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

Opinion piece by Resia Pretorius

Could microclots help explain the mystery of long Covid?

https://www.theguardian.com/commentisfree/2022/jan/05/long-covid-research-microclots

 

I am worried about how much of the microclot theory I am seeing on social media as it's being presented as fact. I hope someone can replicate these findings at least or get some clarity as soon as possible. A lot of people are speaking with their doctors about this as though it is fact, and I'm worried about what happens in the longer term in terms of credibility etc if it all falls apart.

 

https://twitter.com/user/status/1478600481165434883


?

 

It might play a role in some cases, but it cannot explain much of the pathology.

 

Those look like usual bits of dust and chipped plastic.
An ' expert' who is prepared to agree that these look like micro-clotting is pretty hard to take seriously.

 

Indeed - which comes close to 'diagnosis by Tweet'.

Resia Pretorius is part of a Health start up https://afrikanheroes.com/2021/10/15/south-african-healthtech-startup-biocode-raises-473k/

"A collaboration between SU’s Physiological Sciences Department and the Department of Electrical and Electronic Engineering resulted in the launch of the company. Professor Resia Pretorius, Professor Anna-Mart Engelbrecht, and Professor Willie Perold are among the startup’s researchers and founders.
BioCODE is working on a quick test to detect inflammatory chemicals in the bloodstream."

A note for anyone looking for details of Biocode (.co.za) - perhaps just a glitch but my Anti virus software puts a full block on the Biocode website as a 'known threat' which is not very reassuring.

 

Mine does too. But annoyingly it never tells me why any particular page is blocked.

 

Me too. I think many tech start ups are required to big themselves up in order to get funding and sometimes they make over blown claims. I hope that's not what's going on here. I guess we'll have to wait and see. I'm happy for them to go ahead and do the research but I'm not ok with them taking people's money at this stage or encouraging hope that may not be entirely justified yet.

 

As always, this is N=1, so take it for what it’s worth, but a few thoughts:

I was diagnosed with ME/CFS in 2002. In 2006 I presented to the ER with severe upper left abdominal pain that was eventually diagnosed as multiple pulmonary emboli. I had no hx of international travel, surgery, DVT, or anything that would normally provoke at PE. The hematologist did a thorough work-up but couldn’t find a reason for why I had the PE, but did recommend lifelong anticoagulation (I did have DVT & PE after knee and ankle surgery in 1998). So I’ve been on Coumadin and then Xaralto since then but it’s had no effect on my ME/CFS symptoms (or, rather, I’ve continued to deteriorate to the severe form I have now but I doubt that’s due to anticoagulants).

Where it may be a little more complicated is what happened directly after the PE. Despite two days of severe pain and little sleep, the day after I was diagnosed, I actually felt significantly less flu-like than I usually do, which lasted for about 10 days or so. There were a few things going on at that point.

1.) When I initially presented to ER, they did an abdominal CT scan which showed stool stuck in my transverse colon. They simply diagnosed me with constipation and sent me home. Unbeknownst to me, a radiologist took a second look at my scan (and is my unsung life-saving hero as a result!), noticed that the bottom part of my lungs were in the picture and saw what he/she thought was a PE in my right lung prompting a frantic call back from the hospital telling me to return immediately. They were reticent to pump me full of radioactive dye less than 24 hours after doing so for the abdominal CT scan, so checked for DVT with ultrasound but there was nothing. So they started pumping me full of saline to get me to pee a lot and then did the lung CT scan (which showed I had multiple clots in both lungs and so much blood and fluid in my left lung that it had swelled to the point that it was shoving my diaphragm into my colon and keeping stool from passing — I told those mofos the day before I was in a LOT of pain!). What this long story means is that I was getting a lot of saline, which, of course, has been a long-standing treatment in ME/CFS. This has always seemed like the most likely reason for the improvement in my flu-like symptom.

2.) That said, I was placed on the standard treatment of Lovenox for 10 days or so, which correlates with the improvement in symptoms. There are people such as Ken Lassensen who argue Heparin is an effective treatment for ME/CFS and I remember in the early 2000s there were those who swore Heparin made them feel better. I’m very skeptical of these claims but I try to be agnostic. Note: I have been tested for autophospholipid syndrome multiple times and always test negative.

3.) Like others with ME/CFS, I find that opioids not only reduce my pain but also reduce my flu-like symptoms (that icky weak sick feeling, brain fog—it actually improves cognition for me, and generally improves my ability to move) and that effect lasts much longer than the half-life suggests it should. Pain relief will last for the expected period (say 4-6 hours for short-acting morphine) but the sickly feeling will be reduced for a day or two. Once the PE was suspected, I was given a LOT of morphine in the hospital and sent home with a few days of oral Dilaudid. Again, this seems remarkably unlikely for the improvement, especially given the time period of 10 days, but given what I’ve observed over the years that I’ve been on opioids for pain, it's a very remotely potential variable.

I’ve been following the micro-clot findings with a great deal of interest given my clotting issues though my own experience with anticoagulants leaves me a bit skeptical that they will be a good treatment.

 

Not long after I was first diagnosed, I remember reading an article about a woman who claimed she vastly improved on Heparin (which would be around 2000).

Being new to the illness (and naive), I thought it would only be a matter of time before studies demonstrated the benefits and that we would all soon be on Heparin. I was surprised at the time that none of this eventuated. (And people wonder why long-term ME/CFS sufferers are cynical about the latest treatment fad.)

The more things change, the more they stay the same.

 

Was the saline given to you in a drip? I always assumed that was done to increase blood volume, not make people pee, but then I suppose the kidneys excrete the extra after a while.

I read this link quite some time ago, but it has been deleted from its original home and is only available on the internet archive now :

https://web.archive.org/web/2015051...ealth.com/library/showarticle.cfm?libid=16085

I got the original link from here :

https://www.healthrising.org/treati...onic-fatigue-syndrome-mecfs-and-fibromyalgia/

 

Yes.

@Jonathan Edwards has mentioned in his skepticism of the use of saline as a treatment to build blood volume that saline would simply make people pee. That was clearly the reason the ER used it for me.

 

I assume that it was meant to flush the CT contrasts and radio tracers off her system; those can be hard on the kidneys, so it is likely that the doctor wanted to make extra sure all of that would go away. while i am not Michelle (obviously) my background is nursing so i know that side well (that is until 2009)

 

That was precisely what they were doing.

 

Subsequent to Dr Amy Proal, Prof. Carmen Scheibenbogen has now joined this international collaboration. Established ME/CFS researchers adding expertise in viral persistence and autoimmunity domains. We might also hear preliminary findings From Prof. Pretorius's micro-clot evaluation of ME patients in South Africa in a few weeks.

https://twitter.com/user/status/1486641681818656768

 

I finally have gotten down to the original paper. What can you say about representative slides? The cohorts had dramatic gender differences, most importantly the long covid group is large majority female while acute covid is majority male. So even the objective serum measures are hard to interpret. I also wasn't clear if the controls were subjected to only 1 trypsin degradation or both. That would seem not to make sense to me even if there was no visibile pellet.

I guess the results kinda seem underwhelming even if taken at face value. It seems sloppy to throw the single dude's "case report" slides in the middle of this paper. Also, it's worth noting the COI is NOT noted in this paper, and is highly relevant. Perhaps it was formed in between this paper and the treatment paper, about 3-4 months later.

 

A further announcement, with Prof. Akiko Iwasaki also joining the collaboration.

https://twitter.com/user/status/1486944983424843777

 

Can you please say more about that? What did I miss?