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Good news! Norwegian govt funds Rituximab trial - possibly partial, amount not yet announced

WillowJ

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Messages
4,940
Location
WA, USA
I wonder what we might learn if the results of the next phase as not good. Would this mean a) ME is not an autoimmune condition; or b) that simply this drug is not good?

Probably (b). Although maybe (a). I can't offhand think of any research that specifically says patients with ME have similar issues with X cells as this other population who do have an autoimmune condition and are treated successfully with Rituximab.

Comparison studies would be cool I think.

I agree that it would be (b). Lots of our patients have positive ANA, a generic marker for autoimmune disease.

There are some indications that we have stuff going wrong in B cells and T cells, but I don't have any references handy tonight and I'm not sure how this compares to RA and MS. Too late to try to look it up.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
I agree that it would be (b). Lots of our patients have positive ANA, a generic marker for autoimmune disease.

There are some indications that we have stuff going wrong in B cells and T cells, but I don't have any references handy tonight and I'm not sure how this compares to RA and MS. Too late to try to look it up.

I was reading Cort's article this morning and the comments below it. I sure hope people don't place all their hopes on Rituximab or that it and autoimmunity will provide an answer.

I'd like to see someone outside of this phase III drug trial looking more closely at the 'why's?' and 'how's?' because I don't think this trial will be able to - at least not very closely and someone will need to at some point.

Am naturally cautious I suppose. Lot of money involved but it had to be supported. We'll just have to wait and see. Getting used to that aren't we? :(
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
I was reading Cort's article this morning and the comments below it. I sure hope people don't place all their hopes on Rituximab or that it and autoimmunity will provide an answer.

I'd like to see someone outside of this phase III drug trial looking more closely at the 'why's?' and 'how's?' because I don't think this trial will be able to - at least not very closely and someone will need to at some point.

Am naturally cautious I suppose. Lot of money involved but it had to be supported. We'll just have to wait and see. Getting used to that aren't we? :(


I would be amazed if anyone doing a Rituximab trial wasn't doing everything they could to also look at mechanism.

There's also a bigger picture. A confirmatory trial of Rituximab will mean a step-change in how our disease is seen. Rituximab is an immune drug, not a talking therapy or exercise. It will mean we are seen as having an immune disease - which we most certainly do, whether it's auto-immune or not, or has other components such as neurological and so on - and will legitimise our illness, get many more scientists and clinicians interested, and open the floodgates to funding. Any successful confirmatory trial of any immune drug - Rituximab, Ampligen, Valcyte - for ME will do this. At the moment, Rituximab looks very promising and that's why so much effort is going into funding it.

It's not about the % of patients who will eventually benefit from Rituximab directly, although that could be sizeable. The implications are much, much bigger than that.
 
Messages
5,238
Location
Sofa, UK
Fluge and Mella have been looking into what the mechanism might be all along. From the embargoed content at IiME, it looks like they have a very interesting hypothesis and will hopefully be publishing something about that in due course if it pans out. It also looks like they are talking with some of our other researchers about this and the clinical autoimmunity group will all be thinking about the questions above I'm sure. One thing to think about: how autoimmunity might fit into the bigger picture might depend on what it is that the autoimmune antobodies might be attacking...
 

WillowJ

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Messages
4,940
Location
WA, USA
I was reading Cort's article this morning and the comments below it. I sure hope people don't place all their hopes on Rituximab or that it and autoimmunity will provide an answer.

I think it's a leap of logic to assume that when someone says, "if rituximab doesn't work that wouldn't mean it's necessarily not an autoimmune disease" means they think "it's definitely an autoimmune disease and that's the only thing going on".

obviously there are other pathologies, too. you asked about stuff relative to rituxan and I answered relative to that. It could work or partially work, and we have reasons to hope for that. It could fail. We don't know yet. I'm hoping for a good treatment, and this is the soonest thing in the works that offers hope for this.
 

biophile

Places I'd rather be.
Messages
8,977
I wouldn't say that, but they are generally the most skeptical about any "scientific" finding there is. Eg they're skeptical about psychiatry etc. in general too.

Perhaps generally, but I do vaguely recall an article there which uncritically swallowed unscientific ideas about CFS and somatization without much skepticism whatsoever. It is an embarrassment when "skepticism" towards one supposedly dubious diagnostic entity means uncritically accepting questionable ideas about another dubious diagnostic entity.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
We talk about autoimmunity but to what (physical) substans ? We need to know.

Based on Maes paper last year (i forget the title) this is the wrong question. Which substance? Lots of them ... we have autoantibodies to six (IIRC) out of six substances Maes tested. In other words, we don't have a specific autoimmune problem, we have a generalized autoimmune problem (probably). This suggests some kind of failure involving B cells, either producing nonspecific antibodies (which was suggested at the IiME conference) or a complete failure to control autoimmune processes. I doubt the latter as it would probably become fatal very quickly.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
Fluge and Mella have been looking into what the mechanism might be all along. From the embargoed content at IiME, it looks like they have a very interesting hypothesis and will hopefully be publishing something about that in due course if it pans out. It also looks like they are talking with some of our other researchers about this and the clinical autoimmunity group will all be thinking about the questions above I'm sure. One thing to think about: how autoimmunity might fit into the bigger picture might depend on what it is that the autoimmune antobodies might be attacking...

I'm not sure it is about specific antibodies, at least not across the whole CFS population. The one consistent pattern among the CFS literature is non-specific immune system activation. It seems to me the higher than normal results when various autoantibodies are tested in studies is just suggestive of increased immune activation.

I see it as a regulatory loop issue. Induced by a sustained EBV infection (as per that Italian theoretical paper a while back), or adjuvants etc. What Scheibenbogen said at the recent conference was interesting too...
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
There's also a bigger picture. A confirmatory trial of Rituximab will mean a step-change in how our disease is seen. Rituximab is an immune drug, not a talking therapy or exercise. It will mean we are seen as having an immune disease - which we most certainly do, whether it's auto-immune or not, or has other components such as neurological and so on - and will legitimise our illness, get many more scientists and clinicians interested, and open the floodgates to funding. Any successful confirmatory trial of any immune drug - Rituximab, Ampligen, Valcyte - for ME will do this. At the moment, Rituximab looks very promising and that's why so much effort is going into funding it..

Exactly. Lets say for example, that Rituximab clearly works for say, 30% of CFS patients. Then we can go to immunologists, HIV/AIDS researchers etc and ask why - and they will recognise that our current understanding is lacking and the research field should explode. Probably with more Rituximab trials at the start (as measurements taken before and after to see what changed).
 

Gijs

Senior Member
Messages
690
ME is a stress respons disorder just like dr. kogelnik said. All the immuneproblems are secondary but important to tread. We must know what triggers this stressrespons constantly (i do not mean mentally illness!) This will be the key to explain this disease.
 

natasa778

Senior Member
Messages
1,774
ME is a stress respons disorder just like dr. kogelnik said. All the immuneproblems are secondary but important to tread. We must know what triggers this stressrespons constantly (i do not mean mentally illness!) This will be the key to explain this disease.

Chicken and egg question as the immune and stress response systems are closely interlinked and in constant communication. If one is messed up the other one will end up being dysfunctional as well. It is possible also that they then enter a vicious cycle dance, together with other body system, in which one dysfunctional system negatively influences the other in a loop ... so cutting off this negative feedback cycle (in one or several places at once) could be the key. Maybe rituximab does exactly that in some ..
 

Gijs

Senior Member
Messages
690
There are many immune diseases where patiënts do not have a constant active and abnormal stressrespons i think it is specific and unique for ME. Me patients can not handle any stimuli physical and mentally. That is the central problem. Overacivity of the SAM-AX/HPAC AX can explain everything. This puzzle fits. There is an interaction between the parasympathic and immune system macrofagen/gut and Vagus Nerve there can be the key as well.
 

natasa778

Senior Member
Messages
1,774
There are many immune diseases where patiënts do not have a constant active and abnormal stressrespons i think it is specific and unique for ME. Me patients can not handle any stimuli physical and mentally. That is the central problem. Overacivity of the SAM-AX/HPAC AX can explain everything. This puzzle fits. There is an interaction between the parasympathic and immune system macrofagen/gut and Vagus Nerve there can be the key as well.

the nature of immune dysfunction could be different in ME than other immune diseases (I would not call it immune 'disease' anyway, and we do not know of any with same findings )

btw those exact same things above present in autism