The micro-clot finding in Long Covid — implications for the possible aetiology of ME/CFS

I think he means this (from a different preprint paper - EP=Pretorius):

Yes there is potential Competing Interest. MK is a non-executive director and shareholder of Gknowmix (Pty) Ltd. EP is the managing director of BioCODE Technologies. The other authors have no competing interests to declare.
--​

BioCODE Technologies: We develop point-of-care smart sensing solutions that detect novel circulating inflammatory molecules in the blood. These molecules are present during the very early stages of disease.

We combine and synergize concepts from the fields of engineering, physics, biochemistry and physiology to develop innovative inflammatory biomarker sensing solutions.​

 

Thank you @Wyva

Can anyone comment on the risk of bias for this particular situation?

 

I haven't watched this yet.

https://www.youtube.com/watch?v=ZFPleh6z7io

 

Dr Satoshi Akima FRACP 『秋間聰』 on Twitter: „There has been a lot of talk about microthrombosis (“microclots”) in #LongCOVID, along with the usual knee-jerk reactions about anticoagulation. But that may be mistaking effects for causes. A thread..."

https://threadreaderapp.com/thread/1515143282636247041.html

(Haven't read yet, neither through the forum thread nor through the Twitter thread, but seems interesting. )

 

As I mentioned in the other COVID thread (https://www.s4me.info/threads/the-b...arch-and-treatments.14022/page-83#post-414902)

 

Moved post

My own comment relating to blood clotting is a personal story that rests on a comparison of my ME symptom response to long journeys. I realise that it is only my story but it has given me cause to wonder about blood clotting in relation to ME.

I am currently in Cornwall just moving from a state of complete collapse after travelling down by car (split over 2 days) last Thursday and Friday. I missed my birthday on Saturday and was completely unable to respond to phone calls of good wishes. This type of crash has been my response to the journey down here for the last several years.

I can however cross the Atlantic to New York City 3000 milies away without any crash and have been able to do this for the last 8 years (before covid stopped the visits) sometimes more than once a year. This involves all the airport waiting and queuing ( although I have been in a wheelchair for the last few years), an 8 hour flight in squashed seats because we travel economy ( occasionally we are lucky to get extra seats where I can put up my legs) and waiting to get through the US security. I never sleep on flights and I walk frequently to avoid blood clotting so the flight isn't restful. I also have to handle a 5 hour time difference which makes the day a very long one but I am still able to have a catch up with my son. I am tired the following day but not crashed and I can do some 'paced' sightseeing over the following few days.

It is the difference in the effect of the journeys that really perplexes me. One difference is that for the transatlantic journey I am prescribed fragmin. I can't prove it makes the difference but it seems a strongly possible factor when it is repeated time after time. I have factor V Leiden, a blood disorder which increases the risk of blood clotting so I am prescribed low molecular weight heparin which I inject the day before and on the day of flying and again for the return journey. It thins the blood.

"Since early 2020, we and other researchers have pointed out that acute Covid-19 is not only a lung disease, but actually significantly affects the vascular (blood flow) and coagulation (blood clotting) systems." Resis Pretorius.

I will be very interested to see what emerges from this research. I'm not a scientist but hope that those who are can find something of interest.

There would be a way of testing myself further if I tried heparin before the car journey and omitted it before the flight but I doubt if I'd get a prescription for heparin for the car journey, and it shouldn't be omitted before a long flight!

 

moved posts
scienceNews.dk Microclots explain why 1 in 10 people continue having long COVID symptoms

quote:
A few years ago, researchers discovered that fibrinogen, which when blood clots usually accumulate in large polymer networks called fibrin, can occasionally clot into an anomalous amyloid form of fibrin, somewhat in the same way as amyloids do in Parkinson’s disease. This amyloid form of fibrin creates these microclots, which are somewhat resistant to the normal means of proteolytic removal and may lead the immune system to mistakenly produce autoantibodies – in a process that leads to inflammation. This vicious circle bears similarities to post-viral syndromes and to myalgic encephalomyelitis/chronic fatigue syndrome.

“These microclots are more or less easily detected in blood plasma using the thioflavin T stain and a simple fluorescence microscope and are clearly present in up to 30% of the people who have been affected by COVID-19. Although the symptoms of long Covid are multifarious, we believe that these amyloid fibrin microclots can explain symptoms such as breathlessness, fatigue, brain fog, tissue damage, inflammation and coagulopathies,” says Douglas Kell.

 

And the other 9 out of 10 people who have LC?

 

https://twitter.com/user/status/1534604951434960900


https://twitter.com/user/status/1534612098956857348

 

https://twitter.com/user/status/1534627222748815368

 

https://twitter.com/user/status/1534628098339131395

 

I've seen a few references to "platelet hyperactivation" in recent days. What does this actually mean? And would a person with this problem have high levels of platelets?

 

@Arnie Pye

This might explain it a little better.

 

During the 3rd Long Covid Coalition Congress: Thrombosis and Coagulation (YouTube), there was a presentation by Martin Kräter. He is a post-doc at the Max Planck Institute for the Study of Light and works on microfluidics and high-throughput single-cell deformability analysis.

This congress was a 3 hr plus session, with presentations of varying quality, so if interested please jump directly to Martin's talk at 27:00 which runs for 25 mins. At 41:25 he shows something which they think is a real structure, and are assessing to see if it could represent a microclot.

 

This is something I mentioned to Bupesh Prusty when he was making claims about blood cell deformability. Individuals who are less active tend to have slower turnover of RBCs, so an explicit measure of RBC age needs to be measured to prevent confounding.

 

I don't know how Martin prepares the blood cells for analysis, but it's likely closer to whole blood than the spun-down-at-high-g platelet-poor plasma in the Pretorius papers. I would expect the latter are more prone to aggregation and artifactual enlargement.*

I presumed the two cells adjacent to the right in that bottom-right section are RBCs. So that object looks approx 3-4x in width and length. They do look reminiscent of the ThT-coated green bodies, in terms of shape and 'wispiness'. I hope he's able to analyse it further.

* Having said that tho, some of the patients are appreciating that the microclots being shown now are seeming substantially smaller than originally. Hard to know if this is a valid observation, but would be interesting to know if these are longer term LC patients, in whom hypercoagulabillity is normalising over time, compared to earlier samples in more recent LC patients.

https://twitter.com/user/status/1535692591395745792

 

@Hutan

And yet David Berg, owner of HEMEX lab, touted that 80% of ME patients tested positive for hypercoagulation.

My doctor attended one of his workshops in Arizona in early 2000 and it was all the talk that HHV6 was the culprit provoking hypercoagulation. David Berg even diagnosed me based on what my doctor told him regarding my test results