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New Rituximab ME/CFS open-label phase II study with rituximab maintenance treatment

msf

Senior Member
Messages
3,650
SOC, I was trying to suggest that that kind of thing is unlikely, in my view anyway, to be the reason why some people respond to Ritux and some don't - i.e. it's probably not going to be explained by one group having one infection and the other group another infection. What I think we will see instead is that the responders are all at a similar stage of the illness, even if they got there by different routes. Since both EBV and Lyme can persist in B cells, it seems quite likely that both can cause B cell dysfunction that is responsive to Rituximab treatment. I think the amount of time someone has been ill, and how severe their illness is, will determine how much B cell dysfunction they have, and thus how they respond to Rituximab treatment.

On that note, is it just me seeing what I expect to see, or were the major responders in this study ill for longer, on average, than the non- and minor responders?
 

msf

Senior Member
Messages
3,650
No Barb56, it's the same Maes, there is only one who is involved in studying ME, as far as I am aware.
 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
I do wonder if fibro might not also respond to Rituximab.
My own opinion is that it's seems likely there's a strong probability that a subset of fibro patients will respond to rituximab. The fibro population may be very heterogeneous, but perhaps no more than the CFS population.
 

Kati

Patient in training
Messages
5,497
My own opinion is that it's seems likely there's a strong probability that a subset of fibro patients will respond to rituximab. The fibro population may be very heterogeneous, but perhaps no more than the CFS population.
The FM population will likely become more heterogenous with the new definition which does not requires tender points and with the work of psychologizers. Moreover there is a new tendency to bring the pain conditions under one umbrella "chronic widespread pain".


Sad to see.
 
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barbc56

Senior Member
Messages
3,657
No Barb56, it's the same Maes, there is only one who is involved in studying ME, as far as I am aware.

Even a clock is right twice a day. It don't think it takes away from the research since there are so many other references. But there is still a bit of a cringe factor to this guy.

:bang-head::bang-head::bang-head:

Barb
 
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Gijs

Senior Member
Messages
690
Rituximab isn't going to be a medicine for ME/CFS as long they don't know (objective!) for which patiënt it will help. I think it will be helpfull espescially for POTS/ME patiënts because POTS is an almost proven autoimmune disease.
 

lansbergen

Senior Member
Messages
2,512
Even a clock is right twice a day. It don't think it takes away from the research since there are so many other references. But there is still a bit of a cringe factor to this guy.

:bang-head::bang-head::bang-head:

Barb

Well once a psych always a psych but to be honest he always was interested in the biology of it.
 

msf

Senior Member
Messages
3,650
I think some of the disregard that some people have for certain ME researchers stems from the kind of misunderstanding of how science works that Laurence Krauss talks about - that is, new findings do not automatically replace everything that has gone before (in Krauss' example, Einsteinian physics did not replace Newtonian physics, but rather it added a new level of understanding to it). In this way, Fluge and Mella's findings aren't going to replace all previous findings, particularly those that were made by more than one researcher, such as the discovery of active herpes viruses in some ME patients, or the discovery of Lyme and co-infections in others.

Rituximab (or similar treatments) may turn out to be the best way of treating ME, but that doesn't mean that the work of other researchers is irrelevant or worthless.
 

Sidereal

Senior Member
Messages
4,856
I've wondered about this. Aren't autoimmune diseases more common in those of Scandinavian descent?

Dunno. Here's what Fluge/Mella said:

Among patients included in the present study, 41% had one or more first-degree relatives with an autoimmune disease (AD). The prevalence of known AD in the general population was estimated to 3.2% in a study from US [25] and to at least 5% in a study from Denmark [26]. Taking into account that each individual may have on average 4–6 first-degree relatives, and also that several AD to some extent tend to cluster in families, the reported 41% in this study is probably higher than expected and therefore may indicate a genetic predisposition for AD.

Interestingly, recent studies have indicated a possible autoimmune basis for Postural Tachycardia Syndrome (POTS) with autoantibodies to autonomic receptors [27]. Studies have also suggested that in subsets of Chronic Regional Pain Syndrome (CRPS) patients, associations to partly agonistic autoantibodies to β2-adrenergic receptors and to muscarinic-2 receptors were reported [28]. CRPS has been shown to improve after intravenous immunoglobulin therapy, and has been proposed as a prototype of a novel kind of autoimmunity with a possible two-hit process involving pre-existing autoantibodies that may become pathogenic after a triggering event such as trauma or infection [29]. It is worth noting that POTS is detected in approximately 15% of ME/CFS patients [30], and both POTS and CRPS are seen primarily in young women and have features that partly overlap with ME/CFS such as fatigue, brain fog, and central sensitization.

"Brain fog" in a journal article, lol, love it.
 
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Sasha

Fine, thank you
Messages
17,863
Location
UK
That 15% of PWME with POTS seems extremely low - I've seen estimates of 85% and higher. The [30] reference in the paper is this one:

Lewis I, Pairman J, Spickett G, Newton JL (2012) Clinical characteristics of a novel subgroup of chronic fatigue syndrome patients with postural orthostatic tachycardia syndrome. J Intern Med.
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
Fluge & Mella said:
Among patients included in the present study, 41% had one or more first-degree relatives with an autoimmune disease (AD). The prevalence of known AD in the general population was estimated to 3.2% in a study from US [25] and to at least 5% in a study from Denmark [26]. Taking into account that each individual may have on average 4–6 first-degree relatives, and also that several AD to some extent tend to cluster in families, the reported 41% in this study is probably higher than expected and therefore may indicate a genetic predisposition for AD.

@Jonathan Edwards - any mileage in a PR survey of how many first-degree rellies we have and how many have an AD?
 
Messages
15,786
That 15% of PWME with POTS seems extremely low - I've seen estimates of 85% and higher. The [30] reference in the paper is this one:
In studies where they've looked specifically for NMH in ME patients, most had NMH and a minority had POTS.

POTS is not equivalent to Orthostatic Intolerance. It is one type of it, and having tachycardia with a direct known cause (low blood pressure, low pulse pressure) would probably get a label other than POTS.
 

JamBob

Senior Member
Messages
191
In studies where they've looked specifically for NMH in ME patients, most had NMH and a minority had POTS.

POTS is not equivalent to Orthostatic Intolerance. It is one type of it, and having tachycardia with a direct known cause (low blood pressure, low pulse pressure) would probably get a label other than POTS.


Can NMH be autoimmune? Are there any studies into this? Thanks
 

anniekim

Senior Member
Messages
779
Location
U.K
@charles shepherd and @Sasha I think I must be misunderstanding but does the proposed rituxamb study by invest in M.E at UCL not fit the bill of a phase 3 trial here in in the UK?

My understanding is that no definite decisions have yet been made on the protocol for this UK trial, the location, and when the trial will start

Others may be able to provide more information here[/QUOTE]

Great, so it could be a contender as in all adding up to convincing the NHS that rituxamb or something similar would worth being authorised as a treatment for some people with M.E?
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
@Jonathan Edwards - this possibility of OI being another autoimmune issue makes me wonder whether having OI would be an indication that a PWME would respond to rtx.

I don't know if all OI is autoimmune, though - I know astronauts get it, so clearly theirs isn't, and I think that prolonged bedrest can also provoke it but if it's rapid onset, or it's happening in people who aren't bedbound...

Anyway, just a thought.
 

anniekim

Senior Member
Messages
779
Location
U.K
@Jonathan Edwards - this possibility of OI being another autoimmune issue makes me wonder whether having OI would be an indication that a PWME would respond to rtx.

I don't know if all OI is autoimmune, though - I know astronauts get it, so clearly theirs isn't, and I think that prolonged bedrest can also provoke it but if it's rapid onset, or it's happening in people who aren't bedbound...

Anyway, just a thought.
I have had M.E for 17 years but my OI symptoms only became apparent and very rapidly a few years ago when my M.E became more severe. Perhaps I had OI before but not enough to notice....
 
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