Vitamin/mineral Screening Normal range Additional laboratory indexes Critical range Preoperative deficiency Postoperative deficiency Comments; B1 (thiamin). Warfarin, sold under the brand name Coumadin among others, is a medication that is used as a blood thinner. It is commonly used to treat blood clots such as deep vein.
Warfarin - Wikipedia. This article is about the anticoagulation medication. For the rodenticide often called . Less common side effects may include tissue death and purple toes syndrome. Use is not generally recommended during pregnancy. It is recommended that the effects of warfarin typically be monitored by checking prothrombin time (INR) every one to four weeks. Warfarin treatment can help prevent formation of future blood clots and help reduce the risk of embolism (migration of a thrombus to a spot where it blocks blood supply to a vital organ). Thus, common clinical indications for warfarin use are atrial fibrillation, the presence of artificial heart valves, deep venous thrombosis, and pulmonary embolism (where the embolized clots first form in veins). Warfarin is also used in antiphospholipid syndrome. It has been used occasionally after heart attacks (myocardial infarctions), but is far less effective at preventing new thromboses in coronary arteries. Prevention of clotting in arteries is usually undertaken with antiplatelet drugs, which act by a different mechanism from warfarin (which normally has no effect on platelet function). These have a shorter (acenocoumarol) or longer (phenprocoumon) half- life, and are not completely interchangeable with warfarin. Vitamin K Dependent Factors Affected By Warfarin Diet Restriction![]() Several types of anticoagulant drugs offering the efficacy of warfarin without a need for monitoring, such as dabigatran, apixaban, edoxaban and rivaroxaban, have been approved in a number of countries for classical warfarin uses like the more common types of atrial fibrillation, and others in the same drug classes are under development. There is a reversal agent available for dabigatran (idarucizumab). To optimize the therapeutic effect without risking dangerous side effects such as bleeding, close monitoring of the degree of anticoagulation is required by a blood test measuring an INR. During the initial stage of treatment, INR is checked daily; intervals between tests can be lengthened if the patient manages stable therapeutic INR levels on an unchanged warfarin dose. Instead of a blood draw, the point of care test involves a simple finger prick. The target INR level varies from case to case depending on the clinical indicators, but tends to be 2–3 in most conditions. In particular, target INR may be 2. Therefore, bridging anticoagulant therapies (usually heparin) are often used to reverse this temporary hypercoagulable state. Maintenance dose. When warfarin levels are high, people have more risk of bleeding. Conversely, lower levels of warfarin lead to increased risk of blood clots. There is a narrow range where the benefits of warfarin are greater than the risks, its therapeutic window. Certain drugs, herbal medicines and foods can interact with warfarin, increasing or decreasing a previously stable warfarin level. Keeping vitamin K1 intake at a stable level can prevent these fluctuations. Leafy green vegetables tend to contain higher amounts of vitamin K1. Green parts of members of the family Apiaceae, such as parsley, cilantro, and dill, are extremely rich sources of vitamin K; cruciferous vegetables such as cabbage and broccoli, as well as the darker varieties of lettuces and other leafy greens, are also relatively high in vitamin K1. Green vegetables such a peas and green beans do not have such high amounts of vitamin K1 as leafy greens. Certain vegetable oils have high amounts of vitamin K1. Foods low in vitamin K1 include roots, bulbs, tubers, and most fruits and fruit juices. Cereals, grains and other milled products are also low in vitamin K1. International guidelines on home testing were published in 2. All patients must be appropriately selected and trained. Currently available self- testing/self- management devices give INR results that are comparable with those obtained in laboratory testing. This includes people with active bleeding conditions (such as gastrointestinal ulcers), or disease states with increased risk of bleeding e. For patients undergoing surgery, treatment with anticoagulants is generally suspended. Similarly, spinal or lumbar puncture (e. With heparin, risk of maternal haemorrhage and other complications are still increased, but heparins do not cross the placental barrier, so do not cause birth defects. FWS is characterized mainly by skeletal abnormalities, which include nasal hypoplasia, a depressed or narrowed nasal bridge, scoliosis, and calcifications in the vertebral column, femur, and heel bone, which show a peculiar stippled appearance on X- rays. Limb abnormalities, such as brachydactyly (unusually short fingers and toes) or underdeveloped extremities, can also occur. The most common congenital abnormalities associated with warfarin use in late pregnancy are central nervous system disorders, including spasticity and seizures, and eye defects. Similarly, INR levels should be checked to avoid adverse effects. The risk of severe bleeding is small but definite (a typically yearly rate of 1- 3% has been reported). All types of bleeding occur more commonly, but the most severe ones are those involving the brain (intracerebral hemorrhage/hemorrhagic stroke) and the spinal cord. A commonly used score (HAS- BLED) includes known predictors of warfarin- related bleeding: uncontrolled high blood pressure (H), abnormal kidney function (A), previous stroke (S), known previous bleeding condition (B), previous labile INR when on anticoagulation (L), elderly as defined by age over 6. E), and drugs associated with bleeding (e. While their use is recommended in clinical practice guidelines. Protein C is an innate anticoagulant that, like the procoagulant factors that warfarin inhibits, requires vitamin K- dependent carboxylation for its activity. Since warfarin initially decreases protein C levels faster than the coagulation factors, it can paradoxically increase the blood's tendency to coagulate when treatment is first begun (many patients when starting on warfarin are given heparin in parallel to combat this), leading to massive thrombosis with skin necrosis and gangrene of limbs. Its natural counterpart, purpura fulminans, occurs in children who are homozygous for certain protein C mutations. A 1. 99. 9 study in 5. The mechanism was thought to be a combination of reduced intake of vitamin K, which is necessary for bone health, and inhibition by warfarin of vitamin K- mediated carboxylation of certain bone proteins, rendering them nonfunctional. This condition is thought to result from small deposits of cholesterol breaking loose and causing embolisms in blood vessels in the skin of the feet, which causes a blueish purple colour and may be painful. It is typically thought to affect the big toe, but it affects other parts of the feet as well, including the bottom of the foot (plantar surface). The occurrence of purple toe syndrome may require discontinuation of warfarin. No specific treatment is available, but some modalities are under investigation. Risk of bleeding is increased if the INR is out of range (due to accidental or deliberate overdose or due to interactions). When warfarin is being given and INR is in therapeutic range, simple discontinuation of the drug for five days is usually enough to reverse the effect and cause INR to drop below 1. This increased risk is due to the anti- platelet effect of NSAIDS as well as the possible damage to the gastrointestinal mucosa. Other broad- spectrum antibiotics can reduce the amount of the normal bacterial flora in the bowel, which make significant quantities of vitamin K1, thus potentiating the effect of warfarin. Food and Drug Administration (FDA) product insert on warfarin states that alcohol should be avoided. All may increase bleeding and bruising in people taking warfarin; similar effects have been reported with borage (starflower) oil or fish oils. John's Wort, sometimes recommended to help with mild to moderate depression, reduces the effectiveness of a given dose of warfarin; it induces the enzymes that break down warfarin in the body, causing a reduced anticoagulant effect. S- warfarin is 2- 5 times more potent than the R- isomer in producing an anticoagulant response. Heparin must be given by injection, whereas warfarin is available orally. Warfarin has a long half- life and need only be given once a day. Heparin can also cause a prothrombotic condition, heparin- induced thrombocytopenia (an antibody- mediated decrease in platelet levels), which increases the risk for thrombosis. It takes several days for warfarin to reach the therapeutic effect since the circulating coagulation factors are not affected by the drug (thrombin has a half- life time of days). Warfarin's long half- life means that it remains effective for several days after it was stopped. Furthermore, if given initially without additional anticoagulant cover, it can increase thrombosis risk (see below). For these main reasons, hospitalised patients are usually given heparin with warfarin initially, the heparin covering the 3–5 day lag period and being withdrawn after a few days. Mechanism of action. The precursors of these factors require gamma carboxylation of their glutamic acid residues to allow the coagulation factors to bind to phospholipid surfaces inside blood vessels, on the vascular endothelium. The enzyme that carries out the carboxylation of glutamic acid is gamma- glutamyl carboxylase. The carboxylation reaction will proceed only if the carboxylase enzyme is able to convert a reduced form of vitamin K (vitamin K hydroquinone) to vitamin K epoxide at the same time. The vitamin K epoxide is in turn recycled back to vitamin K and vitamin K hydroquinone by another enzyme, the vitamin K epoxide reductase (VKOR). Warfarin inhibits epoxide reductase. When this occurs, the coagulation factors are no longer carboxylated at certain glutamic acid residues, and are incapable of binding to the endothelial surface of blood vessels, and are thus biologically inactive. Vitamin K1 and K2 Benefits Go Far Beyond Blood Clotting. By Dr. Mercola. Most readers here appreciate the importance of vitamin D, as do many physicians. However, there’s another vitamin that is virtually equivalent in terms of benefit that is still sorely underappreciated, and that is vitamin K2. Leon Schurgers is a senior scientist who did his Ph. D work on vitamin K, and I recently had the pleasure of interviewing him on this important topic. Schurgers, all K vitamins actually have more or less the same function, which is related to the first part of the vitamin, called the naphthoquinone ring structure. The two vitamins are only different in their side chains. The Blood Clotting Functions of Vitamins KVitamin K1 is well known for being crucial for proper blood clotting. Schurgers clarifies this by saying that both vitamins K1 and K2 activate certain coagulation factors. Specifically, there are four coagulation factors (Factor 2, 7, 9, and 1. K1 and K2. Schurgers, there’s no risk of over coagulating if you take a lot of vitamin K. In other words, your coagulation factors will not become overactive if you take high amounts of vitamin K1 or K2. So it is quite safe to consume vitamin K when you are not taking an oral anticoagulant drug. In this case, you do need to be cautious. Schurgers: “If you take oral anticoagulants – Coumadins and Warfarins, you have to be careful with K1 AND K2. However, the advice in the United States is to skip everything that contains vitamin K, and that is something I argue against. Because if you take away all the K1 and K2 from the diet, every little interference—if you take a little bit of vitamin K—will have a dramatic effect on the anticoagulant level. However, if you have a steady intake level of vitamin K1 or K2, or both, a little bit of interference is not that bad anymore. So I advocate, please take vitamin K from the diet every day, and put the anticoagulant level on top of that”.. Then have your doctor adjust your dose based upon that. However, it is important you take the same dose of K1 and K2 all the time or else the drug may over- anticoagulate you. Vitamin K Benefits Go Far Beyond Blood Clotting. Vitamin K also has important benefits beyond healthy blood clotting. In the 1. 98. 0s, it was discovered that vitamin K is needed to activate the protein osteocalcin, which is found in your bone. A decade or so later, another vitamin K- dependent protein was discovered: matrix Gla protein (MGP), found in your vascular system. Without vitamin K, these and other vitamin K- dependent proteins remain inactivated, and cannot perform their biological functions. If you inactivate MGP, you end up with serious arterial calcifications, and this is why vitamin K is so crucial for cardiovascular health. Evidence suggests vitamin K can even regress arterial calcification induced by vitamin K deficiency. Schurgers: “There is a very strong correlation between inactive MGP and microcalcifications. It’s very interesting to speculate that vitamin K deficiency is causative of microcalcification, which then sets on a whole cascade of processes leading to atherosclerosis.”. On a side note, when I was in medical school in the late . Key Differences Between K1 and K2. The difference between vitamins K1 and K2 was first established in the Rotterdam Study,1 which Dr. Schurgers was part of. He explains: “We published this in 2. I measured a variety of food items for vitamin K content.. Vitamin K1 is highly available in green, leafy vegetables – spinach, kale, broccoli, and cabbage. However, the absorption of vitamin K1 from food is extremely low. Only 1. 0 percent of the vitamin K, which is found in green leafy vegetables, is absorbed in your body.. And there’s no variable or modification of the consumption that will significantly increase the absorption.. That was when we started to measure vitamin K2 in food items. We discovered that it was only present in fermented foods. Vitamin K2 is produced by bacteria in the fermentation product.. The total amount of vitamin K2 in cheese is lower than K1 in green leafy vegetables. However, all the vitamin K2 is absorbed by the body.. Vitamin K2 in the food item is nearly completely absorbed.. Vitamin K2 Is Important for Cardiovascular Health. The Rotterdam Study found that those who consumed the greatest amounts of K2 had the lowest risk of cardiovascular disease, cardiovascular calcification, and the lowest chance of dying from cardiovascular disease. This was a profound discovery, because such a correlation did not exist for K1 intake. Later on, other studies also showed that while K2 has health benefits, K1 has none. That’s when the investigation into the differences between K1 and K2 began in earnest.“If you absorb vitamin K1 and K2, we showed that K1 is mainly going to your liver and stays there,” Dr. After three to four hours after ingesting a dose of vitamin K1 from food, it is gone. It is taken up by the liver. K2 also goes to the liver, but the liver redistributes it via the low density lipoprotein (LDL) cholesterol fraction.. MK7 is transported more to the vasculature as compared to the vitamin K1. We hypothesized that that is one of the main functions – that K2 has additional benefit in the cardiovascular system, and K1 is more present in the liver.”. So, in addition to activating MGP, which is a potent inhibitor of calcification, K2 also helps prevent arterial calcification by transporting calcium away from areas where it shouldn’t be (in the lining of your blood vessels) to where it’s really needed (such as in your bone). Upon autopsy, many with Alzheimer’s are found to have vascular degeneration, which is thought to produce symptoms of Alzheimer’s. And although there’s limited research in this area, evidence suggests vitamin K2 might help prevent Alzheimer’s by preventing plaque deposition. Schurgers, at least one study has also shown that vitamin K2 has a major function in delivering cellular energy for Parkinson’s disease patients, and may be beneficial in the treatment of this disease. How to Measure Vitamin K Deficiency. Just as you can measure your serum vitamin D level to ascertain whether you might be sufficient or deficient, you can measure your vitamin K1 and K2 levels as well. The problem, however, is that it really only reveals what you ate the day before, which makes it very difficult to judge sufficiency or deficiency. If you consumed a hamburger, for example, with low amount of vitamin K, your vitamin K will probably be very low. So it’s not a very good marker for vitamin K status,” Dr. These blood tests measure the active and inactive forms of MGP. By that, you can more accurately determine whether you’re sufficient in vitamin K or not. These tests are currently being commercialized, and should be available in both Europe and the US in 2. Interestingly enough, Dr. Schurgers has found that virtually everyone is clinically vitamin K- deficient based on these tests. And, it’s particularly noteworthy that, in studies, patients with the highest levels of inactive MGP had the highest chance of dying from cardiovascular disease.“There is always a certain amount of matrix Gla protein, which is circulating in the inactive form, meaning in biochemistry, you need extra vitamin K to activate this form,” he explains. Recommended Dosages. To avoid vitamin K1 deficiency, Dr. Schurgers recommends eating a minimum of 2. He also suggests consuming K2 on a daily basis, which means you need to eat some form of fermented food. Where does this benefit come from?’ The only explanation I can come up with, which is just purely hypothetical, is that 1. Most of the food were in our house for more days and were most likely fermented,” Dr. There are no known side effects of higher dosages, however, so it’s likely better to err on the higher side. At bare minimum, you need 4. Rotterdam Study,2 which was the first study demonstrating the beneficial effect of vitamin K2. In this study, people who consumed 4. K2 daily lived seven years longer than people getting 1. Keep in mind that the K2 content of pasteurized dairy and products from confined animal feeding operations (CAFOs), which comprise most commercial sources, are NOT high in K2 and should be avoided. Only grass- fed animals (not grain fed) will develop naturally high K2 levels. The following table contains estimates of the K2 content of various foods. Food. Vitamin K2 Natto (3. Fermented vegetables made with Kinetic Culture (2 ounces)4. Whole egg mayonnaise 1. Gouda or Brie cheese (1 ounce)7. Miso. 10- 3. 0 mcg. Lamb or duck (1 cup)6 mcg. Beef liver (1 cup)5 mcg. Dark meat turkey (1 cup)5 mcg. Chicken liver (1 cup)3 mcg. Also keep in mind that fermented foods contain a wide variety of different bacteria, and only certain ones—such as Bacillus subtilis—actually make vitamin K2. You can boost the K2 content of fermented foods by making them yourself, using a starter culture specifically designed to optimize K2. My research team found that we could get 4. K2 in a two- ounce serving of fermented vegetables using a starter culture, which is a clinically therapeutic dose. For me, that’s the real take- home message here. Sure, you can swallow vitamin K supplements, but it’s far easier to get vitamin K2 from fermented vegetables. I believe taking this simple step is a really crucial nutritional strategy that can go a long way toward optimizing your health. Eating lots of green vegetables, especially kale, spinach, collard greens, broccoli, and Brussels sprouts, will increase your vitamin K1 levels naturally. You can also obtain about 2. K2 by eating 1. 5 grams of natto each day, which is half an ounce. It's a small amount and very inexpensive, but many Westerners do not enjoy the taste and texture. If you don't care for the taste of natto, do try some fermented veggies made with Kinetic Culture, which will produce high levels of K2. This is what I do nearly every day. As a last resort, take a high- quality K2 supplement.
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