that contain soybean oil such as intravenous lipid emulsions or propofol, may decrease warfarin anticoagulation. The S-enantiomer of warfarin exhibits 2 to 5 times more anticoagulant activity than the R-enantiomer, but the R-enantiomer generally has a slower clearance. It is prudent to monitor the INR and response to warfarin prior to azathioprine initiation, frequently following initiation of azathioprine therapy, and again on azathioprine cessation. The S-enantiomer of warfarin exhibits 2 to 5 times more anticoagulant activity than the R-enantiomer, but the R-enantiomer generally has a slower clearance. Gastrointestinal irritation and impaired hemostasis secondary to platelet inhibition have been observed with relatively small doses of aspirin. Fluvastatin is a weak CYP2C9 inhibitor and the S-enantiomer, the active metabolite of warfarin, is a CYP2C9 substrate. Discontinuation of a barbiturate during warfarin therapy has led to fatal bleeding episodes when the hepatic enzyme-inducing properties of the barbiturate subside.