Is Apheresis an effective treatment for Long Covid and ME?

[andyguitar]

The late Dr Les Simpson(New Zealand) did work on blood(sticky?) in 1980/90s and connections to ME &CFS. .He died in 2015.Here is a link..

That was a good find @Abha and I would urge members to read what Dr Simpson has written. It's about red blood cell deformities (and a bit of other stuff). The deformities of the red blood cells effect microciculation which leads to less oxygen being made available. His evidence for his findings looks pretty good to me. And he also says that the cause maybe "a persisting but unidentified factor in the blood". I wonder if @HTester has come across Dr Simpsons research.

 

[Reading_Steiner]

Never heard of this technique. We know blood flow is an issue, I have an increase in heart rate just prior or during crashes, I supposedly have an enlarged spleen, seen on a CT scan, which is something to do with blood cells is it not ? they initially sent me for ultrasound on my liver because thats the main suspect if you have fatigue, they wouldn't listen if I said I didn't think my liver had any problem, they saw possible kidney stone so thats how I got the CT scan. I got referred to haematology but they wanted me to do further tests before they would accept the referral. I might mention this new video to my doctor, i'm a little bit annoyed that no nhs doctor has ever mentioned to me that specialist services exist for diagnosing me/cfs.

 

[J.G]

I wonder if HTester has come across Dr Simpsons research.

Well! In 2018, Davis et al. published the study "Erythrocyte Deformability As a Potential Biomarker for Chronic Fatigue Syndrome". Link here. Then in 2019, the OMF-funded research paper "Red Blood Cell Deformability is Diminished in Patients with Chronic Fatigue" came out. Link here. The thought that something in the blood - or something that is missing from it - is the cause, is as far as I understand it a working hypothesis.

So yes! The OMF are very much picking up the thread of Dr. Simpson's work; it's an active avenue of enquiry. Though I obviously can't speak for HTester himself, of course

 

[SWAlexander]

Was ist H.E.L.P. apharesis ?

HELP apheresis: Apheresis treatment is available in Europe and many German cities
Ihttps://www.bbraun.com/en/products-and-therapies/extracorporeal-blood-treatment/apheresis.html
Worldwide: https://www.bbraun.com/en/patients/renal-care-for-patients/renal-care-centers.html

 

[Countrygirl]

@Countrygirl...Re 1980s/90 papers

The late Dr Les Simpson(New Zealand) did work on blood(sticky?) in 1980/90s and connections to ME &CFS. .He died in 2015.Here is a link...
https://www.investinme.org/ArticleJ21-Role-of-Impaired-Capillary-Bloodflow.shtml

Cort Johnson also wrote this...
“Sticky Blood” – Antiphospholipid Syndrome, POTS, Chronic Fatigue Syndrome and Fibromyalgia – The Dysautonomia Conference #4
by Cort Johnson | Aug 15, 2018 ...Here is the link..
https://www.healthrising.org/blog/2...ts-chronic-fatigue-syndrome-and-fibromyalgia/

Many thanks, @Abha !

 

[Shanti1]

i had an arterial blood gas test done that showed my venous blood oxygen saturation levels were 36%. the reference range for the lab was 70-80%. maybe this is the test he is talking about? having low venous blood oxygen saturation levels certainly lines up well with the tissue hypoxia theory

I'm almost positive the test Dr. Khan had done was not the same as using a pulse oximeter - Dr. Khan said he had a venous oxygen saturation test, his result was 32 out of a range of 65 - 75, and @dylemmaz said he had an arterial blood gas test done, with a very low result, 36% out of a range of 70 - 80%. @dylemmaz - I'm presuming your arterial blood gas test was done with a blood draw and not a pulse oximeter - is this correct?

I think there is something we are not understanding about the low venous oxygen test....

If you have normal arterial oxygen and low venous oxygen, this is usually GOOD thing, it means that the oxygen in your blood was delivered to and taken up by your tissues.

If you have normal arterial oxygen and high venous oxygen, it means the oxygen was NOT delivered to your tissues and you may have oxygen starvation despite normal arterial O2

In fact, PWME have been shown to have higher than normal venous oxygen saturation and less of a change between arterial oxygen saturation and venous oxygen saturation than healthy controls during exercise.

https://pubmed.ncbi.nlm.nih.gov/24456560/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004422/

So I am confused by Dr. Khan's statement that his venous oxygen being low was a problem, unless he also started out with low arterial oxygen. Thoughts....

Also someone mentioned in another thread that a low esr of say 2 does confer sticky blood. Does anyone know if this is actually true?

Usually, ESR is high in clotting disorders and inflammation so I don't know why PWME have low ESR. Cort writes about it here: https://www.healthrising.org/blog/2019/11/06/clumper-slider-esr-chronic-fatigue-fibromyalgia-poll/

I think apheresis is either a form of or very similar to dialysis. I tried to find the difference between the two and couldn't.

https://cdn.ymaws.com/www.apheresis...910496A7/15.05.07-1615-LONESTARA-Kauffman.pdf

 

[Shanti1]

Usually, ESR is high in clotting disorders and inflammation so I don't know why PWME have low ESR.

Actually, this paper posted earlier by @J.G attributes the low ESR in pwME to the low RBC deformability:
https://ashpublications.org/blood/a...rocyte-Deformability-As-a-Potential-Biomarker

 

[Mary]

If you have normal arterial oxygen and low venous oxygen, this is usually GOOD thing, it means that the oxygen in your blood was delivered to and taken up by your tissues.

Thanks for all the info. But this is puzzling to me - if it's a good thing and I would presume therefore "normal" to have low venous oxygen, why is the "normal" range so high? When I see lab tests, they always have a "normal" range that doctors want you to fit into. And both Dr. Khan and Dylemmaz had quite low levels of venous oxygen, not even close to the normal range. And not to state the obvious (but I am stating the obvious! ), Dr. Khan is a doctor and I presume he would know if having low venous blood oxygen was a good thing or not, and he did not think it was a good thing.

I just found something about low venous oxygen:

A reduction in venous oxygen saturation indicates an increased oxygen consumption/supply-ratio. In the absence of anaemia and arterial hypoxaemia, a low venous oxygen saturation reflects low cardiac output, which may be due to heart failure or obstruction of the circulation as in tamponade or hypovolaemia [3, 25]. Therefore, venous oxygen saturation may be a good indicator of impaired tissue oxygenation [1–3]. Low venous oxygen saturation has previously been associated with impaired outcome in surgical patients, and adequate measures of venous oxygen saturation may have a substantial role in management and treatment of critically ill patients [10].

Peripheral measurements of venous oxygen saturation and lactate as a less invasive alternative for hemodynamic monitoring - PMC (nih.gov)

 

[Shanti1]

@Mary Yes, you solved it.....
It looks like both high and low venous oxygen can indicate problems with tissue oxygenation.

So when there isn't enough perfusion of tissues by blood flow, the body will extract more oxygen than normal.
https://www.lhsc.on.ca/critical-care-trauma-centre/central-venous/mixed-venous-oxygen-saturation

Venous oxygen that is too low can indicate that the body is over-extracting oxygen because so little oxygenated blood is reaching the tissues, We know pwME have low blood volume, so now low venous oxygen makes sense to me. Microclots could also impede the ability of the blood to reach tissue.

Venous oxygen that is too high can indicate that the body is not extracting oxygen from the blood efficiently, as seen in the study above in pwME undergoing exercise. Maybe this is due to mitochondrial dysfunction. Cort explores high Venous oxygen and mitochondrial dysfunction here: https://www.healthrising.org/blog/2...-exertional-malaise-chronic-fatigue-syndrome/

 

[Reading_Steiner]

probably it means that the blood cell are moving super slowly so by the time they get to the end the cells had more time to extract the oxygen, if it gets super low at the end it could mean that they extracted so much that they were effectively 'empty' because below 30% or what not it doesn't diffuse properly due to concentration gradient. how do we measure this value though ? I only have a wristband thing and the value looks normal.

 

[Martin aka paused||M.E.]

HELP apheresis: Apheresis treatment is available in Europe and many German cities
Ihttps://www.bbraun.com/en/products-and-therapies/extracorporeal-blood-treatment/apheresis.html
Worldwide: https://www.bbraun.com/en/patients/renal-care-for-patients/renal-care-centers.html

“Was it help apheresis?” not “what is..”

 

[SWAlexander]

@Mary Yes, you solved it.....
It looks like both high and low venous oxygen can indicate problems with tissue oxygenation.

So when there isn't enough perfusion of tissues by blood flow, the body will extract more oxygen than normal.
https://www.lhsc.on.ca/critical-care-trauma-centre/central-venous/mixed-venous-oxygen-saturation

Venous oxygen that is too low can indicate that the body is over-extracting oxygen because so little oxygenated blood is reaching the tissues, We know pwME have low blood volume, so now low venous oxygen makes sense to me. Microclots could also impede the ability of the blood to reach tissue.

Venous oxygen that is too high can indicate that the body is not extracting oxygen from the blood efficiently, as seen in the study above in pwME undergoing exercise. Maybe this is due to mitochondrial dysfunction. Cort explores high Venous oxygen and mitochondrial dysfunction here: https://www.healthrising.org/blog/2...-exertional-malaise-chronic-fatigue-syndrome/

"the significant decrease in deformability of RBCs from ME/CFS patients may have origins in oxidative stress,"

Not sure, maybe I posted this link before:
Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
https://www.researchgate.net/public...cephalomyelitisChronic_Fatigue_Syndrome_MECFS

 

[SNT Gatchaman]

Is it really the normal pulse O2 oximeter he talks about? Because afaik that’s being used in every clinic so that would have been discovered immediately… in general when you have a very low oxigen level you get intranasal O2 or being referred to the ICU

No, it's a formal blood gas analysis, from a blood draw. This is typically arterial, but can be venous. Blood gas analysers are usually close to the patient to prevent deterioration (simplistically, the gases leeching out) and so are usually present in ICUs. You used to be able to put the syringe on ice to quickly transfer to the lab as well. ABG and VBG show the partial pressures of oxygen, CO2, as well as acid/base level, not just the oxygen saturation.

I'm almost positive the test Dr. Khan had done was not the same as using a pulse oximeter - Dr. Khan said he had a venous oxygen saturation test, his result was 32 out of a range of 65 - 75, and @dylemmaz said he had an arterial blood gas test done, with a very low result, 36% out of a range of 70 - 80%. @dylemmaz - I'm presuming your arterial blood gas test was done with a blood draw and not a pulse oximeter - is this correct?

Mary, that is correct. Dylemmaz must have also had a venous blood gas test, as an arterial saturation of. 36% is incompatible with life.

Dr. Khan is a doctor and I presume he would know if having low venous blood oxygen was a good thing or not, and he did not think it was a good thing.

He's a respiratory physician, so he would definitely know about this stuff. See this link too.

 

[Mary]

Does anyone know if one's blood were "sticky" as in Long Covid with microclots or ME/CFS (if ME/CFS in fact made one's blood "sticky"), whether that would show up with any dialysis or apheresis procedure?

Dr. Khan's microclots clogged the apheresis machine 4 times I think and it had to be cleaned out. I'm wondering if this would have happened if he had been having a different dialysis or apheresis procedure - or was the HELP protocol necessary to cause this to happen?

It just seemed to me that if one had lots of blood clots, they would clog the machine regardless of what it was being use for. In dialysis some sort of filter is used to clean the blood and I'm assuming apheresis has a similar filter, and that it's this filter which got clogged with Dr. Khan - though of course, I may be wrong about this.

My doctor's office does something called ozone dialysis (I haven't had it done [yet]). And I'm wondering, assuming my blood is "sticky", whether it might clog his machine too - whether or not it would be worth an experiment, though a bit pricey! (I think the cost is around $400 ) Also, I don't know whether using ozone in this way would be a good thing - his website says that the "03D infusion" removes impurities, inflammatory proteins; unneeded inactive proteins; diseased cells; and dead cells.

I'm also wondering whether my doctor's machine could be used for the HELP apharesis process.

@SNT Gatchaman or anyone?

 

[andyguitar]

or was the HELP protocol necessary to cause this to happen?

Probably as it uses the drug Heparin.

 

[Mary]

Probably as it uses the drug Heparin.

This is what I'm wondering - whether the heparin is necessary to cause this effect.

If you run something clogged with a substance through a filter, that substance generally will clog the filter. So I'm wondering if something in the HELP protocol - e.g., heparin - is necessary to cause what happened with Dr. Khan's blood, or whether the microclots all on their own without the heparin or anything else would clog the dialysis or apheresis filter.

 

[andyguitar]

So I'm wondering if something in the HELP protocol - e.g., heparin - is necessary to cause what happened with Dr. Khan's blood,

I dont think it can be done without Heparin. The Heparin removes fibrogen and cholesterol from the blood plasma. It sounds like the Heparin combines with the fibrogen and cholesterol to form a clot and these are then removed by the filter. So it not really removing clots from the whole blood. If you like the Heparin is forming a clot.

 

[SNT Gatchaman]

Dr. Khan's microclots clogged the apheresis machine 4 times I think and it had to be cleaned out. I'm wondering if this would have happened if he had been having a different dialysis or apheresis procedure - or was the HELP protocol necessary to cause this to happen?

It just seemed to me that if one had lots of blood clots, they would clog the machine regardless of what it was being use for. In dialysis some sort of filter is used to clean the blood and I'm assuming apheresis has a similar filter, and that it's this filter which got clogged with Dr. Khan

Conventional haemodialysis / haemofiltration (as used for renal replacement therapy) uses a semi-permeable membrane, that allows counter-current diffusion to rid the blood of undesirable solutes (e.g. urea, potassium). Those circuits don't clog frequently in the setting of e.g. alternate daily dialysis, but may clog in the ICU setting of continuous haemofiltration.

VA- or VV- ECMO circuits in ICU will need their filters changed every three or four days, I believe. This is not performed until needed due to patient risk during each changeover. The patient is heparanised to preserve the circuits for as long as possible. Heparin should be protective against filter occlusion. That it isn't in his case is a relevant observation, implying that the coagulation process is impaired despite the heparin, so presumably impacting a different part of the coagulation cascade.

EDIT: HELP apheresis seems to make use of heparin to "precipitate out" LDL cholesterol, lipoproteins and fibrinogen. I'm not clear on the balance of anticoagulation vs precipitation here, to answer @Mary's question.

I infer from Twitter posts etc that Dr. Khan was having filtration for around 3-4 hours at a time. I presume the apheresis technique is broadly comparable to the above, so it would be unusual to block the filter 4 out of 7? times. The medical and technical staff presumably commented to him that this was atypical, as otherwise a non-specialist would have regarded this as par for the course.

Suspect this indicates that his blood is genuinely abnormal (despite the "normal" coagulation tests). Whether that generalises to all long Covid or all ME patients is unclear. Would be interesting if a complete panel of coagulation tests would also be normal (surely not). That is a potential biomarker.

The low SvO2 might be a useful "cheap" surrogate in the meantime.

 

[Shanti1]

If you run something clogged with a substance through a filter, that substance generally will clog the filter. So I'm wondering if something in the HELP protocol - e.g., heparin - is necessary to cause what happened with Dr. Khan's blood, or whether the microclots all on their own without the heparin or anything else would clog the dialysis or apheresis filter.

In the second video on the original post starting at 7min, it is explained that in, this case, the heparin used in HELP apheresis works as an absorbent for specific molecules to draw them out of the blood (I know that seems counter-intuitive) that regular apheresis does not.

I get what you are saying though, why wouldn't the "micro-clots" be filtered out just by virtue of their size when they go through a filter? Especially if they have the ability to "clog" the filter? Perhaps they are not fully formed clots, but rather fully form during the HELP apheresis process? Just a guess,

On another note, the clots found in long-COVID are distinctly different from clots found in other pathologies.
Dr. Etherisius Pretorius authored the paper, Persistent clotting protein pathology in Long Covid/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased level of antiplasmin, which first brought the micro-clot issue in long-COVID into the public eye.

Both in the paper, and here in this video where she presents her work, she explains that micro-clots in COVID-19 patients are resistant to normal enzymatic breakdown, unlike clots in other conditions. She further explains in the video that the reason for the resistance to fibrinolysis (enzymatic breakdown) is the incorporation of the COVID-spike protein into the clot and how it alters the clot behavior. She also discusses how COVID microclots have a different composition from normal clots, even apart from the spike protein.

 

[Mary]

@andyguitar , @SNT Gatchaman , @Shanti1 - thanks for your replies! When I get a bit more energy, I'll go over them in more depth