Blood Thinners

In anticipation of my upcoming appointment and in an effort to better educated myself, I'm curious about oral blood thinners. Since APS is due to a build up of fibrin, my thought is that we need a fibrinolytic. There are several categories of "blood thinners" including anti platelet drugs, ones that work on the clotting factors, etc.

Ive seen a lot of people on Coumadin, and am wondering if this is the drug of choice even though I believe it works on clotting factors other than fibrin? I'm not sure where in the clotting cascade the meds are meant to target. I have a medical background which is why I'm curious.

Thanks!

Elke

7 Replies

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  • I think the point is that people with APS get better by getting the blood to flow better regardless of how. For instance, the APS antibody I have attacks myelin. It is considered a "secondary antibody." What I have read about it is that they really don't know why anticoagulation works, but it does. At one hospital I read they don't test for the antibody since they don't know what it does. (Great!) I'm on Eliquis and Plavix and I have seen good results with it, so that is really the most important thing to me. But I'm sure other people can give you a more scientific explanation than "it works."

  • Im not sure where you get the idea that APS is due to a build up of fibrin! APS is a autoimmune disease, the immune system produces abnormal antibodies called antiphospholipid antibodies. These target proteins attached to fat molecules (phospholipids), which makes the blood more likely to clot.

    Therefore anyone who has the disease with raised antibodies, will take an anticoagulant - to thin the blood. Some will only need Aspirin - an anti platelet, some will need something stronger like warfarin and some will use LMW heparin because it works differently and seems to work better for some people. Others will need a combination of warfarin and a anti platelet like aspirin or clopidogrel. Now there are the new oral anticoagulants however the ONLY one that has been trialled and deemed safe for use so far with APS is Rivaroxaban and that is for those who have venus clots or needed an INR 2-3 only.

  • Allow me to clarify. The build up of fibrin is not the cause of APS, but rather what happens due to the faulty clotting mechanism caused by APS, which is an autoimmune disease. There are many, many publications both online and in medical journals that specifically mention fibrin with regard to APS. While fibrin is one factor in the clotting cascade, it is not the only one. PubMed, Dr Jacob Teitlebaum, Dr David Berg, Hemex laboratories all specifically refer to fibrin as the problematic constituent in the "sticky blood." It's not an issue with platelet function causing clots, although platelets can become abnormally lowered (immune-mediated thrombocytopenia) as a related disorder.

    I was just curious if anyone was familiar with the "how's" of the drugs and why one would be favored over another.

  • I don't have a medical background, but I am married to one who does, and I do have a background that includes stats and probability/risk so I can read the research and get most of it. I'll throw the medical terms around with abandon here, most of them I'll probably use correctly - I do still have a habit of mixing up my -otomys and -ectomys which causes much hilarity when in the company of surgeons, but we shouldn't run into that here.

    I was at same stage as you (possibly, from your post) just over a year ago, about to be put on anti-coagulation, for life, and did a fair bit of research myself, particularly on NOACs, I'll try and summarise:

    Four main drug groups, simplified method of action:

    - anti platelet (clopidogrel/plavix, aspirin)

    act directly on binding sites on platelets, inhibiting aggregation. Irreversible (until your body replaces the platelets).

    - warfarin (=coumadin, and other VKAs)

    Vit K antagonists, reduce vit K via a fairly long convoluted metabolic pathway, vit k deficiency reduces clotting factor production but doesn't affect clotting factors already in the blood (approx 48h time to act, 40hr half life in vivo). Reversible with Vit K but _not_ immediate effect (if any doctor tells you it is, they are wrong). Variable dosage, requires monitoring.

    - Low Molecular Weight Heparins (LMWHs - fragmin, lovenox, etc.)

    Target clotting factor Xa which is late on in the clotting cascade - just before fibrin I think. Injectable only, not oral. Fast action, short half life, not reversible.

    - NOACs (rivaroxaban, apixaban, etc.)

    Newer oral anticoagulants, mostly antagonise FXa (not sure on all of them) - i.e. the action is similar to Heparin. Fast action, short half life (<24hr). Not currently reversible, but wears off in about the time the warfarin antidote takes to work, antidotes developed but not tested/licensed yet.

    Which is best for APS ? No one knows. Really. My first neurologist warned me when my tests came back LA+ve that "the evidence base is very thin", he wasn't joking (actually there is lots of evidence - decades worth in the case of warfarin, less for NOACs but enough to show that they work as well but are much safer, however, the vast majority of it does NOT apply to APS, restrict yourself to APS-specific evidence and there is very very little).

    Which are licensed for APS (to my knowledge) ? Warfarin. Only. [And that may be therefore be what you get]. It has been historically used and licensed because it was all there was. LMWHs are licensed for use in pregnancy (only), again because that is all there is (or was - not sure about NOACs) - warfarin being teratogenic. LMWHs _are_ used where warfarin fails (there are people here on it long term), and where warfarin cannot be used (bridging for surgery, or fast acting top-ups for warfarin therapy if INR goes low, for example) - but this is, I believe, all unlicensed (again it comes back to it being the only option).

    However for your question, the history of use of both warfarin and LMWH (and in particular the use of LMWH to "top up" when warfarin goes too low) would tend to indicate that point of action is not that important for treating APS symptoms or preventing APS-induced thrombosis. There is no reason from this to suppose that NOACs should be any worse than LMWHs, but no reason why they should be any better.

    The only evidence published so far for NOACs and APS is the RAPS study which others have pointed out - but it only applies to a very narrow criteria (why they are balkanising us in this way I do not know).

    Some other things you might want to be aware of:

    - there is no consensus among doctors on what level of warfarin (what INR range) is needed for APS, particularly for arterial (there are some small scale studies but they have conflicting results, notably the retrospective studies conflict with prospective, which if know what you are talking about should instantly raise a massive red flag). My own doctors couldn't agree and I was referred in to the warfarin clinic multiple times with different target ranges. Way to build confidence...

    - warfarin (or other VKA) requires regular monitoring of INR with venous blood samples. APS patients are renowned for being unstable and therefore needing more frequent checking. This can be hard on your elbows if your veins are lousy (say after much use for contrast injections etc.), as mine now are. Weekly monitoring meant permanently bruised (you bruise much mroe once on warfarin) and painful elbows for me. It is also not a small inconvenience to have to attend a clinic every week.

    - fingerprick testing either in-clinic or self testing may be available, be aware that it isn't accurate for APS and (for that reason), NONE of this testing equipment is licensed for APS patients. Many of us use it nonetheless, but it is unlicensed and therefore exactly the same status as NOACs [I was denied rivaroxaban because it was unlicensed for APS, and told I had to have warfarin, which I now manage by self testing with equipment that is itself unlicensed for APS and I had to sign disclaimers to say I understood that - I am sure it makes sense to some doctor somewhere...]

    - warfarin is also a pain because it interacts (often unpredictably) with just about every other drug in existence, alcohol, nicotine (and probably caffeine), and a lot of food. I have found advice on both alcohol and food (e.g. cranberries) to be inconsistent or contradictory - again, doesn't inspire confidence that anyone knows what they are doing

    - if you are arterial/stroke APS then I found Khamashta did a review here: rheumatology.oxfordjournals... - he is a useful starting point for searching publications, works (or worked) with prof Hughes. Also edited the APS medical textbook (ISBN 184996940X).

    - ask them (again if your are arterial) what your personal stroke risk is and personal bleeding risk on anti-coagulation (if you had AF you're supposed to have this reviewed every year). The correct answer is "we don't know" because there are lots of scoring systems and data to back them up - but they don't apply to APS.

    - doctors are, in my experience, very poor at statistics and probability / risk (worryingly, because evidence based medicine depends on it). If anyone tells you that warfarin is really safe because there is "only 1-3% risk of serious bleeding" then tell them they are talking out of their backside (because I omitted to do that because I just wanted out of that consultation). In fact (a) that figure is from general warfarin population and doesn't apply to APS and (b) it is per-patient-year so if you are a patient in your 40s being put on anti-coagulation for the rest of your life, your total risk is way different (and yes I do know you don't just add up or multiply the risk by the number of years).

  • Thank you for having the possibility also to read what you have written!

    Kerstin

  • Patients have an individual plan for anticoagulation or anti platelet therapy or in some cases both, as you will be aware some patients are ok just on Aspirin, I am but also take low dose naltrexone which helps me with a multitude of conditions. hopkinslupus.org/lupus-trea...

    MaryF

  • OK. First let me explain I am the English major – with no degree in science. But my father was a doctor. I'm sure you realize that the clotting cascade is very complex. My take away from what I have read is that the immune system can target a number of different steps in the cascade and this explains why us patients have such diverse reactions to the various medications. Some of us are symptom-free on warfarin, others on heparin, and others on others. And regarding fibrin – I recently read that the viruses that are linked to people developing APLS, mono, my myc oplasma pneumonia and chicken pox, all "hide out" inside blood vessels and platelets and use a fibrin encouraging chemical to stay hidden from the immune system. So, according to the scenario, an immune systems is justified in it's attacks,.. it's a fascinating topic. I look forward to future research that may explain these complications to me, the English major.

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