Is Apheresis an effective treatment for Long Covid and ME?

[Reading_Steiner]

Could it be possible to check if the red blood cells are 'going through' properly in ME people by using some sort of radioactive chemical that binds to the red blood cells and then do some sort of scan that has a high enough resolution to see clusters of red blood cells where they are piling up in the capillaries in a 'traffic jam' creating highlight spots on the scanner output ?

 

[godlovesatrier]

I don't think we're saying long covid can be caused by vaccinations no. We're saying there's a direct correlation between blood samples under microscope showing red blood cell abnormalities and what MIGHT be hyper coagulation (but we don't know) and these symptoms appearing just after literally any of the vaccines on the market or covid19 infection.

With similar sorts of things being seen under microscope in chronically ill patients like those with ME. It's all speculative but it seems quite clear there's some sort of direct correlation.

 

[Shanti1]

A vaccine causing long-covid and a vaccine possibly aggravating an already perturbed immune system, potentially contributing to altered RBC behavior ie, being "sticky" are pretty different outcomes. I think the latter is more plausible than the former.

The spike protein present in the blood during an actual COVID infection is thousands of times higher than the spike protein fragments that make it into the blood after vaccination. In fact, at first, it was thought that spike protein didn't make it into the blood from the vaccines, but a May 2021 paper using an "ultrasensitive single-molecule array" showed extremely small amounts of the S1 fragment of the spike protein on days 1-7 after the first moderna vaccine injection, but not after the second, presumably because the immune system clears it. Basically, if you keep lowering the detection limit on your testing, eventually you will find something, but personally, I don't think it is enough to cause a problem. I think the more likely scenario would for vaccine reactions is stirring up the immune response.

 

[SWAlexander]

Shanti1
"I think the more likely scenario would for vaccine reactions is stirring up the immune response. "
The system is on heightened alert. Even more so if there were previous immune response challenges.

 

[Pyrrhus]

The authors in the RBC deformability paper think the lack of RBC flexibility develops because of the higher level of reactive oxygen species found in RBC of pwME.

Anyone interested in how oxidative stress impairs Red Blood Cell (RBC) deformability might be interested in this paper:

Red blood cell oxidative stress impairs oxygen delivery and induces red blood cell aging (Mohanty et al., 2014)
https://doi.org/10.3389/fphys.2014.00084

Studies from our laboratory have shown that oxidative stress plays a significant role in damaging the RBC membrane and impairing its deformability.

Personally, I wonder if a reduced level of RBC membrane phospholipids may be relevant here:

Dysregulation of the Kennedy Pathway and Tricarboxylic Acid Cycle in ME/CFS (Che et al., 2021) (Pre-print)
https://forums.phoenixrising.me/thr...cle-in-me-cfs-che-et-al-2021-pre-print.84668/

This metabolomics paper found decreased levels of certain membrane phospholipids in ME patients compared to controls, notably phosphatidyl-choline, phosphatidyl-ethanolamine, and related plasmalogens. This confirms previous research findings of decreased membrane phospholipids.

It shows a possible association between phospholipid metabolism and Ron Davis's work on RBC Deformability

 

[Gingergrrl]

I wasn't able to read the entire thread and have a few questions for those who were able to follow it all

He mentioned a venous oxygen saturation test

Was it ever determined what this "venous oxygen saturation test" was? Is it the same thing as an "arterial blood gas test" or something different?

I hear yesterday from a doctor that 2 clinics doing plasmapheresis are opening up, one in New York and one in California. If anyone has further info please. post.
Is this what Dr. Scheibenbogen was doing????

I don't know the answer but was also curious re: the clinic mentioned that might be opening up in California? Also, re: your question about Dr. Scheibenbogen, my understanding was that her studies used "immuno-adsorption" (but I am not totally sure how this differs from "apheresis")?

I wonder if others had such evidence of having 'sticky' blood, Hughes Syndrome/Antiphospholipid Syndrome?

I am also wondering about this.

I am told plasmapheresis is a different process to what is happening in Germany.

My understanding (and I am hoping that someone will let me know if I am right or wrong ) is that plasmapheresis or "PLEX" is most commonly done in the US vs. immuno-adsorption is more commonly done in Europe & Asia. I am still unclear how the technique being referred to as "Apheresis" matches with those two techniques or if it is something different?

 

[Mary]

Was it ever determined what this "venous oxygen saturation test" was? Is it the same thing as an "arterial blood gas test" or something different?

It's different. An arterial blood gas test measures oxygen in the blood flowing from the heart, through the arteries, to the tissues in the body.

Venous oxygen saturation test measures oxygen in the blood returning to the heart from the tissues, flowing through the veins.

 

[Gingergrrl]

It's different. An arterial blood gas test measures oxygen in the blood flowing from the heart, through the arteries, to the tissues in the body.

Venous oxygen saturation test measures oxygen in the blood returning to the heart from the tissues, flowing through the veins.

Thank you so much for explaining that! Are they both blood tests except the first is drawn from an artery and the second is drawn from a vein (like any regular blood test)? Also, what would be the purpose of the second test (meaning what specifically is it measuring in relation to clotting or other factors)?

 

[SNT Gatchaman]

In ME, the RBCs may be completely normal, and able to deform appropriately. But what if the micro-thrombi circulating with them are sufficient to impede their passage through the smallest capillaries? This would mean the RBCs don't get damaged, but are slow.

Slower RBC transit would mean that more O2 is extracted from each RBC, leading to lower SvO2, as observed by Dr. Khan on his venous blood gas. The tissues are still being starved of O2 overall, as the absolute flux of RBCs is decreased due to their slower transit.

A mild-moderate ME patient might have an amount of micro clot that impaired tissue oxygenation during exertion but not at rest. A more severe patient might have so much micro clot affecting their micro-circulation, that they are compromised even at rest.

You may be interested in this paper which describes the actual physical changes in the RBCs of pwME: https://ashpublications.org/blood/a...rocyte-Deformability-As-a-Potential-Biomarker. So maybe it is a combo.

Thank you @Shanti1! While I'm still spit-balling...

Could the onset of the disease perhaps start with viral-induced platelet dysfunction and the resulting formation of fibrinogen micro-clots? As it takes hold and especially in those with increased exertion, later metabolic damage to the RBCs ensues, which causes them to be less deformable. I'm thinking how the disease might start with one thing wrong, that leads to a cascade and self-reinforcement.

In patients that recover, severe rest might have allowed the balance to tip more favourably, letting the RBCs start to regain their deformability and ultimately (months) there is clearance of the micro-clots.

Of course these observations may all be downstream from immune dysfunction. Good to see studies revisiting the potential theories of old, that were not duly followed-up over recent decades.

 

[andyguitar]

Good to see studies revisiting the potential theories of old, that were not duly followed-up over recent decades.

Yes it is, but unfortunate that pathology gets ignored.

 

[Gingergrrl]

I have one other question (for anyone in this thread)... is the "apheresis" technique in this thread that is used to dissolve these micro-clots the same as when plasmapheresis is used for autoantibodies?

 

[Mary]

Are they both blood tests except the first is drawn from an artery and the second is drawn from a vein (like any regular blood test)?

Yeah, I think they are both blood tests. There was some confusion about the difference between these tests and what is measured by a pulse oximeter - I just checked and a pulse oximeter "under optimal conditions" measures arterial oxygen, not venous. But you can get a blood draw as well for arterial oxygen saturation. I think the term arterial blood gases refers generally to tests for both arterial and venous blood oxygen levels. It also measures some other things.

Also, what would be the purpose of the second test (meaning what specifically is it measuring in relation to clotting or other factors)?

Re the venous oxygen saturation - I don't think there's a simple answer. I think I'm getting a rough idea though. Did you watch the video in the first post with Dr. Khan? He mentions his venous oxygen saturation test result which was 32, and the normal range was 65-75 (!) I believe this was diagnostic for Long Covid. It might be applicable to ME/CFS as well . . . so I don't think it specifically has to do with clotting factors or anything, it just demonstrates low oxygen levels - @dylemmaz also had very low venous oxygen: 36% out of a range of 70 - 80%, but I don't know if he has Long Covid.

 

[andyguitar]

is the "apheresis" technique in this thread that is used to dissolve these micro-clots the same as when plasmapheresis is used for autoantibodies?

.
No the micro clots are removed by using the drug Heparin. But there are some similarities in the sense that blood is removed from the patient into a machine which filters the blood/plasma and then returns the "cleaned" blood to the body. So the Heparin does not actually go into the patient.

 

[Reading_Steiner]

A new user put this in their introduction https://www.researchgate.net/public...ED_WITH_HYPOPERFUSION_AND_PERSISTENT_BIOCLOTS

 

[SWAlexander]

A new user put this in their introduction https://www.researchgate.net/public...ED_WITH_HYPOPERFUSION_AND_PERSISTENT_BIOCLOTS

Excerpted below.
Tissue hypoperfusion implies a lower contribution of oxygen and nutrients to the tissues, although there is no obvious damage to the tissues, the normal functioning of the organs and systems is affected, especially those that require a greater contribution of oxygen and nutrients, which are mainly the musculoskeletal system, the brain and the lungs, so that in a state of hypoperfusion it will produce its own symptoms that correspond to these organs and systems. Chronic fatigue associated with tissue hypoperfusion.

 

[SWAlexander]

I have one other question (for anyone in this thread)... is the "apheresis" technique in this thread that is used to dissolve these micro-clots the same as when plasmapheresis is used for autoantibodies?

There are older reports, I consider need to be revised. Dr. Jaeger´s and colleges latest article from 18 April 2020:
https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2020.34.s1.04989

New results may be available after studies by Dr. Jaeger and new joining colleges completed their research after Nov.

 

[MonkeyMan]

I hear yesterday from a doctor that 2 clinics doing plasmapheresis are opening up, one in New York and one in California. If anyone has further info please. post.

Is this the one in New York?
https://nybloodcenter.org/products-and-services/clinical-services/apheresis-services/

Has anyone from this board tried plasmapheresis? If so, did it help? (Apologies if this was posted already, I don't have the strength to read through this whole thread).

 

[Countrygirl]

I have a genetic tendency to a blood clotting disorder and had my first (superficial) clot when aged 15. I had several throughout my adult life, and now have had a number of TIAS, and small strokes. I gather about 8% of the population have a genetic tendency to develop clotting disorders, so perhaps this makes some of us prone to mico-clots following certain viral infections?

 

[EtherSpin]

Ok, to sum it up in my understanding:

Viruses like EV and SC19 might create proteins that are recognized by the platelets in a manner that cause blood coagulation. That seems to be a piece of the puzzle.
Viruses can cause excessive fibrin production. That eventually leads to accumulation. It builds fibrin blocks. These affect blood flow and lead to hypoxia in some parts (tissues, nerves) of the body.
This should lead to fermentation (lactate) due to anaerobic metabolism (although it should be noted that many pwME have low pyruvate pointing towards problems with glycolysis).
The response of the immune system to the pathogens additionally produce inflammation (epithelial inflammation that damages the cells).
Furthermore, the pathogens produce proteins that due to molecular mimicry let the body produce AAB.

The big??? is what is P.E.M. Is it low ATP (bc of hypoxia) being used up or do we have to think along the inflammatory axis: Stressors like exercise as potent stimulators of the innate immune response( IL-6, MIF) Any preexisting immune dysfunction would be revved up/restarted including autoimmune triggers.....?!?

I would not expect apheresis to cure this problem but being a highly effective treatment if it's the hypoxia route. And maybe both are very much linked together.

would that help inform Davis and team of a particular avenue or flavour of drug to try via the Nanoneedle ? presumably not applicable to the yeast version of the tests (where nanoneedle has CFS blood)

 

[Canned]

Has anyone from this board tried plasmapheresis? If so, did it help? (Apologies if this was posted already, I don't have the strength to read through this whole thread).

Yes I tried it and it did not help.