Is Apheresis an effective treatment for Long Covid and ME?

Countrygirl

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ruben

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Sadly then it would seem thread has ran its course. Or have I misunderstood something. But I would love to be proved wrong. The microclots issue though one would have thought surely have some significance
 
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Dr Charles Shepherd of the ME Association said he had tried it without success and I have heard of a couple of others but neither reported improvement

In my case it was a plasma exchange. Like in plasmaexchange the first step of help apheresis is that the plasma gets separated from the blood cells. In help, the plasma then gets treated and filtered, in plasmaexchange the plasma is being completely removed and replaced by synthetic plasma.

I would love to be be wrong but that’s why I don’t see why help apheresis should work for cfs while plasmaexchange doesn’t.
 

SWAlexander

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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?

Did you ever had a Factor V (Or F5) test? This is how I found out have this genetic mutation.
Mayo Clinic explains:
https://www.mayoclinic.org/diseases-conditions/factor-v-leiden/symptoms-causes/syc-20372423
 

SNT Gatchaman

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Sadly then it would seem thread has ran its course. Or have I misunderstood something. But I would love to be proved wrong. The microclots issue though one would have thought surely have some significance

I think it depends if the above-referenced plasmapheresis is different to H.E.L.P. aphersis. The latter is aimed at clearing the microclots, which the former may not be addressing.

In help, the plasma then gets treated and filtered, in plasmaexchange the plasma is being completely removed and replaced by synthetic plasma. I would love to be be wrong but that’s why I don’t see why help apheresis should work for cfs while plasmaexchange doesn’t.

I don't have sufficient knowledge or direct experience, but plasma exchange preserves the separated off cellular components of blood. Could the microclots persist along with the cellular component, unless specifically targeted by HELP?
 

SWAlexander

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I think it depends if the above-referenced plasmapheresis is different to H.E.L.P. aphersis. The latter is aimed at clearing the microclots, which the former may not be addressing.



I don't have sufficient knowledge or direct experience, but plasma exchange preserves the separated off cellular components of blood. Could the microclots persist along with the cellular component, unless specifically targeted by HELP?

Until we have Dr. Jaeger's research results published, we may look to the manufacturer for explanation what there machines do: https://www.fresenius-kabi.com/us/products/apheresis-collection-systems
 

Reading_Steiner

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Could a biomarker be as simple as putting a band around someones wrist thats moderately tight and then seeing whether red marks appear after and how long they stay for ? I noticed that i've started getting them quite prominently after removing my heart rate monitor thing, they remain there for at least 10 minutes. I googled and I couldn't find a proper explanation for why we get red marks after wearing things but I wonder if it could be informative about what those red blood cells are doing.
 

SWAlexander

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Countrygirl

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Sadly then it would seem thread has ran its course. Or have I misunderstood something. But I would love to be proved wrong. The microclots issue though one would have thought surely have some significance

It was different to Apheresis, @ruben. I discussed this with Dr Weir who has spoken to Dr Jaeger and Asad and he explained that whereas plasmapheresis wouldn't work, apheresis, as conducted by Dr Jaeger, would.
 

Shanti1

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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/
Seems it could be another dysregulated pathway that may contribute to the RBC membrane issue, prob as a result of the initial trigger that then causes all these downstream effects. Looks like phosphatidyl-ethanolamine decreases membrane fluidity, and phosphatidyl-choline increases it.

Influence of phospholipid species on membrane fluidity: a meta-analysis for a novel phospholipid fluidity index
https://pubmed.ncbi.nlm.nih.gov/22052236/

Of course, much of it has to do with the saturation of the fatty acids in the membrane. We know omegas integrate into the RBC cell membranes as that is where they are measured for Omega Index scores offered by various labs.
 

SWAlexander

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I was told I have antiphospholipid syndrome.

Is Factor V Leiden and antiphospholipid syndrome?
Significant associations have been reported between these complications and the presence of antiphospholipid antibodies, notably the lupus anticoagulant and anticardiolipin antibodies. Factor V Leiden is a genetic disorder associated with an increased risk of venous thrombosis.
 

Shanti1

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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)?
I checked some of the labs in the US and they don't run venous oxygen saturation (SvO2). I think it needs to be done in a hospital or office set up to measure it because it needs to be done immediately before the O2 begins to disintegrate. Also seeing that it is usually done from a central venous catheter, but I think it can be done peripherally as well.

A low SvO2 can signify low tissue perfusion. Basically, the tissues are not getting enough O2 so, even though arterial O2 looks normal, as the RBCs pass very slowly through the sludgy capillaries (or due to low BP, heart failure, or other causes of low tissue perfusion), the body extracts more O2 than normal from the blood to compensate for the low perfusion.

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.

Yes, I think so. Through the info I learned in this thread, I have come to believe this RBC deformability and sub-clinical hypercoagulability are likely an issue for many, I certainly feel it is the case for me. It seems perfectly logical that a virus or other toxin could trigger the inflammation that triggers RBC membrane changes and clotting factors. The only thing I'm not certain of is that we have the same resistant microclots as COVID patients instead of regular "stickiness" or maybe small clots that continually form and dissolve.
In cancer pathology, the cancer causes a hypercoagulation state in order to "hide" from the immune system in clumped platelets and metastasize. I wouldn't be surprised if pathogens do the same (something else to research).

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?
The technique is a specific type of apheresis called HELP apheresis.

Until we have Dr. Jaeger's research results published, we may look to the manufacturer for explanation what there machines do: https://www.fresenius-kabi.com/us/products/apheresis-collection-systems
This link describes regular apheresis. If you are interested specifically in how HELP apheresis works, including the use of heparin to remove substances from the blood, see this link: https://vpjournal.net/article/view/3015

Could a biomarker be as simple as putting a band around someones wrist thats moderately tight and then seeing whether red marks appear after and how long they stay for ? I noticed that i've started getting them quite prominently after removing my heart rate monitor thing, they remain there for at least 10 minutes. I googled and I couldn't find a proper explanation for why we get red marks after wearing things but I wonder if it could be informative about what those red blood cells are doing.
If you have mast cell issues, that could be the cause....
 
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