Blood clot drug totally ineffective as post-Covid treatment, research finds. Results from UK-wide trials on anticoagulant Apixaban

Its always good to have a spare explanation of one fails!!
Since it doesn't seem to have much to do with Long Covid it might have been better to keep the powder dry.

 

From the commentary above, I take it that this morning's breathless headlines, like this one in the Guardian, are highly misleading:

Covid blood-thinner drug treatment dangerous and does not work – study
https://www.theguardian.com/world/2...g-treatment-dangerous-and-does-not-work-study
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To breakdown the issues with this headline specifically:

[Covid blood-thinner drug treatment] ---> the blood-thinning drug included in the study does not actually address the hyperactivated platelets caused by COVID-19.
[dangerous] ---> what are the dangers, specifically? Are these dangers also found in other medications that DO address both hyperactivated platelets and microclots?
[and does not work] ---> do we have any studies on the efficacy of other anti-clotting medications that address both hyperactivated platelets and microclots?

 

As stated above, this has very little to do with long covid, so I don't think this damages the blood clotting hypothesis for LC (which I remain quite skeptical about).

 

I think you are misinterpreting. The headline, article, and paper are about one particular drug, not blood thinners / blood clotting in general, or other potential mechanisms, such as platelet activation.

 

Dr Resia Pretorius has had the protocol including anti clotting and anti platelet since the beginning when they analysed the make up of the clots (https://europepmc.org/article/PPR/PPR436609).

Its a bit surprising I think to not see some benefit from half this protocol on its own however.

 

Article now posted as preprint: https://www.medrxiv.org/content/10.1101/2022.12.07.22283175v1

So a half-therapeutic dose for a couple of weeks showed no benefit and this was framed as "Blood clot drug totally ineffective as post-Covid treatment". Wow.

 

I am hoping people here can help me understand more about the microclots, anticoagulants and ME...

I know people with ME who have been on anticoagulants for months to years and they've had no change in their ME (for better or worse). Not all of these people are on the same class of blood thinner.
In the microclot theory, at what point should improvements be noticed and to what degree?

 

We don't have enough data yet. The "microclot" theory is unproven/not accepted. There is strong evidence of hypercoagulability in LC, and cardiovascular events are clearly significantly increased post COVID, even in those without symptoms of LC. There is some evidence that hypercoagulability is present in ME also.

If we were to accept this as true in LC and ME, how long does it stay true? The longest anyone can have had LC is not quite 3 years, versus 30-40+ years for ME in many cases. Does hypercoagulability become less of a feature, only present in the onset years? Is there survivorship bias when looking at long-term ME?

Regardless, I think your comment about people experiencing no change in ME suggests that hypercoagulability is not the fundamental cause. It may well be a downstream effect in some, many or even all. Treating it may be helpful in some, but we don't have the tools to guide this adequately.

However, your friends that have been on anticoagulants (presumably for reasons unrelated to ME) are unlikely to have been on both anti-platelet and anticoagulant treatments. As noted above those treating "microclots" have for the last 18 months proposed a two anti-platelet and direct oral anticoagulant regimen. Studies needed.

While I think hypercoagulability is going to be very important, we need to properly understand the interlinked immune dysregulation, immunometabolic and immunothrombosis aspects. I think the answer to this disease — when it comes — is going to be hard to put into just a couple of sentences.

 

Thank you very much

 

I think this may be misleading.

There is good evidence for an increase in clot-related events for several months after Covid. It is likely that a relatively high proportion of the people involved have residual ill-health due to lung damage just on the basis of clotting being a common comorbidity of being ill.

But I think it may be unhelpful to relate this to 'Long Covid' in the sense of suggesting that clotting events might be the cause of felling ill in any way like ME.

I think there may be a confusion a bit like the confusion between osteoporosis and back pain. Osteoporosis produces fractures that give episodes of acute pain chiefly in the thorax. It has nothing to do with the common chronic lumbar back pain that most people get. Osteoporosis is, in itself completely painless.

Similarly, whatever the cause of more frequent clots after Covid is it is very likely completely asymptomatic most of the time - maybe a rise in circulating fibrinogen or something.

So no, I don't think there is any evidence for any link between clotting and Long Covid in the sense that is of interest to people here. I am not aware of any reliable evidence for increased clotting in ME.

 

Link?

 

Answered in the negative as above. I thought we had some, but nothing reliable.