Is Apheresis an effective treatment for Long Covid and ME?

[perrier]

Sulodexide looks like an interesting medication (aka Aterina). It is 80% low molecular weight heparin and 20% low molecular weight chondroitin. What makes it unique is that almost all heparin is given either IV (regular heparin) or subcutaneous injection (low molecular weight heparin) and this is an oral formula. Here is an informative post on the research on the use of heparin in ME/CFS.
https://livingwithchronicfatiguesyndrome.wordpress.com/2016/08/23/heparin-for-me/
It seems worth trying, too bad Sulodexide may be hard to get a hold of.


Take home on TEG: it can tell you if you have a clotting problem (microclots included), but not if you specifically have resistant long-covid type micro-clots.

Heparin subcutaneous was tried here, and there was not result. ME doctors were using it regularly about 10 years ago.

 

[Martin aka paused||M.E.]

thesis there is that the endothelial lining is damaged and needs to be healed.

Yes, please look at my Lp-PLA2 levels
She will visit Dr Jaeger'sclinic next week. I know one ME patient who will be there.

 

[perrier]

https://go.drugbank.com/drugs/DB062...4F2ivsGb4Wiwqsguw4-9VZeuWRYPU5EZPY8UCbjP3OXpY

reference for the medication the Tunisians are using @Countrygirl

 

[Martin aka paused||M.E.]

I posted about my concerns that apheresis alone won't cure ME. Pretorius seems to have it on her radar

 

[perrier]

Yes, please look at my Lp-PLA2 levels
She will visit Dr Jaeger'sclinic next week. I know one ME patient who will be there.

Thanks Martin. Dr. Pretorius said that she will be looking at 20 new patients coming to see Dr Jaeger. She will test their blood before treatment, and then after the filtration. I wish we could know more about the ME patient (s) in terms of number. Dr. Pretorius study is only to start in January, and that is hard for the very severe.

 

[Shanti1]

@JES @perrier Thank you both for your comments regarding heparin/pentoxifylline/Bromelain having been tried by pwME without great results I had seen @Martin aka paused||M.E. make a similar comment on another thread. It does seem though, that now and then, there is someone for whom these things do make a difference, but I agree, they are not going to be the magic bullet.

@Martin aka paused||M.E. Is your friend still responding to pentoxifylline?

 

[perrier]

I posted about my concerns that apheresis alone won't cure ME. Pretorius seems to have it on her radar
View attachment 45464

Bravo Martin. Dr. Pretorius did say in the interview that Dr. Jaeger is putting some patients on anticoagulants after the Apheresis. It is an interesting interview. I think that Dr. Amy Proal could help us with more information.

 

[Martin aka paused||M.E.]

Is your friend still responding to pentoxifylline?

I only heard of one responding well but he posted here on this board. I don't know. For me it was a hell ride on it.

 

[Shanti1]

I only heard of one responding well but he posted here on this board. I don't know. For me it was a hell ride on it.

Oh sorry, it was someone else who reported on their friend.

 

[Shanti1]

Yes, please look at my Lp-PLA2 levels

It is quite high, especially for someone who is young. To me, Lp-PLA2 indicates very active plaque and endothelial inflammation as it is secreted by inflammatory "foam cells", which are basically macrophages that have eaten too much oxidized LDL cholesterol and are now fat and bloated and deciding to settle down in the arteries for the long-haul.

 

[Martin aka paused||M.E.]

It is quite high, especially for someone who is young. To me, Lp-PLA2 indicates very active plaque and endothelial inflammation as it is secreted by inflammatory "foam cells", which are basically macrophages that have eaten too much oxidized LDL cholesterol and are now fat and bloated and deciding to settle down in the arteries for the long-haul.

The thing that is quite shocking is that I have an increased risk of over 89% for heart attack and stroke.

But I'm convinced if all has to do with fibrinogen.

 

[Shanti1]

I posted about my concerns that apheresis alone won't cure ME. Pretorius seems to have it on her radar

Do you know in the image associated with this post what Dr. Pretorius is referring to when she says, "not only can the S1 (S1 portion of the spike protein) do this, but also enterovirus"? Is she referring to causing abnormal clots or autoantibodies?

Here are some interesting images from Dr. Pretorius's presentation in this video:
When you add spike protien to fibrinogen, that is when you get the abnormal resistant clot.

This one shows that if you add thrombin (to get clot formation) you don't get abnormal clots, only when you add the spike protein does it happen.

 

[perrier]

Is there anyone here with a contact ability to Dr. Proal. She apparently would have the most info regarding ME patients during the Aphaeresis project which is coming up next week, presided over by Dr. Pretorius.

 

[Martin aka paused||M.E.]

not only can the S1 (S1 portion of the spike protein) do this, but also enterovirus"?

I said this, not her. It's bc EV and S1 similarly infect endothelial cells. Where is infection+inflammation there are AAB. This is why there is the end of the former sentence about molecular mimicry.
To be clear: that's my statement, not Dr. Jaeger's. I just wanted to check if Dr. Pretorius knows about it. She does obviously.

 

[Shanti1]

@Martin aka paused||M.E. Ahh, thanks for clarifying. It is one of my big questions, what in ME/CFS would cause resistant clot formation to occur (we know it is spike protein in COVID)? Most of the pathogens thought to trigger ME/CFS are not associated with excess clotting and the antiphospholipid antibodies don't seem like they would be responsible.
I don't doubt that ME/CFS involves hypercoagulation, RBC deformability, altered blood flow, poor oxygen extraction secondary to capillary shunting/mitochondrial dysfunction, but I'm holding out for proof on the resistant variety of the microclot, especially with no low SvO2 detected in studies.

 

[Martin aka paused||M.E.]

@Martin aka paused||M.E. Ahh, thanks for clarifying. It is one of my big questions, what in ME/CFS would cause resistant clot formation to occur (we know it is spike protein in COVID)? Most of the pathogens thought to trigger ME/CFS are not associated with excess clotting and the antiphospholipid antibodies don't seem like they would be responsible.
I don't doubt that ME/CFS involves hypercoagulation, RBC deformability, altered blood flow, poor oxygen extraction secondary to capillary shunting/mitochondrial dysfunction, but I'm holding out for proof on the resistant variety of the microclot, especially with no low SvO2 detected in studies.

SvO2 is not an adequate measurement as Asad explains. Some have normal values but blood clotting.

 

[Shanti1]

Regarding the normal O2 saturation in ME studies Asad says here that this has NO meaning re micro clots > it's a non-specific parameter

I was taking this to mean arterial O2 via oxygen saturation metere or arterial draw, but you are saying he is referring to SvO2? I think I will need to watch the video. Thank you.

 

[Shanti1]

@Martin aka paused||M.E. Thanks for posting the video, well worth watching. (https://forums.phoenixrising.me/thr...-long-covid-and-me.85939/page-18#post-2375233).
@SNT Gatchaman You might want to take a look, esp @22m-25m to see if it influences your research plan. Dr. Khan basically says SpVO2 can be high, normal, or low in Long-COVID. Clots/thickened endothelial walls can lead to poor oxygen extraction (high SpVO2) or excess clotting factors and compromised circulation can lead to slow passage of blood through capillaries (low SpVO2) or, it can be normal, not because circulation is normal, but perhaps because these two factors are "fighting" with each other. I guess we have to wait for direct detection of resistant microclots in ME/CFS for an answer.

 

[SNT Gatchaman]

@Shanti1 Yes there seem to be competing forces that could affect the venous-side oxygen saturation.

• Micro-clot aggregates and endothelial inflammation → ↓ O2 tissue transfer → ↑ SvO2
• Tissue hypoxia → metabolic adaptations → ↓anaerobic threshold → ↑SvO2
• ↓RBC deformability +/- micro-clots impeding → ↑capillary transit time → ↑opportunity for O2 extraction → ↓SvO2

They are measuring SvO2 at rest in the patient's current, compensated state. That's why I think it's really useful to know what happens to it following exertion (PEM). Can it give a clue as to which of the above factors is at play?

If SvO2 drops precipitously (and then slowly recovers) following exertion that suggests to me that there is worsening RBC deformability.

Asad's SvO2 was 33% on arrival at the clinic (it would seem from his Twitter posts). He was pretty sick and may have been in prolonged PEM.

 

[Countrygirl]

Amy Proal, PhD

@microbeminded2

Replying to
@microbeminded2

@cstroeckw
and 4 others
4/ In fact, here is an image from one of Resia’s papers on platelet hyperactivation/clotting. Notice how platelets have receptors that recognize a wide range of #viral proteins. That is part of why we think her work can be directly applied to ME/CFS: https://pubmed.ncbi.nlm.nih.gov/32279287/