Antidote: Coumadin

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I and every other clinician who treats patients with the common blood thinner warfarin (Coumadin) have a problem. The effect of the drug is delayed. If gauging the effect of the drug wasn't difficult enough by the time delay, the problem is made worse because other medications such as antibiotics cross-react and slow the metabolism of Coumadin, while foods that contain vitamin K neutralize its effects.     
As a result, managing the effects of Coumadin as a blood thinner requires frequent monitoring of blood tests, and getting it right is part of the art of medicine. Unfortunately, the number too often slips high or low, increasing the risk of either bleeding or clotting.                   
For the last few years scientists have been getting closer and closer to a suitable oral replacement. Derived from the saliva of ticks, and working by a totally different mechanism than Coumadin, studies have been ongoing on two drugs, dabigatran (Pradaxa), a direct thrombin (factor X) inhibitor which was approved by the FDA last month for blood thinning stroke patients with atrial fibrillation, and rivaroxaban (Xarelto), a factor Xa inhibitor which seems to be on the verge of approval. Both of these new drugs are patient friendly, not requiring blood tests or a special diet. The only real downside of these drugs versus warfarin is that they lack a ready antidote.
For all the negative press and publicity that occurs when a drug fails, it would be appropriate to see a media frenzy welcoming in these two great, new drugs. Don't expect it any time soon. Warfarin, take a bow, your time in the forefront is rapidly drawing to a close.
Marc Siegel, MD, is an internist and professor of medicine at New York University and the author of False Alarm: The Truth About the Epidemic of Fear
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