Is Apheresis an effective treatment for Long Covid and ME?

[Martin aka paused||M.E.]

I mean for example tilting the team towards trying more of the drugs that effect clotting factors

What I can tell you is that Pretorius said that if it’s chronic (LC) it’s too late and normal anticoagulants don’t help (like heparin shots). Amy said that it is to extrapolate to ME. So I think that wouldn’t be successful. I will talk to Jaeger again. She seems to be very interested in my case (EV infection and trajectory). I will try everything to get this apharesis. Otherwise last resort is Valcyte and we all know how dangerous this try would be.

 

[junkcrap50]

Dr. Kahn, from the BBC interview, said that these apheresis treatments has significantly improved his Long Covid. But he says that he's not entirely recovered. Do we know what his plan is to do next? Is he going to continue doing HELP apheresis until he's cured? He's already done 13, I've heard.

 

[Martin aka paused||M.E.]

Dr. Kahn, from the BBC interview, said that these apheresis treatments has significantly improved his Long Covid. But he says that he's not entirely recovered. Do we know what his plan is to do next? Is he going to continue doing HELP apheresis until he's cured? He's already done 13, I've heard.

The only thing I know is that he will return to UK soon and wants to visit me before. But I didn’t ask him how many rounds he’ll do… No he is not cured but much better.

 

[ChookityPop]

Is there an HELP apheresis Clinic near Kiel in Germany?

 

[aquariusgirl]

What I can tell you is that Pretorius said that if it’s chronic (LC) it’s too late and normal anticoagulants don’t help (like heparin shots). Amy said that it is to extrapolate to ME. So I think that wouldn’t be successful. I will talk to Jaeger again. She seems to be very interested in my case (EV infection and trajectory). I will try everything to get this apharesis. Otherwise last resort is Valcyte and we all know how dangerous this try would be.

Martin..to be clear.....the implication here is that Amy Proal thinks HELP APHERESIS could be beneficial for ME/CFS patients?

 

[MonkeyMan]

Martin..to be clear.....the implication here is that Amy Proal thinks HELP APHERESIS could be beneficial for ME/CFS patients?

Good question. For what it's worth, Dr Jaeger seems to think so. Here's an excerpt from this interview with her (at 11:25) -

Interviewer: Because the symptoms of Long COVID are similar to the symptoms of ME, and I know there's been a bit of joined-up cooperation with the groups representing both sets of patients ... Are you able to say at this time, is that too big a stretch, is that putting two plus two and getting ten? Do you think there is a link between the treatment, that we could see given to ME patients as well?

Dr Jaeger: Yes, of course! I think there is a big overlap, and we will try this also. And I have already tried, and it works. So, we just, I think you can cure everybody with vessel diseases from this disease, but now we just try to focus to enlarge the evidence. So we're combining it now with MRIs, and lactate measuring, and other stuff to convince and make a PET scans before enough to help treatment and so, I think the world needs HELP machines.

 

[perrier]

Here's an issue I don't get: OK Covid folks have micro clots. They have not been ill that long, comparatively. But folks with ME have been ill for years and years and years. and blood does regenerate and so does tissue. So, do they too have micro clots? After 10-15 years of illness. Then the question becomes: what is driving the body to make these micro clots, assuming this thesis is correct. Some initial virus? Still not having left body? or what? Any help with this appreciated. Thanks.

 

[SNT Gatchaman]

Here's an issue I don't get: OK Covid folks have micro clots. They have not been ill that long, comparatively. But folks with ME have been ill for years and years and years. and blood does regenerate and so does tissue. So, do they too have micro clots? After 10-15 years of illness. Then the question becomes: what is driving the body to make these micro clots, assuming this thesis is correct.

They appear to be showing micro-clots in LC patients that are 12 months or more in. This suggests that the micro-clot process is long-lived — so, potentially decades. As an aside: are these the "something in the blood" Ron Davis found?

So the question becomes are they self-perpetuating or is the factor that created them persiting and continuing to create them. As I read it the Pretorius team seem to be suggesting that the micro-clots contain inflammatory mediators that are protected. The clots are resistant to breakdown but the mediators presumably still take effect, causing inflammation in the micro-circulation, affecting vessels and circulating cells. They seem to be stating that the balance shifts away from fibrinolysis, so that clots persist / continue to be created from fibrinogen. Removing the clots allows the balance to shift back to fibrinolysis and the microclots are resolved over time.

New RBCs could continue to be damaged: by effectively smaller or more irregular capillaries; or by the inflammatory mediators in the micro-clots; or by the increased oxygen extraction as they transit the capillary bed more slowly.

This is all a very attractive concept. There are many reasons why ME could be a disease of the micro-circulation and that might explain its "invisibility" to standard clinical investigative techniques. Sex-differences in the macro- and micro-circulation are now understood that could favour the female predisposition. Children tend to recover more frequently — is this because children have more dynamic potential in recovering their micro-circulation, both in map heterogeneity, but also in capillary diameter (vs RBCs)?

Disease onset could be a feature of the burden of micro-clots initially formed (immune over-response?). Genetic predisposition and symptom range could even be due smaller capillary diameters in some or all body tissues.

There is much to investigate prompted by the micro-clot finding in LC patients that could be relevant to ME. Getting rid of the clots safely sounds like priority 1 though: initially mechanically, then maybe pharmaceutically.

 

[Breagjam]

This may have been stated elsewhere, but did Dr. Kahn pretty much meet all of the criteria for ME? (Within his long Covid symptoms)

 

[SNT Gatchaman]

This may have been stated elsewhere, but did Dr. Khan pretty much meet all of the criteria for ME? (Within his long Covid symptoms)

I'm pretty sure he has been open with his descriptions of POTS / orthostatic intolerance, PEM, brain fog, sensory hypersensitivity and sleep disruption on previous videos and Twitter. Not sure if he's commented on GI / GU symptoms, infection, chemical sensitivities etc. Sounds like he at least qualifies for atypical ME.

 

[sb4]

I have tried googling to find out the covid microclot diameter in order to compare it to Ron Davis "something in the blood" diameter range but I have been unsuccessful.

I found that microcapilaries "They have an inner diameter of 0.5 µm and an outer diameter of 0.7 µm".

When searching for Rons Something in the blood I found this forum post "I don't think Ron Davis has given a size estimate other than to say "it's big." My impression when he talks about breaking it apart and seeing what it's made of is that he's talking about a "particle" made up of many molecules as opposed to just one large molecule. "

A blood cell is apparently "6 - 8 μm" in diameter. A clump of RBC would be more than enough to block off some of the smaller capilaries. Just guess it depends on how big Ron is refering to.

Anybody know if he ever specified the range of sizes he though the thing in the blood was?

 

[SWAlexander]

sb4, maybe this link will help.
http://book.bionumbers.org/how-big-is-a-human-cell/

 

[SNT Gatchaman]

A blood cell is apparently "6 - 8 μm" in diameter. A clump of RBC would be more than enough to block off some of the smaller capilaries. Just guess it depends on how big Ron is refering to.

Yes, they could be blocked or at least have a slow-moving traffic jam of RBCs.

I found that microcapilaries "They have an inner diameter of 0.5 µm and an outer diameter of 0.7 µm".

I think capillary diameters are generally 5-10 µm. A healthy RBC is a bi-concave disc that can usually just fit through a capillary, but has to fold (like a taco) to squeeze through smaller capillaries. It has long been established that RBC deformability and morphology are abnormal in ME.

I think the question is: are the micro-clots or clumps of them sufficient to narrow capillaries further by physical occlusion or do they induce inflammatory changes in the endothelium (esp. pericytes) as well as conformational changes in the RBCs. I suspect it's the latter.

----

This model would impair energy metabolism and shift it from aerobic -> anaerobic, due to the the slower RBC transit and impaired capillary blood-tissue gas exchange.

PEM would be a unique disease feature, explainable by this model. The compensated, at-rest, metabolic needs could be exceeded by increased blood flow, further compromising some previously available capillary channels. This could either be simply by more backed-up RBCs in more capillaries, and/or further damage to RBCs deformability and oxygen delivery as they traverse these inflamed, narrow channels with a "minefield" of micro-clots containing inflammatory mediators.

The notable feature of PEM is variation in delay to symptom, post-exertion. This could be a direct result of time to effect of further RBC damage or capillary occlusion (remembering that the tissues have compensated to some degree, by shifting metabolic pathways). Or it might be explained by the larger traffic jam of RBCs compromising the oxygen saturation in the venous-side, blood pool which injures more and more circulating white blood cells.

I'd like to track venous oxygen saturation over days, post-exertion when PEM occurs (if this could be done safely).

 

[junkcrap50]

When searching for Rons Something in the blood I found this forum post "I don't think Ron Davis has given a size estimate other than to say "it's big." My impression when he talks about breaking it apart and seeing what it's made of is that he's talking about a "particle" made up of many molecules as opposed to just one large molecule. "

I thought the "something in the blood" was relatively small, and big wouldn't be a accurate description. I thought it was way too small for filtration to remove it from blood in his lab tests. Good thinking by the way.

Pretty sure there was previous discussion on sizes of the "something in the blood" on here somewhere. I think people were listing the range of exosome sizes as many spectulated it was an exosome. They can carry miRNA inside of it. I don't think it by itself is causing the hypo-perfusion or blockages, as I don't remember that being discussed with respect to the "something in the blood." Rather the "something in the blood" was what was causing healthy cells to act as CFS cells, and vice versa. Of course, due to cell metabolism & mitochondrial disruption caused by this something in the blood, RBCs could subsequently cause microclots and obstructions.

Here's an infographic on sizes I found:

 

[SWAlexander]

Consider some other possibilities such as abnormality of red blood cells.
Example: Sickle cell anemia red blood cell disorder in which there aren't enough healthy red blood cells to carry oxygen throughout your body.
Or look at spherocytosis that causes red blood cells destroy faster than they are replaced (40 days instead of 129 days).

 

[SNT Gatchaman]

Thank you @junkcrap50 for the infographic above.

When searching for Rons Something in the blood I found this forum post "I don't think Ron Davis has given a size estimate other than to say "it's big." My impression when he talks about breaking it apart and seeing what it's made of is that he's talking about a "particle" made up of many molecules as opposed to just one large molecule. "

A blood cell is apparently "6 - 8 μm" in diameter. A clump of RBC would be more than enough to block off some of the smaller capilaries. Just guess it depends on how big Ron is refering to.

Anybody know if he ever specified the range of sizes he thought the thing in the blood was?

For comparison, looking at the Pretorius paper's figure 5, the smallest microclots seem to be 2-8 µm. Larger forms seem to be 50 µm or more. I'm unsure if they only clump to form larger aggregates when circulating in the larger vessels that the blood is drawn from, but even the smallest here look to have the potential for significant mechanical flow limitation in the micro-circulation.

 

[sb4]

I found a forum post by @Janet Dafoe clarifying that the thing in the blood is big and "Big = larger than 10,000 molecular weight. Proteins, protein groups or antibodies (including autoantibodies). Amino acids are smaller, around 300 molecular weight."

This seems to indicate that blood clots would be too big to be the something in blood. Also I take your point junkcrap, in rons experiment I should imagine that even if there where clots it wouldn't cause the cell to act sick as the test, I assume, was done in a test tube thing so the blood wouldn't have to go through small spaces to get to the cell.

 

[SWAlexander]

#LongCovid sticky blood. (Content warning: trying - and failing - to squeeze a drop of blood from my finger)
@doctorasadkhan @resiapretorius

https://twitter.com/i/web/status/1455465937000439813

@ClaireHastie1
and
@resiapretorius
We are on it my dear friend. We are close. We will try demonstrate that this is core to the pathology in #LongCovid & #MECFS.
@DrAnnaNZ

 

[BrightCandle]

I have known I had very thick blood and I couldn't complete home blood tests using lancets since 2016 if not earlier. I have ever since the condition developed and I can't get close to that much blood out of a lancet prick as that women, one to two drops is about the limit of it. I thought this was a well known aspect of the condition so presumably someone has researched into this before now?

 

[Countrygirl]

Dr. Kahn, from the BBC interview, said that these apheresis treatments has significantly improved his Long Covid. But he says that he's not entirely recovered. Do we know what his plan is to do next? Is he going to continue doing HELP apheresis until he's cured? He's already done 13, I've heard.

He said he might be coming to see Dr William Weir who runs an ME clinic in my home. Asad was originally supposed to be coming here in September but had the opportunity to go to Germany at the same time. Meanwhile, I have pencilled him in for an appointment for the next clinic in December or January.

I really look forward to meeting him, if he still wants to keep his appointment.

I think I will need to allocate a two-hour appointment if he is able to come.