Opinion Challenging the current hypothesis that thrombosis is responsible for the post-COVID-19 condition, 2024, Carson, Davey Smith, Garner et al

RaviHVJ

RaviHVJ

Senior Member (Voting Rights)
Abstract:

People with the post-COVID-19 condition suffer symptoms that persist beyond 12 weeks following acute COVID-19 infection. Fatigue, shortness of breath, and cognitive dysfunction (“brain fog”) are common. Scientists, clinicians, and patients debate the pathophysiology. One pathophysiological hypothesis is that prothrombotic changes associated with acute COVID-19 persist, causing clots that lead to symptoms. This theory, arising from a research team in South Africa and supported by a paper in Nature Medicine, has been widely disseminated on social media and entered the public narrative as a cause of the post-COVID-19 condition.

We describe the development of this theory, examine the findings of a Cochrane review that critically appraises the “microclot” beliefs, and critically appraise the influential study relating clotting biomarkers to cognitive deficits. We conclude the inferences for the hypothesis are not based on evidence, unlicensed use of antithrombotic medication is not justified, and apheresis should not be considered outside of a well-designed clinical trial.

https://www.sciencedirect.com/science/article/pii/S2475037924001316

Study authors include Paul Garner and Alan Carson
 
So Garner and Carson are essentially using the microclots literature as a way to rubbish the biomedical literature around Long Covid writ large. Very telling that they write "Furthermore, there is a body of research in neuroscience, psychology, and evolution that explains the presence of PCC in those not severely unwell initially," citing the Oslo Fatigue Consortium's position paper. The standards of evidence they require from biomedical research are orders of magnitude greater than those they require of research supporting their own pet theory.

Also I'm in no position to evaluate the microclots literature, but their critiques of it seem a little weak and forced.

"The team found that the phenomenon termed “microclots” were not clots but amyloid fibrin(ogen) particles" - has this ever not been utterly obvious? There's a reason they applied a new term to the particles rather than calling them clots.

"These were also found in the studies appraised in healthy individuals, in patients with acute COVID-19, and in persons with diabetes" - this has also been known for a long time. The question isn't whether they're found in healthy people and people with other disease states, but whether there's a correlation between microclots and Long Covid.

"There was no evidence linking the amyloid fibrin(ogen) particles to the pathophysiology of PCC" - it's still early days in research into Long Covid and microclots. As far as I can tell, researchers are still at the stage of working out how best to identify and quantify microclots in an objective manner.

It just reads as an oversimplified hit job.
 
RaviHVJ said:
As far as I can tell, researchers are still at the stage of working out how best to identify and quantify microclots in an objective manner.
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I think Garner and Carson are on solid ground in their critique of 'micro-clots' which aren't even micro-clots, they are precipitates in test tubes. I think the researchers are still at the stage of trying to find out whether they have measured anything real to be honest.

The story around micro clots is that they obstruct small blood vessels in living patients. But we know what obstruction of small blood vessels in living people looks like and we don't see that in Long Covid, so it seems a pretty dead horse to flog.

Their support of the Oslo Fatigue Consortium is obviously absurd, but that is a different issue.
 
Jonathan Edwards said:
I think Garner and Carson are on solid ground in their critique of 'micro-clots' which aren't even micro-clots, they are precipitates in test tubes. I think the researchers are still at the stage of trying to find out whether they have measured anything real to be honest.

The story around micro clots is that they obstruct small blood vessels in living patients. But we know what obstruction of small blood vessels in living people looks like and we don't see that in Long Covid, so it seems a pretty dead horse to flog.

Their support of the Oslo Fatigue Consortium is obviously absurd, but that is a different issue.
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I was hoping you’d chime in - I have 0 scientific background so have never known what to make of microclots. Always good to see what an expert makes of the evidence :)
 
Odd way to spend their time. There are pretty much no real arguments here, so I don't really know why this commentary exists other than to add a citation to their Cochrane review and their Oslo op-ed. Given the authors, however, this actually makes the hypothesis more interesting. They just have a special talent of being wrong, to the point where if they think something is wrong, it's more likely to be right.

But really there are no arguments here. This has been researched by a handful of people, and I'm pretty sure that there has been more attention devoted to dismissing it than at researching it. I almost never see this mentioned in the patient community other than as a research hypothesis, one of many. There are people willing to try anything, and that shouldn't be surprising given the level of disability, but the hypothesis isn't based on treatments, so it's mostly irrelevant here.

To actually cite themselves as evidence of a preferred alternative psychosocial explanation is pretty laughable, in part because of how completely hollow their entire argumentation is, far weaker than even the microclot theory, but also the fact that it's framed entirely as "fatigue syndromes", which is the majority of LC patients but far from all. And simply ignores PEM/PESE, which is even more common and the most disabling aspect, something they're still in denial of.

But at least this keeps them busy, away from their usual nonsense. So I guess that's good. The difference between the patient community and them of course is that we want to know what's really true and will accept the outcome of rigorous scientific research, in part because there are many hypotheses, while they have only one model, the same Freud came up with 150+ years ago. But that hasn't happened yet, because it is researched by a handful of people, less than the number of therapists an average rehabilitation clinic providing useless alternative medicine that is harmful to many.

I don't think they understand that in science, hypotheses aren't challenged in a debate, they are falsified by the scientific method. So frankly I welcome them doing that. In fact stand on every street corner with a trumpet and scream it loud. Nobody cares.

In fact, I think this deserves a meme:

microclot.jpg
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rvallee said:
I almost never see this mentioned in the patient community other than as a research hypothesis, one of many. There are people willing to try anything, and that shouldn't be surprising given the level of disability, but the hypothesis isn't based on treatments, so it's mostly irrelevant here.
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I wouldn't be so sure. The big problem with ME/CFS is that even the most mainstream biomedical inclined physicians specialising in it have a tendency to pick up fringe ideas like this. So, currently, people are being treated with triple anticoagulant therapy on the basis of 'micro clots' and by physicians who people with ME/CFS may have to rely on as their best medical allies. It is an uncomfortable situation.
 
Pretty thin.
Where is the pathology if this is going on?
Where are the physical signs of embolisation?- rash, nail fold infarcts....
The bright dots in muscle are almost certainly nerves in my opinion, not amyloid.
And so on.
 
Merged thread

Fibrinaloid microclots in long COVID: assessing the actual evidence properly
Douglas B. KellM. Asad KhanEtheresia Pretorius

We have read with interest an opinion piece on fibrinaloid microclots in the plasma of patients with long COVID and related diseases.

In the article by Hunt et al., the authors first claim that “We initially critically appraised the research studies that had led to demand for apheresis treatment” (citing their Cochrane review). We wish to point out that several of the authors of that paper and one of its reviewers (Carson) are now authors of the article by Hunt et al., while Garner is a Cochrane Editor. Cochrane has thus far refused to append an online comment, where we point out erroneous facts (however, the rebuttal can be found at http://dbkgroup.org/dealing-with-clots/). Repeating erroneous facts, when the authors know them to have been rebutted, is poor practice.

Hunt et al. then claim to “describe the development of the {microclot} theory,” a claim that unfortunately bears no relation to the true version but rather represents their opinion of the theory. Readers might instead imagine that those of us who actually did develop the theory might be best placed to discuss its development accurately. The microclot theory is airily described as “arising from a research team in South Africa” when in fact the joint program led by Pretorius and Kell is of over 10 years duration and has produced more than 60 joint peer-reviewed publications.

We also wish to point out the comment “We conclude the inferences for the hypothesis are not based on evidence….” We are not quite sure if the authors suggest that there are no such entities as microclots (ie, that we made it up), whether they do not believe that microclots have an amyloid nature, or if they are indeed upset that we call the entities “microclots.” Our first definition of the term “microclots” in the article by Pretorius et al. was given as anomalous (amyloid) deposits (microclots).

As with all new discoveries, there might be different opinions. Rather than sitting on the side line and writing opinion pieces, we should rather come together as researchers to determine the nature and content (by further robust experimental design) of this novel entity and in fact debate the terminology to be used if there are disagreements.
LINK
 
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You are correct. It was discussed here

I only searched the titles so I didn't see it.

Threads now merged
 
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There was also a letter to the editor responding to the rebuttal - "Reported particles are not blood clots, so anticoagulant drugs are not a plausible treatment" (18 October 2024). Sadly a lot of LC patients will dismiss the general critique due to the authorship; it would have been better coming from a group of respected haematologists rather than Garner et al.

Link | PDF
 
It is a pity that they have not recruited some haematologists.
The main objection to the story is that the lumps in the pictures cannot have been there in the patients because they would have been centrifuged out. Whether or not you call them clots is probably less important.

It intrigues me that haematologists have not said more about this. When I spoke to an eminent haematologist friend they seemed sceptical but perhaps not wanting to be seen to be saying so in public
 
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