Transitioning from Dalteparin to Riva... - Sticky Blood-Hugh...

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Transitioning from Dalteparin to Rivaroxaban

My Hematology team have decided to take me off Dalteparin 15,000 IU/0.6 ml to Rivaroxaban 15 mg, this is because a recent DEXA scan has shown I have severe Osteoporosis in spine and hip, and they say Dalteparin can worsen Osteoporosis.

They said I have to take both Dalteparin and Rivaroxaban together for two days to get the Rivaroxaban loaded, and then just stop Dalteparin, they did not say if I should leave a time gap between the two.

Does this sound right please?

14 Replies

Do you have APS/Hughes? Riveroxaban studies show it is not the best avenue for this. Why are you on theses meds?


Yes I have APS, I had PE just before Christmas.


Can you reveal why you were put on Dalteparin in the first place and how long you were on it for?

Ive been on it for 8 years and my DEXA scans have improved not got worse. They actually have no proper trials that proves LMWH increases the risk of osteoporosis, its only that unfractioned heparin does, so the assumption is that LMWH will do too.

If its not caused by your fragmin then there is no reason to change.

As I said Id be interested to know why you were on it and if Rivaroxaban is a suitable substitute, as it would not be for me.


I have been on Dalteparin since December 23 because of PE. I raised the concerns you mention, but my Hematology team were adamant I move to Rivaroxaban. I think I will continue with Dalteparin until I see them again on 28 February.


As you know the recent RAPS trial advised that those that needed an INR above 3 should not be placed on Rivaroxaban. Do you think you would be on 3 or above if you were placed on warfarin and was there any reason why you were not transitioned from LMWH onto warfarin after your PE which is the normal protocol?

I had a Xray done of my hands after I developed trigger thumb in both thumbs and it showed early osteoporotic changes. My Rheumatologist at the Lupus Centre advised I came off LMWH and consulted with Haematology who suggested a warfarin substitute (which was strange given my allergy to warfarin). I did some research. First I was told by a number of people in radiology that X-rays of hands are not conclusive evidence of osteoporosis so a DEXA of hips was a more conclusive way forward and that again was good. I stayed on LMWH! Funnily enough both trigger thumbs spontaneously disappeared! So Im glad I stuck to my guns.

My advice to you is to look for the reasons why you have developed Osteoporosis. Do you have a thyroid problem? Do you have Celiac Disease? Any other conditions other than Lupus or did anyone in your family have it like your mother or an aunt? If you can get to the bottom of whats causing the problem then you may not have to change your anticoagulant. If you don't you may well have changed it for nothing and still not got any closer to improving whats at the root cause of your real issue.

I hope you can work things through with them at the end of Feb.


> As you know the recent RAPS trial advised that those that needed an INR above 3 should not be placed on Rivaroxaban.

This is not actually true - the RAPS trial result actually says nothing about those needing high-intensity anticoagulation, other than that they weren't in the study and therefore further research would be required. Same for those with arterial thrombosis.

Outwith the trial, after publication, various people have advised that the trial does not apply to those with INR >3, but that is very different to saying that the trial advised against it, which it does not.

There is a logical and intuitive reason why Rivaroxaban should not be used for INR>3 - since RAPS showed equivalent performance to warfarin at 2-3, logically it would be inferior to warfarin at 3-4 (unless a higher dose was used, but no higher dose is tested or licensed). However, drug effects in the human body are seldom linear and often illogical and counter-intuitive. Warfarin at 3-4 has been found to perform no better than at 2-3 in multiple trials with APS (cited in the RAPS write up and current UK APS guidelines) - non-linear, illogical, counter-intuitive and quite possibly wrong - but there is no clinical trial that refutes those results, no trial evidence showing that 3-4 is better, none. Yet many recommend INR >3 for APS (and for many, it appears it works better - we just don't know how to select the patients).

Conversely, given that RAPS used a lab-test surrogate outcome, there is no logical reason why the test would behave differently and therefore that the outcome would be any different for arterial clotters, none (if anyone has one, please speak up) - but because arterial clotters were not included in the trail, the results do not apply to them and hence people recommend against it. Even if logically, intuitively, the results would have been exactly the same for them.


Hi Ray46 - perhaps I worded it incorrectly, however this directly from the study under "Discussion" page e435, first column, "We caution, therefore, that our results are not applicable to patients with antiphospholipid syndrome and venous thromboembolism who need greater than standard- intensity anticoagulation or with stroke or other arterial thrombosis." As "greater than standard" means >3, than I think that is what they were advising.

Additionally, at some point on this Forum I have posted either a tweet of an article from Prof Beverly Hunt (and who would argue with her), that no one who has had an arterial clot or needed an INR >3 should be placed on this DOAC, as it has never been trialed and therefore the safety of it has not been tested. Trials did in fact start for this group of patients, but I believe had to be abandoned due to bad outcomes. I may be wrong on that but again I think it is on this Forum if you would care to do a search.


In fact Ive found it for you!


So, if I am, say, a single-positive stroke patient:

RAPS trial (successful) - doesn't apply to me as stroke is arterial

TRAPS trial (triple positives, failed) - doesn't apply to me as I am not triple +ve

So we are left, again, with absence of evidence (which is not evidence of absence).

Prof Hunt's statement makes sense from a strict evidence-based-medicine position, but it presumes that there is an alternative which does have evidence. Problem is when you start dividing APS patients into subgroups there is very little evidence for _anything_, and warfarin evidence contradicts (some trials show no better than aspirin, some claim to show 3-4 INR is superior, others that 2-3 is superior). Doctors with different opinions tend to point out flaws with the trials that they disagree with, but if you take out _all_ the flawed trials you are left with... no efficacy evidence. On the other hand we do have evidence (large scale general, but RAPS papers state it as applicable) that NOACs are much safer than warfarin, and the RAPS results also show improved quality of life compared to warfarin.

But what I really would like to know is if Prof Hunt statement is based on knowledge or belief that the lab tests used in RAPS would give a different result (non-equivalent performance) for an arterial clotter - because those tests are not a million miles away from the INR test, and if the INR test behaves differently for arterial clotters then we have a problem.

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Ray46 I cant answer that question but what I would say is that Prof Hunts experience and exposure to patients is second to none. Therefore even if there is now specific trial outcome that dictates protocol, she would have enough clinical experience to know what would best fit a particular patient.

The problem is Ray that sero-negative patients are not always sero-negative, they may be on one day but not on another. Single, double or even triple positive patients, unless they repeatedly test them over a long period of time, tend to find those tests change. That is why it has been said on here and else where that classification criteria is good for disease classification but not for clinical diagnostic purposes. Patients are individual and its clear this disease affects us in many different ways - look at identical twins who can have the same or similar symptoms and one can be triple positive and the other negative!

Sometimes clinical judgement and experience is all that we have, used with information like trials that can point in the right direction. At the end of the day it still won't suit everyone.


Are you under one of our recommended specialists? They can be found on our charity website: Also under 'pinned posts' over on the right hand side of our forum, you need somebody who fully understands the issues of medicating a patient with Hughes Syndrome/APS, this is also helpful for your own GP. Make sure also that your Thyroid is adequately tested, unfortunately often it is not which is why a lot of us order our own panels of tests on line, rather than being told we are fine, due to the narrow testing, also your B12, Folate, Ferritin and vitamin D. MaryF


I agree with SBM...i would question your healthcare provider about this... maybe he isnt current, no offense meant.


Thank you, I will definitely have a robust conversation with them.

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I've been on Rivaroxaban 20mg + 100mg for a few years now and for me it was a miracle. I would query the 15mg dose you are given -is this the 2 week starting dose? My Haem has me on this med as he said a small dose for APS is like a small dose of Warfarin-doesn't keep you adequately anti coagulated. I couldn't keep a stable INR and also clotted on LMWH. Also it's a lot easier when travelling long distance 10+ hours and different time zones.

I do stress this is what is working for ME and has kept me well. Had a bone scan also recently which showed slight osteopenia and just advised to keep Calcium intake a bit higher-cheese yoghurt salmon etc. I see my Haem 6 monthly and Rheumy 4 monthly and both are great and advise me to come sooner if I have a problem.


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