Lab result explainedBlood count (CBC)Last updated November 10, 2026

PT/INR blood test: normal range, what a high or low INR means, and warfarin targets

Prothrombin time and INR (PT/INR) · Coagulation panel (PT/INR, often with PTT) · reported in PT in seconds; INR as a ratio with no units (some reports also give PT as a percentage of normal, "prothrombin activity")

Prothrombin time (PT) measures how many seconds it takes your blood plasma to clot after a clotting trigger (tissue factor and calcium) is added; the INR (international normalized ratio) is the same result converted to a standardised scale so that values from different laboratories and reagents can be compared. If you are not taking a blood thinner, a normal PT is about 11 to 13.5 seconds and a normal INR is 0.8 to 1.1 (some labs accept up to 1.2). The test checks the clotting factors made by the liver that depend on vitamin K (factors II, VII, IX and X) plus factors V and fibrinogen, which is why it is used for three different jobs: monitoring warfarin, assessing liver function, and investigating bleeding or bruising.

For people on warfarin (Coumadin, Jantoven), the INR is the number that sets the dose. The usual target is 2.0 to 3.0 for atrial fibrillation, deep vein thrombosis and pulmonary embolism, and 2.5 to 3.5 for a mechanical mitral valve or a mechanical valve with extra risk factors. Below the target the drug is not preventing clots; above it the bleeding risk climbs, gently up to about 4.0 and then steeply, so an INR above 4.5 to 5 needs a same-day call to whoever manages your warfarin, and an INR above 9 or any bleeding is an emergency. The newer anticoagulants (apixaban, rivaroxaban, dabigatran, edoxaban) do not need INR monitoring and distort the PT unpredictably, so an INR on these drugs is not interpretable in the usual way.

If you are not on warfarin and your INR is high, the most likely explanations are liver disease (the liver makes the clotting factors; INR is part of the MELD score used to grade cirrhosis), vitamin K deficiency from poor intake, malabsorption or a long antibiotic course, a medication effect, or, acutely, disseminated intravascular coagulation in a very ill person. A mildly low INR (0.8 to 0.9) with no blood thinner is not a disease and does not mean your blood is "too thick"; it is simply the bottom of the normal range.

PT/INR at a glance

What it is: PT is the clotting time in seconds through the extrinsic and common pathways (factors VII, X, V, II and fibrinogen); INR is PT standardised across laboratories.
Normal (no blood thinner): PT about 11–13.5 seconds; INR 0.8–1.1 (up to 1.2 on some reports). Labs differ in the PT seconds but the INR is comparable everywhere.
On warfarin: target INR 2.0–3.0 for most conditions; 2.5–3.5 for mechanical mitral valves or high-risk mechanical valves. Below 2.0 under-protected; 3.0–4.5 modestly over; above 4.5–5 call the same day; above 9–10 or any bleeding is an emergency.
High INR not on warfarin: liver disease, vitamin K deficiency (poor diet, malabsorption, antibiotics, newborns), DIC, inherited factor VII deficiency, some medications, or a sample problem (underfilled tube, very high hematocrit).
Low INR on warfarin: missed doses, more vitamin K in the diet, an interacting drug or supplement (rifampin, carbamazepine, St John's wort), or an absorption problem; raises clot risk.
Next step on warfarin: dose adjustment and a repeat INR within days; off warfarin: liver tests, a PTT, and sometimes a vitamin K trial or clotting factor levels.

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What PT/INR measures

Clotting proceeds through a cascade of enzymes that ends with thrombin converting fibrinogen into a fibrin mesh. The PT tests the branch started by tissue factor: the laboratory adds thromboplastin (tissue factor plus phospholipid) and calcium to your citrated plasma and times the clot. The result depends on factor VII, which has the shortest half-life of all the factors (about 6 hours), then X, V, II (prothrombin) and fibrinogen. Factors II, VII, IX and X all require vitamin K to become active, which is why warfarin, a vitamin K antagonist, prolongs the PT, and why factor VII's short half-life makes the PT the first test to move when the liver falters or vitamin K runs short.

Different thromboplastin reagents have different sensitivities, so the same plasma can clot in 13 seconds in one lab and 15 in another. To fix this, each reagent is assigned an International Sensitivity Index (ISI) against a WHO standard, and the INR is calculated as (patient PT ÷ mean normal PT) raised to the power ISI. An INR of 2.5 therefore means the same degree of anticoagulation wherever it is measured. The INR was designed for warfarin monitoring; it is also used in liver disease, although it is less well standardised there because the deficiency pattern differs.

The sample is drawn into a light-blue-top tube containing citrate, which must be filled to the line: an underfilled tube or a hematocrit above 55 percent leaves too much citrate for the plasma and falsely prolongs the PT. Heparin contamination from a line, a delay of more than 24 hours before testing and clotted samples also produce spurious results. The PT is not affected by food, though vitamin K intake over the preceding days affects the true result in people on warfarin; the test does not need fasting. Point-of-care fingerstick INR meters used in anticoagulation clinics and at home agree with laboratory INR to within about 0.3 to 0.5 units in the 2 to 4 range and are less reliable above that.

Normal range for PT/INR

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (PT in seconds; INR as a ratio with no units (some reports also give PT as a percentage of normal, "prothrombin activity"))	Notes
Not on anticoagulants, PT	About 11–13.5 seconds	Depends on the reagent; some labs 10–14. Use the printed range.
Not on anticoagulants, INR	0.8–1.1 (up to 1.2 on some reports)	Comparable between laboratories.
Warfarin, standard target	INR 2.0–3.0	Atrial fibrillation, DVT, pulmonary embolism, most bioprosthetic valves, bileaflet mechanical aortic valve without risk factors.
Warfarin, higher target	INR 2.5–3.5	Mechanical mitral valve, older mechanical valve designs, mechanical valve with atrial fibrillation or previous clot.
Warfarin, mildly supratherapeutic	INR 3.1–4.5	Bleeding risk modestly raised; usually managed by holding or reducing a dose and rechecking in a few days.
Warfarin, high	INR 4.5–9 without bleeding	Same-day call; doses held, sometimes a small oral dose of vitamin K, repeat INR within 1 to 2 days. Risk of major bleeding rises steeply above 4.5.
Warfarin, very high	INR above 9–10, or any INR with significant bleeding	Emergency: oral or intravenous vitamin K; for serious bleeding, prothrombin complex concentrate or plasma.
Liver disease	INR 1.2–1.5 mild impairment; above 1.5 significant; above 2.0 with other features suggests liver failure	An INR of 1.5 or more is one of the defining features of acute liver failure; INR contributes to the MELD score for transplant priority.
Newborns	PT slightly longer than adults for the first days	Vitamin K stores are low at birth, which is why the vitamin K injection is given.

High PT/INR (blood clots more slowly)

On warfarin, a high INR means the dose is currently too strong for you. Common reasons are a new interacting medicine (antibiotics such as trimethoprim-sulfamethoxazole, metronidazole and fluoroquinolones; fluconazole; amiodarone), a stretch of illness or poor eating that cut vitamin K intake, diarrhea, a bout of heavy drinking, a change in thyroid status or a dosing error. The bleeding risk rises slowly up to an INR of about 4.0 and then steeply: in a classic cohort, the risk of intracranial hemorrhage roughly doubled for each unit of INR above 4, and patients with an INR above 6 who were not treated had a meaningful risk of major bleeding over the following two weeks. That is why 4.5 to 5 is the usual "call today" line and 9 to 10 the "treat now" line even without symptoms.

Off warfarin, a prolonged PT with a normal PTT points to factor VII, which is the first to fall in early liver disease and vitamin K deficiency. The liver makes all the relevant factors, so in cirrhosis, hepatitis and acute liver failure the INR tracks how much synthetic function is left; an INR above 1.5 with jaundice and confusion defines acute liver failure. Vitamin K deficiency arises from poor intake (prolonged illness, eating disorders, alcohol dependence), fat malabsorption (celiac disease, cystic fibrosis, bile duct obstruction, bariatric surgery) and broad-spectrum antibiotics that wipe out gut bacteria; a dose of vitamin K that corrects the INR within 24 to 48 hours confirms the diagnosis and distinguishes it from liver disease, which does not correct.

A high INR with a high PTT and low platelets and fibrinogen in someone who is very ill suggests disseminated intravascular coagulation, which accompanies sepsis, major trauma, obstetric emergencies and some cancers. Isolated inherited factor VII deficiency is rare, as is a lupus anticoagulant strong enough to prolong the PT. The direct oral anticoagulants prolong the PT to a variable and unreliable degree (rivaroxaban and edoxaban more, apixaban barely at all), so an INR of 1.4 on apixaban says little about how anticoagulated you are.

Common causes

Warfarin dose too high for current circumstances
Interacting drugs, reduced vitamin K intake during illness, diarrhea, alcohol binges, worsening heart failure or liver congestion, hyperthyroidism and dosing errors all push the INR up; the INR responds over 2 to 5 days because factor half-lives range from 6 to 72 hours.
Drug interactions with warfarin
Trimethoprim-sulfamethoxazole, metronidazole, ciprofloxacin, fluconazole, amiodarone, many statins at high dose, tramadol, acetaminophen above 2 g a day for several days, and some chemotherapy raise the INR; most anticoagulation clinics ask to be told before any new prescription.
Liver disease
Cirrhosis, alcoholic and viral hepatitis, fatty liver with advanced fibrosis and acute liver failure reduce factor synthesis; the INR rises in proportion to the loss of function and is part of the MELD and Child-Pugh scores.
Vitamin K deficiency
Poor intake, fat malabsorption (celiac disease, Crohn's disease, cystic fibrosis, bile duct obstruction, bariatric surgery), prolonged broad-spectrum antibiotics and newborns who did not receive vitamin K; corrects within 1 to 2 days of vitamin K.
Direct oral anticoagulants
Rivaroxaban and edoxaban prolong the PT noticeably, apixaban slightly, dabigatran mainly the PTT; none is monitored by INR and the result should not be used to adjust these drugs.
Disseminated intravascular coagulation
Sepsis, major trauma, placental abruption, acute leukemia and snake envenomation consume clotting factors and platelets; PT, PTT and D-dimer rise while fibrinogen and platelets fall.
Inherited or acquired factor deficiency
Factor VII deficiency prolongs only the PT; deficiencies of factors X, V, II or fibrinogen prolong both PT and PTT. Acquired inhibitors and amyloidosis (factor X) are rare causes.
Massive transfusion or dilution
Large-volume fluid or red cell replacement after major bleeding dilutes clotting factors; plasma is given to correct it.
Sample and laboratory artefact
Underfilled citrate tube, hematocrit above 55 percent, heparin contamination from a line, delayed processing or a clotted sample each falsely prolong the PT; a repeat on a properly collected sample resolves it.

Symptoms that can go with it

Often none, particularly in the 3 to 5 range on warfarin
Easy bruising, bleeding gums when brushing, nosebleeds that take longer than 10 minutes to stop
Blood in urine (pink or red), black tarry stools or visible blood in stools, vomiting blood or coffee-ground material
Heavier or longer menstrual periods
Prolonged bleeding from cuts, or large bruises after minor knocks
Severe headache, sudden weakness, confusion or vision change on an anticoagulant, which can mean bleeding in the brain and is an emergency
Jaundice, swollen abdomen, confusion or spider-like skin vessels when liver disease is the cause

Low PT/INR (blood clots faster than target)

If you are not taking an anticoagulant, an INR at or just below the bottom of the range (0.8 to 0.9, or a PT of 10 to 11 seconds) is normal and has no clinical meaning. The PT is not a test for a tendency to clot; people with high clotting risk (from factor V Leiden, antiphospholipid syndrome, cancer or immobility) have a normal PT. A short PT can occasionally reflect a high factor VII or fibrinogen level, oral estrogen, or a sample that was activated during a difficult draw, none of which needs treatment.

On warfarin, a low INR means you are below your target and not fully protected against clots. In atrial fibrillation the stroke risk at an INR below 2.0 is roughly double that in the 2.0 to 3.0 range, and strokes that occur at low INRs tend to be more severe; for a mechanical heart valve, time below range is the main driver of valve thrombosis. The usual causes are missed or late doses, a sustained increase in vitamin K-rich foods (large servings of kale, spinach, collards, broccoli, Brussels sprouts) or a new multivitamin containing vitamin K, a drug that speeds warfarin metabolism (rifampin, carbamazepine, phenytoin, phenobarbital), the herbal St John's wort, or vomiting and malabsorption of the tablets.

Some people need unusually high warfarin doses because of CYP2C9 and VKORC1 gene variants, and a few have true warfarin resistance. If the INR stays low despite good adherence, the clinic will usually review diet, medicines and supplements, confirm the tablets are being absorbed, and raise the dose stepwise; the INR takes 3 to 5 days to reflect each change because of the long half-life of factor II.

Common causes

Missed, late or under-dosed warfarin
The most common reason; even one or two missed doses can drop the INR below 2.0 within a few days. Pill organizers, a fixed time and an alarm are the standard fixes.
Increased dietary vitamin K
A cup of cooked kale, spinach or collard greens provides 500 to 1,000 µg of vitamin K, several times a typical day's intake; a sudden increase lowers the INR within days. The advice is a consistent intake, not avoidance.
Drugs that speed warfarin metabolism
Rifampin, carbamazepine, phenytoin, phenobarbital, griseofulvin and some HIV drugs induce the liver enzymes that clear warfarin; the INR can halve within a week or two of starting them.
St John's wort and other supplements
St John's wort induces CYP2C9 and CYP3A4 and lowered INR by about 20 to 25 percent in a controlled study; coenzyme Q10 (vitamin K-like structure), high-dose green tea extract and multivitamins containing vitamin K can also lower it.
Vomiting, diarrhea and malabsorption
Warfarin is absorbed in the upper gut; persistent vomiting or severe diarrhea can prevent absorption and lower the INR.
Hypothyroidism
Low thyroid hormone slows the breakdown of clotting factors, so more warfarin is needed; as thyroid treatment takes effect, the INR rises again.
Genetic variation and warfarin resistance
VKORC1 and CYP2C9 variants explain up to a third of the variation in warfarin dose; rare VKORC1 mutations cause true resistance requiring very high doses.
Normal variation (no anticoagulant)
An INR of 0.8 to 0.9 or a PT at the low end is the normal range; it does not indicate a clotting disorder and needs no action.

Symptoms that can go with it

None from the low INR itself
On warfarin, a low INR raises clot risk: a swollen, painful calf or thigh (DVT), sudden breathlessness or chest pain (pulmonary embolism), or sudden weakness, facial droop or speech difficulty (stroke), all of which are emergencies
With a mechanical heart valve, new breathlessness, a change in the valve click or a stroke can indicate valve thrombosis

Read it alongside

PTT (activated partial thromboplastin time) — tests the other branch of the cascade; a high PT with a normal PTT points to factor VII (early liver disease, vitamin K deficiency, warfarin), both high suggests a common-pathway factor, DIC or severe liver disease.
Platelet count — bleeding with a normal PT/INR and PTT but low platelets has a different cause; both abnormal in DIC and advanced cirrhosis.
Fibrinogen and D-dimer — low fibrinogen with high D-dimer confirms consumption (DIC) when PT and PTT are both prolonged.
ALT, AST, bilirubin and albumin — a high INR with low albumin and raised bilirubin indicates reduced liver synthetic function rather than vitamin K deficiency.
Hemoglobin — a falling hemoglobin with a high INR suggests occult bleeding, most often from the gut.
Creatinine and eGFR — kidney function affects the dosing of the direct oral anticoagulants and the bleeding risk on any anticoagulant.
Vitamin K response — an INR that normalizes 24 to 48 hours after vitamin K confirms deficiency; failure to correct points to liver disease or a factor deficiency.
Mixing study and factor assays — ordered by haematology when a prolonged PT is unexplained, to distinguish a missing factor from an inhibitor.

What usually happens next

On warfarin with an out-of-range INR: the clinic adjusts the weekly dose (usually by 5 to 20 percent) and repeats the INR within 3 to 7 days; expect to be asked about missed doses, new medicines, illness, alcohol and changes in what you eat.
An INR of 4.5 to 9 without bleeding on warfarin is usually managed by holding one or two doses, sometimes with a small oral dose of vitamin K (1 to 2.5 mg), and a repeat INR in 1 to 2 days; above 9 to 10, oral vitamin K is given even without bleeding.
If you are not on an anticoagulant and the INR is 1.2 to 1.5 with no symptoms, it is usually repeated on a correctly filled tube with liver tests and a PTT; a persistent mild rise with normal liver tests is often vitamin K deficiency and a short course of vitamin K is both treatment and diagnostic test.
If liver disease is suspected, the INR is read with albumin, bilirubin, platelets and imaging; in known cirrhosis it is tracked over time as part of the MELD score rather than treated on its own.
Before surgery or a procedure, an INR of 1.5 or below is generally required; warfarin is usually stopped 5 days beforehand, sometimes with a short-acting injectable anticoagulant as a bridge for high-risk conditions, and the INR is checked the day before.
If you repeatedly fall outside range despite good adherence, ask about home INR self-testing, a review of all medicines and supplements, and whether a direct oral anticoagulant would be an option for your condition (not for mechanical valves or antiphospholipid syndrome).

Diet, lifestyle and natural levers with evidence

What can move PT/INR once the cause is known. Nothing here replaces finding the cause.

Keep vitamin K intake consistent (on warfarin)

Strong evidence

Warfarin works by blocking vitamin K, so the amount you eat sets the dose you need. Day-to-day swings in leafy-green intake are a leading cause of unstable INRs. In a randomised trial, patients with unexplained INR instability given 150 µg of vitamin K daily spent more time in range and had fewer out-of-range results than placebo, and other small trials showed similar improvements, although a Cochrane review judged the overall evidence limited. The practical advice is to eat greens regularly in similar amounts rather than to avoid them, and to tell the clinic before starting a multivitamin or a supplement containing vitamin K.

Do not start vitamin K supplements on warfarin without the clinic's knowledge; the dose will need adjusting and the INR rechecking.

Avoid St John's wort on warfarin

Strong evidence

St John's wort induces the liver enzymes that clear warfarin. In a controlled crossover study in healthy volunteers it reduced the INR response to a warfarin dose by about 20 to 25 percent, and case series describe INRs falling below range within one to two weeks of starting it, with recovery after stopping. It is the herbal product with the clearest evidence of a clinically important interaction.

Stopping St John's wort while on warfarin raises the INR again over 1 to 2 weeks; either change needs an INR check.

Alcohol: avoid binges and keep intake low and steady

Moderate evidence

Acute heavy drinking inhibits warfarin metabolism and raises the INR for a day or two, while sustained heavy drinking induces metabolism and lowers it, and chronic alcohol-related liver damage raises the baseline INR independently. Systematic reviews of warfarin interactions rate alcohol as a probable cause of INR instability and bleeding; keeping intake to no more than one to two drinks a day, and the same from day to day, is the usual advice.

Ginkgo, garlic, ginger, fish oil and other bleeding-risk supplements

Preliminary evidence

These do not change the INR much in controlled trials (a crossover study of ginkgo and ginger with warfarin found no significant INR effect, and 3 to 6 g a day of fish oil did not alter INR in small trials), but they reduce platelet function and have been linked in case reports to bleeding on warfarin. High-dose vitamin E (above 400 IU) and cranberry juice in large quantities have similar case-report signals. Most anticoagulation clinics ask patients to mention them and to avoid high doses rather than banning them.

Stop ginkgo, high-dose fish oil and vitamin E a week before surgery, and report any new bruising or bleeding.

Correct dietary vitamin K deficiency (not on warfarin)

Moderate evidence

Adults need about 90 to 120 µg of vitamin K a day, supplied mainly by leafy greens, broccoli, Brussels sprouts and vegetable oils; a high INR from pure dietary deficiency, seen with prolonged poor intake, eating disorders or long antibiotic courses, corrects within days of resuming these foods or taking a small oral dose. If malabsorption is the cause (celiac disease, bile duct obstruction, bariatric surgery), food alone is not enough and the underlying condition needs treating.

Acetaminophen and NSAID awareness

Moderate evidence

Regular acetaminophen above about 2 g a day for several days raises the INR on warfarin (one case-control study found a roughly tenfold increase in the odds of an INR above 6 at 9 g or more per week); occasional doses do not. NSAIDs such as ibuprofen and naproxen do not change the INR but impair platelets and irritate the stomach, roughly doubling the risk of gastrointestinal bleeding on an anticoagulant. Acetaminophen in modest doses remains the preferred painkiller; tell the clinic if you need it daily.

When to see a clinician promptly

On warfarin: an INR above 4.5 to 5 without bleeding needs a call to your anticoagulation clinic or prescriber the same day; an INR above 9 to 10 needs urgent advice, usually vitamin K.
Any significant bleeding on an anticoagulant, whatever the INR: vomiting blood, black or bloody stools, blood in urine, a nosebleed that will not stop after 15 minutes of pressure, or heavy bleeding from a cut: emergency department.
A severe headache, sudden confusion, weakness, slurred speech, vision loss or a fall with a head knock while on an anticoagulant, even with no visible injury: emergency, possible intracranial bleeding.
A swollen painful leg, sudden chest pain or breathlessness, or stroke symptoms while your INR has been below range: possible clot, emergency.
A high INR with jaundice, confusion, drowsiness or a swollen abdomen in someone with or without known liver disease: possible liver failure, same-day assessment.
A newly raised INR in someone not on anticoagulants, with unexplained bruising, bleeding gums or prolonged bleeding, needs assessment within days.

Frequently asked questions

What is a normal INR level?

If you are not taking a blood thinner, a normal INR is 0.8 to 1.1, with some laboratories accepting up to 1.2. On warfarin the "normal" is your target range: 2.0 to 3.0 for atrial fibrillation, DVT and pulmonary embolism, or 2.5 to 3.5 for a mechanical mitral valve and other high-risk valves. An INR of 1.0 on warfarin means the drug is not working, not that you are normal.

What is a normal PT (prothrombin time)?

About 11 to 13.5 seconds in most laboratories, with some ranges running 10 to 14 depending on the reagent used. Because the seconds vary between labs, the result is usually converted to an INR, which is standardised and is the number to use for comparing results over time or between laboratories.

Is an INR of 1.2 or 1.3 bad?

Not usually. An INR of 1.2 is at the top of many normal ranges, and 1.3 is a mild prolongation that often reflects a sample problem, mild vitamin K deficiency after an illness or antibiotics, early liver disease, or a direct oral anticoagulant. It is not a bleeding risk on its own and is typically repeated with liver tests. Before surgery, most teams accept an INR up to 1.5.

What INR is dangerously high?

On warfarin, bleeding risk rises modestly between 3 and 4.5 and steeply above that. An INR above 4.5 to 5 should be reported the same day; above 9 to 10 is treated with vitamin K even if you feel fine; and any INR with active bleeding is an emergency. Off warfarin, an INR above 1.5 in someone with liver disease or above 2 with no explanation needs prompt investigation rather than being dangerous in itself.

What does a low INR mean?

On warfarin, an INR below 2.0 (or below 2.5 for a mechanical mitral valve) means you are under-anticoagulated and clot risk is raised; the usual reasons are missed doses, more vitamin K in your diet, a new interacting medicine or St John's wort. Not on warfarin, an INR of 0.8 or 0.9 is simply the low end of normal and does not mean your blood is too thick or that you are at risk of clots.

What foods affect INR?

Foods high in vitamin K lower the INR on warfarin: kale, spinach, collard and turnip greens, Swiss chard, broccoli, Brussels sprouts, asparagus and green tea in large amounts, plus vegetable oils and vitamin K-containing multivitamins. The goal is a consistent intake from week to week rather than avoidance. Alcohol binges raise the INR; grapefruit has little effect on warfarin; cranberry juice and mango have been linked to raised INRs in case reports but not consistently in trials.

What is the difference between PT, INR and PTT?

PT (prothrombin time) times the tissue-factor pathway and is the test affected by warfarin, liver disease and vitamin K. INR is the PT converted to a standardised scale so results match across laboratories. PTT (partial thromboplastin time) times the other branch of the clotting cascade and is used to monitor heparin and to detect hemophilia, von Willebrand disease and lupus anticoagulant. The two are often ordered together to localise a clotting problem.

Do I need to fast for a PT/INR test?

No. The test is not affected by a recent meal. Take your warfarin at the usual time unless the clinic tells you otherwise, and make sure the tube is filled to the line, because an underfilled sample falsely raises the result. Tell the clinic about any new medicine, supplement, illness or change in diet since the last test, since those explain most unexpected results.

References

Prothrombin time test and INR (PT/INR). MedlinePlus, US National Library of Medicine (2023)View source
Prothrombin time test. Mayo Clinic (2024)View source
Vitamin K: fact sheet for health professionals. National Institutes of Health, Office of Dietary Supplements (2021)View source
Holbrook A, Schulman S, Witt DM, et al.. Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest (2012)
Witt DM, Nieuwlaat R, Clark NP, et al.. American Society of Hematology 2018 guidelines for management of venous thromboembolism: optimal management of anticoagulation therapy. Blood Advances (2018)
Otto CM, Nishimura RA, Bonow RO, et al.. 2020 ACC/AHA guideline for the management of patients with valvular heart disease. Circulation (2021)
Hylek EM, Chang YC, Skates SJ, Hughes RA, Singer DE. Prospective study of the outcomes of ambulatory patients with excessive warfarin anticoagulation. Archives of Internal Medicine (2000)
Hylek EM, Go AS, Chang Y, et al.. Effect of intensity of oral anticoagulation on stroke severity and mortality in atrial fibrillation. New England Journal of Medicine (2003)
Holbrook AM, Pereira JA, Labiris R, et al.. Systematic overview of warfarin and its drug and food interactions. Archives of Internal Medicine (2005)
Sconce E, Avery P, Wynne H, Kamali F. Vitamin K supplementation can improve stability of anticoagulation for patients with unexplained variability in response to warfarin. Blood (2007)
Jiang X, Williams KM, Liauw WS, et al.. Effect of St John's wort and ginseng on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. British Journal of Clinical Pharmacology (2004)
Tripodi A, Mannucci PM. The coagulopathy of chronic liver disease. New England Journal of Medicine (2011)

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