Stanford MECFS working group meeting 2023

Ash said:
When reading the wiki bit on this drug it says not safe for long term use because of decalcification of bones.
How does this fit in for us, in layman’s terms? If anyone knows.
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The theory seems to go that cells which are in a metabolic trap can be released with the right stimulus. So if the right drug is identified, presumably it wouldn't need to be taken long term anyway.

I don't know how likely it is that the trap idea is correct, of course, it is still a theory at present.
 
What are thoughts on testing type I interferon inhibitor therapy in ME like is done in SLE? Since they’ve found similar levels of increased IFNa in ME as in SLE. Type I interferon (which includes IFNa) is activated in more than 50% of SLE patients and is considered an important pathogenic factor. There is at least one existing approved drug anifrolumab (Saphnelo) which is an anti-IFNa receptor monoclonal antibody.
 
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Ash said:
When reading the wiki bit on this drug it says not safe for long term use because of decalcification of bones.
How does this fit in for us, in layman’s terms? If anyone knows.
Click to expand...

If the problem is being locked into metabolic shunt, as seems to be the suggestion then once a drug has unlocked the situation it should no longer be needed.

Etidronate can be used over quite long periods along as it has to be intermittent. Maybe if the shunt kept coming back you could re-unlock it repeatedly.

I am afraid I cannot see scrap of evidence for any of this being relevant to ME.
 
And sorry if this idea has already been hashed out and isn’t relevant, but how about clinically testing IL-1 inhibition in ME/CFS patients as proof of concept to see if illness symptoms are indeed driven by inflammation or not? This would circumvent the issue found with testing corticosteroids because of their confounding neuropsychiatric effects
 
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Jonathan Edwards said:
I am afraid I cannot see scrap of evidence for any of this being relevant to ME.
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I think the theory was at least partly inspired by the subset of people who've experienced overnight remissions. It's happened to me twice, and it is odd.

That doesn't necessarily mean it's significant, and even if it is there are other potential explanations. Having since experienced the overnight magic of the Astra-Zeneca Covid vaccine, I'd be more inclined to think it was some kind of immune shift. The first jab provoked a recovery in function as rapid and impressive as the remissions decades earlier, although not nearly as long-lasting.
 
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