Is Apheresis an effective treatment for Long Covid and ME?

[Breagjam]

I reached out to Dr. Benjamin Natelson in NYC, he responded to me:



I think that's a bit short-sighted...the current therapies are a bit more aggressive than just aspirin.

That’s a disappointing response.
What does he mean “data nonexistent”? No large scale study of microclots?
Don‘t let Dr. Khan see this response

 

[andyguitar]

I think that's a bit short-sighted...the current therapies are a bit more aggressive than just aspirin.

Sounds like someone who has not bothered to look at all the information that's available.

What does he mean “data nonexistent”? No large scale study of microclots?

It's just another ill informed comment @Breagjam

 

[smithsj]

Sounds like someone who has not bothered to look at all the information that's available.
It's just another ill informed comment @Breagjam

Well he's right that there isn't much (any?) data. Absence of evidence is not evidence of absence though. Hopefully he'll regret his statement next month...

 

[andyguitar]

Well he's right that there isn't much (any?) data.

There is more to science than double cross over placebo blind trials, is thats what he means.

 

[Akasha]

Data nonexistent. Read the abstract for the article. Seems to imply we need to measure and address platelet dysfunction. RECOVERY-aspirin study just published. 10,000 inpatients RCT, no benefit from asa. Chance of targeted outpatient therapy based on TEG being helpful seems remote and doubt its worth studying.

Just "read the abstract" and "doubt its worth studying"?
I'm sorry but It sounds lazy and arrogant to me. Platelet hyperactivation is proved by microscopy in Pretorius paper. In fact, if he would have read it, he'll know his questions are addressed inside.
Pretorius group proposed that a treatment covering the enzymatic pathway, platelets and lysis of microclots is needed EARLY in the disease, prehospital. Platelet hyperactivation needs dual channel blockade (ASA+clopidogrel) and the over activation of the enzymatic coagulation pathway needs a DOAC. That's why only ASA is not enough.

But what would I know? I only read the paper...

 

[Akasha]

Talking about ASA...
A bit after my onset, my pediatrician told me not to have ASA ever again. He gave me some pills for my pain that had too much salicylic acid and I developed massive hematomas on my legs (from just minor falls). I haven't taken even an aspirin since then.
I can't link this event with the micro clotting. If I had clots, I guess ASA wouldn't have that effect on my blood, right?

Any insights would be really appreciated

 

[SWAlexander]

Maybe this brings more clarity.

PROF RESIA PRETORIUS von Willebrand
"When patient’s general tests do not show that there is an issue with coagulation.
Even the primary tests everything comes normal and people are concerned so but that's the answer is very simple the d-dimer the massive inflammatory molecule presence of von Willebrand are all trapped inside the micro clots that are the insoluble part of the plasma and most of these pathology tests look at the soluble part of the plasma. So the soluble part if you compare soluble with soluble you don't find differences and we also confirmed that there's no real you know…."
If you watch

and open the Transcript you can hear and read it trapped inside the micro clots.

 

[SNT Gatchaman]

Timestamps for the above video:

• Background to starting research into long COVID
• Introduction to micro-clots in long COVID paper
• Micro-clots resistant to trypsin digestion
• Contents of micro-clots: promoting persistence and inflammation
• If coagulation is abnormal, why are standard blood tests normal?
• Micro-clots and endothelial dysfunction causing oxygen deprivation in micro-circulation
• Reference to HELP apheresis
• Neuroinflammation and damaged blood-brain barrier (which might take longer to recover)
• Possible reasons for vulnerability to long COVID (unclear, some with co-morbidities, some may be genetic predisposition)
• Defining long COVID in terms of persistent micro-clots and platelet hyperactivation (biomarker)
• This is a real biological disease and not psychological

 

[SWAlexander]

Thank you SNT Gatchaman .

 

[Shanti1]

[QUOTE="
It turns out alpha-2-antiplasmin is a serine-proteases inhibitor (ref) (ref). Nattokinase, serrapeptase, and lumbrokinase are all serine-proteases

Can you say more on serine-proteases? HOw are these related to just the amino acid serine? So one can measure the amino acid serine in serum and in urine. Do these have any relation to serine proteases?
Also curious if you thinj they are relevent to many with CFS or are they specific to COVID? Does the link to the articles you've given discuss the role of serine protease in COVID?

@vision blue
The thought is that Alpha2-Antiplasmin is found in high amounts in COVID microclots. It is a serine protease inhibitor and is one of the factors that contribute to the resistance of the microclots to break down by the enzyme plasmin. Plasmin is a serine protease, meaning that the amino acid serine plays a key role in the enzyme's catalytic center (the part of the enzyme that binds to fibrin to break it down).

Nattokinase, serrapeptase, and lumbrokinase are also serine proteases that break down fibrin and share similarities in structure to plasmin. The question is if the antiplasmin in the microclots would also inhibit these exogenous serine protease enzymes or perhaps they are different enough in structure that they are not impacted by antiplasmin. It seems that doctors are using nattokinase and have good results, so it may be a theoretical, non-clinically relevant concern.

Since antiplasmin irreversibly binds to plasmin, nattokinase (and other enzymes) could actually be useful in overcoming the inhibition of antiplasmin. If someone wanted to incorporate a non-serine protease that also has fibrinolytic activity, they could use bromelain, which contains cysteine proteases.

 

[SlamDancin]

@Shanti I did a little trial of NattoK and Bromelain and they both made me sicker and even after cessation I never returned to the baseline I was at before. It’s been a couple months now at most. Be careful with these

 

[Shanti1]

@SlamDancin thanks for sharing that. I also couldn't tolerate bromelain, nattokinase, or serrapeptase, but I stopped as soon as I realized I felt worse with them. Fortunately, I came back to baseline. I'm sorry to hear you are still not recovered. How long did you take them for?

I think pwME need to be careful with any new supplement or medication. It can be difficult to know if feeling worse is a herx or detox reaction or if something is simply not good for our biology. At this point, if I feel poorly with something, I usually just stop as it is too risky to gamble on it being a herx that I have to push through. For my personal biology, I have also started to be able to distinguish between a herx and something that is just aggravating me. I hardly tolerate any supplements.

 

[SWAlexander]

How awful, @SWAlexander !

Please recover soon.

Thank you. I´m on the mend. Sleeping is my way of recovering. On 14 -15 Dec. 12 hours sleep, 15-16 Dec. 9 hours sleep.

 

[SWAlexander]

@SlamDancin thanks for sharing that. I also couldn't tolerate bromelain, nattokinase, or serrapeptase, but I stopped as soon as I realized I felt worse with them. Fortunately, I came back to baseline. I'm sorry to hear you are still not recovered. How long did you take them for?

I think pwME need to be careful with any new supplement or medication. It can be difficult to know if feeling worse is a herx or detox reaction or if something is simply not good for our biology. At this point, if I feel poorly with something, I usually just stop as it is too risky to gamble on it being a herx that I have to push through. For my personal biology, I have also started to be able to distinguish between a herx and something that is just aggravating me. I hardly tolerate any supplements.

I took Bromelain once to reduce pain and sinuses swelling. I had a big anaphylaxis reaction.

 

[Crux]

It's possible that Lactoferrin may be a good additional treatment as it inhibits viruses and is antithrombotic.
This paper includes lysosyme and ovatransferrin, derived from eggs as antiviral, antithrombotic substances.

https://www.futuremedicine.com/doi/10.2217/fvl-2020-0170

" In addition, lactoferrin-derived peptides inhibit angiotensin II pro-inflammatory activity through binding to the angiotensin II receptor type 1 [69], and lactoferrin as well as other peptides in cow’s milk have an antithrombotic effect [71]. "

This paper is about how lactoferrin inhibits plasminogen activation, which can cause inappropriate blood clotting if not regulated.

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5986228/

" Here, we demonstrate a so far unknown function of LF in regulation of fibrinolysis and unravel the molecular determinants and mechanism whereby lactoferrin blocks plasminogen activation."

@SWAlexander , @Learner1 , may find this interesting.

 

[Martin aka paused||M.E.]

So. If I would like to look at my blood for Christmas what microscope would I need and what centrifugal speed?
Josh found sth very interesting. RBC clotting in a crash but normal when at baseline.
He has 200 patients in his study now.
Pics shared with permission:

 

[SWAlexander]

Martin I don´t know if my answer fits your need.
I found it very helpful emailing question like yours to different labs. Some are very willing to help.
However, F9 (Christmas factor) clotting is a X chromosome disorder and very few labs test for it.

If you like Mayo Clinic has a video, partially on F9,

 

[Martin aka paused||M.E.]

However, F9 (Christmas factor) clotting is a X chromosome disorder and very few labs test for it.

I don't think that his findings have anything to do with it because the blood looks normal when not crashed

 

[SWAlexander]

It's possible that Lactoferrin may be a good additional treatment as it inhibits viruses and is antithrombotic.
This paper includes lysosyme and ovatransferrin, derived from eggs as antiviral, antithrombotic substances.

https://www.futuremedicine.com/doi/10.2217/fvl-2020-0170

" In addition, lactoferrin-derived peptides inhibit angiotensin II pro-inflammatory activity through binding to the angiotensin II receptor type 1 [69], and lactoferrin as well as other peptides in cow’s milk have an antithrombotic effect [71]. "

This paper is about how lactoferrin inhibits plasminogen activation, which can cause inappropriate blood clotting if not regulated.

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5986228/

" Here, we demonstrate a so far unknown function of LF in regulation of fibrinolysis and unravel the molecular determinants and mechanism whereby lactoferrin blocks plasminogen activation."

@SWAlexander , @Learner1 , may find this interesting.

Yes, it is very interesting. Thank you. I remember now watching a video on LF a few months ago:
Lactoferrin And COVID-19: Previous Evidence And Mechanism Against COVID-19

 

[SWAlexander]

I don't think that his findings have anything to do with it because the blood looks normal when not crashed

If the blood looks normal before a crash, are you sure it is F9 (Christmas factor)?
I think you are on something very interesting.