Hadn’t thought of that. Actually, from what I understand, the status of warfarin is mostly okay now because they test for unusual sensitivity to it before they administer it?
Prescription warfarin—actually they might use related molecules these days with the same basic mechanism of action—kills 10s of thousands per year: they die from loss of blood because the warfarin-like molecules have inhibited the clotting mechanism more than intended. So for example someone I was friends with died (in his sleep) this way.
Nevertheless, warfarin-like molecules have positive expected global utility because clots cause so much negative utility. So for example I was on it for about 6 years. You’re supposed to get a blood test every 2 weeks for as long as you’re on it.
Since Alex was a grad student in pharmacy, he’ll probably correct any untruths in the above in the unlikely event there are any.
ADDED. “Unusual sensitivity” is the wrong way to describe it.
This is actually not relevant as warfarin dosage is determined by regular testing and dose adjustment. Your inborn metabolic rate is a very small effect compared to, for example, dietary preferences. (for those who are unfamiliar with the agent, warfarin antagonises the effects of vitamin K and so must be adjusted against dietary intake)
Unfortunately there are many people in the health sector offering tests that, whilst factually correct, are irrelevant to a patient’s care.
The influence of the genotype varies from “typical sensitivity” to “may require greatly decreased warfarin dose”. A range that is all but irrelevant, regular testing or no (think for example of the initial dosage).
There is the option of being tested for polymorphisms of 1-2 of the most relevant metabolic enzymes, which account for some of the bleeding risk. My impression is that genotyping is not routinely done. Also, warfarin is risky in normal metabolizers (many many drug/food/disease interactions). I agree with Richard on the overall cost-benefit. (ETA: Though there are new expensive drugs approved for some of the same indications—rivaroxaban and dabigatran—that show some promise of being safer.)
Are you referring to warfarin here or am I imagining things?
(Blinks.)
Hadn’t thought of that. Actually, from what I understand, the status of warfarin is mostly okay now because they test for unusual sensitivity to it before they administer it?
Prescription warfarin—actually they might use related molecules these days with the same basic mechanism of action—kills 10s of thousands per year: they die from loss of blood because the warfarin-like molecules have inhibited the clotting mechanism more than intended. So for example someone I was friends with died (in his sleep) this way.
Nevertheless, warfarin-like molecules have positive expected global utility because clots cause so much negative utility. So for example I was on it for about 6 years. You’re supposed to get a blood test every 2 weeks for as long as you’re on it.
Since Alex was a grad student in pharmacy, he’ll probably correct any untruths in the above in the unlikely event there are any.
ADDED. “Unusual sensitivity” is the wrong way to describe it.
Of note, 23andme tests for genetically determined warfarin tolerance. I can copypasta their references on demand.
This is actually not relevant as warfarin dosage is determined by regular testing and dose adjustment. Your inborn metabolic rate is a very small effect compared to, for example, dietary preferences. (for those who are unfamiliar with the agent, warfarin antagonises the effects of vitamin K and so must be adjusted against dietary intake)
Unfortunately there are many people in the health sector offering tests that, whilst factually correct, are irrelevant to a patient’s care.
Someone tell the NHS, which is sponsoring a large trial to explore just that question.
The influence of the genotype varies from “typical sensitivity” to “may require greatly decreased warfarin dose”. A range that is all but irrelevant, regular testing or no (think for example of the initial dosage).
There is the option of being tested for polymorphisms of 1-2 of the most relevant metabolic enzymes, which account for some of the bleeding risk. My impression is that genotyping is not routinely done. Also, warfarin is risky in normal metabolizers (many many drug/food/disease interactions). I agree with Richard on the overall cost-benefit. (ETA: Though there are new expensive drugs approved for some of the same indications—rivaroxaban and dabigatran—that show some promise of being safer.)