WARNING: BLEEDING RISK
-
Warfarin sodium can cause major or fatal bleeding [see Warnings and Precautions].
-
Perform regular monitoring of INR in all treated patients [see Dosage and Administration].
-
Drugs, dietary changes, and other factors affect INR levels achieved with warfarin sodium therapy [see Drug Interactions].
-
Instruct patients about prevention measures to minimize risk of bleeding and to report signs and symptoms of bleeding [see Patient Counseling Information].
|
|
WARFARIN SUMMARY
Warfarin sodium is an anticoagulant that acts by inhibiting vitamin K-dependent coagulation factors.
Warfarin sodium tablets,USP are indicated for:
- Prophylaxis and treatment of venous thrombosis and its extension, pulmonary embolism (PE).
- Prophylaxis and treatment of thromboembolic complications associated with atrial fibrillation (AF) and/or cardiac valve replacement.
- Reduction in the risk of death, recurrent myocardial infarction (MI), and thromboembolic events such as stroke or systemic embolization after myocardial infarction.
Limitations of Use
Warfarin sodium tablets, USP have no direct effect on an established thrombus, nor does it reverse ischemic tissue damage. Once a thrombus has occurred, however, the goals of anticoagulant treatment are to prevent further extension of the formed clot and to prevent secondary thromboembolic complications that may result in serious and possibly fatal sequelae.
|
|
NEWS HIGHLIGHTSMedia Articles Related to Warfarin
Genotyping Lowers Warfarin Risk in Hip or Knee Replacement Source: Medscape Anesthesiology Headlines [2017.09.26] Considering variants of three genes that affect response to warfarin improved the safety of using the drug. Medscape Medical News
Published Studies Related to Warfarin
Genetics and the clinical response to warfarin and edoxaban: findings from the
randomised, double-blind ENGAGE AF-TIMI 48 trial. [2015] anticoagulant rather than warfarin... INTERPRETATION: CYP2C9 and VKORC1 genotypes identify patients who are more likely
Relationship between time in therapeutic range and comparative treatment effect
of rivaroxaban and warfarin: results from the ROCKET AF trial. [2014] CONCLUSIONS: The treatment effect of rivaroxaban compared with warfarin for the
Outcomes of temporary interruption of rivaroxaban compared with warfarin in
patients with nonvalvular atrial fibrillation: results from the rivaroxaban once
daily, oral, direct factor Xa inhibition compared with vitamin K antagonism for
prevention of stroke and embolism trial in atrial fibrillation (ROCKET AF). [2014] CONCLUSIONS: TI of oral anticoagulation is common and is associated with
Efficacy and safety of rivaroxaban compared with warfarin in patients with
peripheral artery disease and non-valvular atrial fibrillation: insights from
ROCKET AF. [2014] CONCLUSION: Patients with PAD in ROCKET AF did not have a statistically
Apixaban vs. warfarin with concomitant aspirin in patients with atrial
fibrillation: insights from the ARISTOTLE trial. [2014] CONCLUSION: Apixaban had similar beneficial effects on stroke or systemic
Clinical Trials Related to Warfarin
Warfarin Adverse Event Reduction For Adults Receiving Genetic Testing at Therapy INitiation (WARFARIN) [Recruiting]
The WARFARIN Study is a clinical trial designed to determine if the use of genetic
information related to warfarin sensitivity can help create a dose of warfarin that will
result in less hospitalizations and deaths related to warfarin.
Drug Interaction Study of Isavuconazole and Warfarin in Healthy Male Subjects [Completed]
The purpose of this study is to assess the effect of multiple doses of isavuconazole on the
pharmacokinetics (PK) of warfarin after single dose administration.
Applying Pharmacogenetic Algorithms to Individualize Dosing of Warfarin [Completed]
The purpose of this study is to determine whether DNA analysis improves the efficiency of
dosing and safety in patients who are being started on warfarin therapy. Warfarin, a blood
thinner (anticoagulant) prescribed to 1-2 million patients in the United States, is a
leading cause of drug-related adverse events (e. g., severe bleeding), in large part due to
dramatic (20-fold) differences between individuals in dose requirements. At least half of
this variability now can be explained by 3 common genetic variants, age, body size, and sex;
however, warfarin therapy continues to begin with the same dose in every patient with the
correct individual dose determined by trial and error. This study proposes to determine
genetic variations the same day from DNA simply obtained by swabbing the inside of the cheek
and use this information to determine the proper dose regimen individually in each patient.
The aim is to show that the investigators can achieve more rapid, efficient, and safe dosing
in up to 500-1000 individuals who are initiating warfarin therapy for various clotting
disorders across a large healthcare system in order to demonstrate improved dosing
effectiveness, efficiency, and safety with genetic-based dosing, which could lead to a
nationwide application resulting in as much as a $1 billion dollar annual benefit in
healthcare outcomes.
Pharmacogenetics of Warfarin Induction and Inhibition [Completed]
This research study will help determine how a person's genetic makeup affects their response
to drugs, the ability of the body to break down drugs, and their potential to experience an
interaction between drugs. The investigators are investigating the drug interactions with
the commonly used anticoagulant drug called warfarin. Warfarin is used for the treatment and
prevention of life-threatening abnormal blood clots such as deep vein thrombosis, heart
attacks, and strokes. The investigators chose warfarin for this study because it is a
commonly used drug and must be monitored closely to avoid side effects. The investigators
are interested in studying whether individuals with certain genetic profiles react
differently to warfarin when it is combined with other drugs. This research is being done to
see if certain genetic profiles require us to adjust warfarin doses differently than is
needed for the general population. Genetic profiles of subjects are determined from their
participation in the Pharmacogenetics Registry study (investigator Richard Brundage,
University of Minnesota).
The study hypothesis is: Functionally defective CYP2C9 alleles attenuate the
warfarin-fluconazole inhibitory interaction and exacerbate the warfarin-rifampin inductive
interaction.
Genetic Response to Warfarin in Healthy Subjects [Completed]
The purpose of this study is to determine the importance of genetic differences on
individuals' response to warfarin in a group of healthy subjects. Warfarin is also known by
the "trade name" Coumadin and is in a class of medications called anticoagulants or "blood
thinners." Warfarin works by reducing the blood's ability to make clots. It is used to
stop blood clots from forming or growing larger in your blood and blood vessels. Warfarin
is prescribed for many conditions, including for people with certain types of irregular
heartbeat, people with replacement or mechanical heart valves, people who have suffered a
heart attack, people who have had orthopedic surgery, or who have a history of having blood
clots. Warfarin is used to prevent or treat deep vein thrombosis (swelling and blood clot
in a vein), pulmonary embolism (a blood clot in the lung), and strokes (a blood clot in the
brain). Researchers have found that certain genes may affect how a person's body will break
down or react to warfarin. If genetic information can help doctors better determine the
best dose of warfarin before it is first given, this may help the doctors get patients to
the correct levels of blood thinning and thereby reduce the risk of bleeding or the risk of
developing a blood clot. The expectation of this study is that this information will
ultimately improve warfarin therapy while lessening the risks associated with dosing errors.
This study is considered investigational because the subjects are healthy and not being
prescribed warfarin for clinical care.
Reports of Suspected Warfarin Side Effects
International Normalised Ratio Increased (9),
Drug Interaction (6),
Drug Ineffective (2),
Skin Exfoliation (2),
Pyrexia (2),
Completed Suicide (2),
Hallucination (2),
Toxicity TO Various Agents (2),
Renal Impairment (2),
Diarrhoea (2), more >>
|
PATIENT REVIEWS / RATINGS / COMMENTSBased on a total of 1 ratings/reviews, Warfarin has an overall score of 6. The effectiveness score is 8 and the side effect score is 6. The scores are on ten point scale: 10 - best, 1 - worst.
| Warfarin review by 44 year old female patient | | Rating |
Overall rating: | |           |
Effectiveness: | | Considerably Effective |
Side effects: | | Moderate Side Effects | | Treatment Info |
Condition / reason: | | heart condition |
Dosage & duration: | | 3 mg. warfarin taken 1 time daily for the period of 3 years |
Other conditions: | | none |
Other drugs taken: | | none | | Reported Results |
Benefits: | | Taking 3 mg of warfarin sufficiently thinned my blood so that I did not find it difficult to do everyday tasks. I immediately felt better after I started the regimen in the spring of 2003. My cough went away and I had a lot more energy.
I took this regimen for about 3 years, everyday. I also found it easier to concentrate and think (what was I doing before it???) It was as if my brain cleared up or something. I breathed easier and I was more willing to tackle regular household chores. I worked over 50 hours/week before and during this treatment. |
Side effects: | | The side effects of warfarin on me did not become apparent until a couple of years later. I started feeling weak and I bruised easily. I acquired more broken blood vessels/capillaries veins in my feet and calves. I was tired and started feeling cranky. I stopped taking warfarin for 6 months but then went back to it after I had the old feeling of "thick" blood. During the 6 months that I wasn't taking warfarin, I felt better, had more energy. But then the downside: my blood was getting too thick and I was starting to get headaches. So I went back on it. This time my doctor said I might have to increase dosage to 4 mg. since I hadn't been taking the warfarin. However, when I had my thrombin checked, I was okay at 3 mg.; I took this for another 3 months and then started feeling the old way and quit again. The same scenario was repeated (started feeling like I had "thick" blood and now I had increasingly bad headaches). I went back on 3 mg. of warfarin in August of this year but only took them for 3 months. Then I started a vitamin/mineral/COQ10 regimen and stuck with it and am still doing that. I credit most of the perfect blood feeling (for lack of a better term) to Vitamin E and the fact that I also changed my diet. I try to eat a lot of veggies and fruits, and I have been a vegetarian for almost two years (not super strict - but I feel disgusted about eating meat and therefore never eat it unless it is buried in some food. I do eat salmon and tuna. The final straw for me with warfarin was that I started feeling really mad about things. The littlest things would make me angry, anger that was way out of proportion to the incident. When my teenaged daughter started crying after I ripped into her for staying longer at a social visit, and I heard my words echoing in my house, I knew that was it. I quit warfarin and started taking 81 mg. of aspirin daily (I had a headache every morning after I went off warfarin). I started the vit./min. regimen in November, gradually adding supplements as I learned about their benefits, but it wasn't until 3-4 weeks ago that I realized I wasn't having any headaches and I was able to stop taking 81 mg. of aspirin. Also, since starting the stricter diet and the vit./min. supplements (also some herbs), I have not had an anger "fit" (of course, I am also more prone to control my anger because I really didn't like how I had been), I do not feel depressed. I have told everyone in my family about this because it seems so remarkable. Why didn't the doctors tell me? |
Comments: | | Treatment consisted of simply taking 3 mg. of warfarin daily and getting my blood thrombin checked every two months. I was not a very good patient about getting my blood thr. checked so I'm sure when I was feeling weak and bruised/bled so easily, my blood was getting too thin. And then when I would quit the warfarin for several weeks, sometimes months at a time, my blood would get too thick. I really like my doctor though, because he tells me to do what makes me feel best, and I think that's smart advice. I must say add that I always loved the feeling of donating blood before I took warfarin because it gave me the same feeling as I initially had with warfarin (at the very beginning of my treatment). I would like to donate blood now but they don't let me because I don't weigh enough (which makes no sense at all). Couldn't they take less blood? Who determined how much blood you can give anyway? |
|
|
Page last updated: 2017-09-26
|