Nature - Chronic post-COVID-19 syndrome and chronic fatigue syndrome: Is there a role for extracorporeal apheresis?, 2021, Bornstein et al

Kalliope

Kalliope

Senior Member (Voting Rights)
Nature - molecular psychiatry
Chronic post-COVID-19 syndrome and chronic fatigue syndrome: Is there a role for extracorporeal apheresis? - Bornstein et al

Abstract
As millions of patients have been infected by SARS-CoV-2 virus a vast number of individuals complain about continuing breathlessness and fatigue even months after the onset of the disease.

This overwhelming phenomenon has not been well defined and has been called “post-COVID syndrome” or “long-COVID” [1].

There are striking similarities to myalgic encephalomyelitis also called chronic fatigue syndrome linked to a viral and autoimmune pathogenesis.

In both disorders neurotransmitter receptor antibodies against ß-adrenergic and muscarinic receptors may play a key role.

We found similar elevation of these autoantibodies in both patient groups.

Extracorporeal apheresis using a special filter seems to be effective in reducing these antibodies in a significant way clearly improving the debilitating symptoms of patients with chronic fatigue syndrome.

Therefore, such a form of neuropheresis may provide a promising therapeutic option for patients with post-COVID-19 syndrome.

This method will also be effective when other hitherto unknown antibodies and inflammatory mediators are involved.
 
Extracorporeal apheresis using a special filter seems to be effective in reducing these antibodies in a significant way clearly improving the debilitating symptoms of patients with chronic fatigue syndrome.
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?

'clearly'?

So ME has been cured then?

Am I the only one who doesn't know?

Is it just me or....is the world full of......
 
Kalliope said:
Therefore, such a form of neuropheresis may provide a promising therapeutic option for patients with post-COVID-19 syndrome.
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I'm struggling to understand this sentence. I don't know what "neuropheresis" mean.

Urban Dictionary says:

An imaginary procedure a neurosurgeon conjures when attempting to drop their balls on the table to ensure colleagues agree with their research plan.
“Start milrinone, see if she improves, plan for angio after neuropheresis catheter.”
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Does it have other meanings?
 
From the paper
"Targeting neurotransmitters AB in ME/CFS
Based on recent studies employing the monoclonal anti-CD20 antibody rituximab [9] in patients with ME/CFS there is reason to believe that the reduction of these neurotransmitters AB may be a promising target for therapy. In these studies, depletion of CD20+ B cells with rituximab led in a majority of patients with ME/CFS to a complete or at least partial remission. Since this beneficial effect occurred only several months after initiation of treatment with rituximab, it may be attributed to the wash-out of the autoantibodies due to the elimination of the short-lived antibody producing plasma cells related to the CD20+ memory B cells. A more immediate therapeutic strategy with less side effects may involve immune apheresis or other forms of extracorporeal apheresis such a neuro- or cerebropheresis [10].

Using immunoadsorption in patients with post-infectious ME/CFS with an IgG-binding column for 5 days in an observational study with ten patients induced a rapid improvement in seven patients [11, 12]. We have also used extracorporeal apheresis (INUSpheresis) enabling a significant reduction of total IgG and all neurotransmitter receptors of up to 50% as well as inflammatory proteins such as CRP or RANTES. In a clinical observation in patients with ME/CFS, extracorporeal apheresis used over either 2 or 4 days induced a significant improvement of symptoms based on disease-specific scores. ME/CFS patients with a clear-cut infection-triggered increase of autoantibodies seemed to have the most significant and sustainable clinical benefits. However, it is also highly conceivable that clinical improvement seen in patients subjected to therapeutic extracorporeal apheresis may have multiple causes, not only related to reduction in autoantibodies against neurotransmitters but also other yet unknown autoantibodies, inflammatory proteins, and rheological factors."


References

Ref 9 is to the 2015 phase 2 publication from Fluge and Mella, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0129898

Ref 10, Extracorporeal apheresis therapy for Alzheimer disease—targeting lipids, stress, and inflammation, https://www.nature.com/articles/s41380-019-0542-x

Ref 11 Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME (2018) Scheibenbogen et al

Ref 12 Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Efficacy of Repeat Immunoadsorption. Scheibenbogen et al. 2020
 
Kalliope said:
No it's this. This looks dodgy...
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Indeed.

Interesting co-authorship. From a quiick glance, nobody from the Scheibenbogen team involved, but in addition to the three staff members from the private clinic linked above, mostly affiliations with renowned universities, including two authors from the Institute of Psychiatry, Psychology & Neuroscience, King’s College London, UK.
 
Andy said:
From the paper
"Targeting neurotransmitters AB in ME/CFS
Based on recent studies employing the monoclonal anti-CD20 antibody rituximab [9] in patients with ME/CFS there is reason to believe that the reduction of these neurotransmitters AB may be a promising target for therapy. In these studies, depletion of CD20+ B cells with rituximab led in a majority of patients with ME/CFS to a complete or at least partial remission. Since this beneficial effect occurred only several months after initiation of treatment with rituximab, it may be attributed to the wash-out of the autoantibodies due to the elimination of the short-lived antibody producing plasma cells related to the CD20+ memory B cells. A more immediate therapeutic strategy with less side effects may involve immune apheresis or other forms of extracorporeal apheresis such a neuro- or cerebropheresis [10].

Using immunoadsorption in patients with post-infectious ME/CFS with an IgG-binding column for 5 days in an observational study with ten patients induced a rapid improvement in seven patients [11, 12]. We have also used extracorporeal apheresis (INUSpheresis) enabling a significant reduction of total IgG and all neurotransmitter receptors of up to 50% as well as inflammatory proteins such as CRP or RANTES. In a clinical observation in patients with ME/CFS, extracorporeal apheresis used over either 2 or 4 days induced a significant improvement of symptoms based on disease-specific scores. ME/CFS patients with a clear-cut infection-triggered increase of autoantibodies seemed to have the most significant and sustainable clinical benefits. However, it is also highly conceivable that clinical improvement seen in patients subjected to therapeutic extracorporeal apheresis may have multiple causes, not only related to reduction in autoantibodies against neurotransmitters but also other yet unknown autoantibodies, inflammatory proteins, and rheological factors."


References

Ref 9 is to the 2015 phase 2 publication from Fluge and Mella, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0129898

Ref 10, Extracorporeal apheresis therapy for Alzheimer disease—targeting lipids, stress, and inflammation, https://www.nature.com/articles/s41380-019-0542-x

Ref 11 Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME (2018) Scheibenbogen et al

Ref 12 Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Efficacy of Repeat Immunoadsorption. Scheibenbogen et al. 2020
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Is this not what Dr Scheibenbogen worked on? Or am I inaccurate ?
 
Seems like as a treatment it is too invasive and not long enough lasting. But would apheresis at least help us as a diagnostic — if it improved symptoms dramatically, we’d at least know that yes, there is something in our blood? (or would it prove something in plasma?)

Apherisis is offered at hematology centers to blood cancer patients I believe.
 
I don’t really understand the process, but it sounds rather like a ‘fishing exercise’ if you will pardon the pun:

Not clear what either no response or a positive response actually means, though obviously interesting if you get a positive response even if it is transitory.
 
Getting around to reading the whole article, I thought the following was interesting. I don't think we yet have good evidence for HPA axis dysfunction including abnormally low levels of cortisol in ME/CFS. The authors say they didn't find low levels of cortisol levels in Long Covid patients in those treated with dexamethasone. The inference is 'if we didn't find altered levels of cortisol even in these patients, then hydrocortisone is unlikely to be useful in Long Covid generally'. That's an interesting observation given Avi Nath's (NIH) excitement about trialling hydrocortisone in Long Covid.

Hypothalamic–pituitary–adrenal–hypofunction has been described in patients with ME/CFS as a consequence of activated immune-inflammatory pathways [17].

Most patients with severe Covid-19 disease have been receiving dexamethasone and may have an adrenal pre-damaged by the inflammatory process [18]. Therefore, there may be a predisposition for adrenal insufficiency [19] explaining some of the symptoms of the ME/CFS in post-COVID-19 patients. However, we have tested HPA-axis function in patients post-COVID-19 that have received dexamethasone and did not observe any blunting of adrenal cortisol levels (unpublished observation). Based on these findings, replacement with hydrocortisone may not be indicated to improve the severe signs of patients with a post-COVID-19 fatigue syndrome.
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