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Astounding Norwegian research breakthrough with Rituximab can solve CFS mystery!!!

Discussion in 'Rituximab: News and Research' started by urbantravels, Oct 19, 2011.

  1. livingwithcfids

    livingwithcfids

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    Ten patients in the rituximab group (67%) and two patients in the placebo group (13%) saw at least moderate reductions in fatigue.

    In most of the patients, improvements were transient and faded within eight to 44 weeks.

    But three patients, two in the rituximab group and one that got the placebo, continue to be symptom free 2 1/2 years after their treatments. Those three patients have all returned to full-time jobs, researchers say.

    One person in the placebo group has made full recovery from ME/CFS for 2.5 years? How is this even possible?



    http://www.webmd.com/chronic-fatigu...-drug-may-also-treat-chronic-fatigue-syndrome
     
  2. kurt

    kurt Senior Member

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    There are spontaneous remissions sometimes in ME/CFS, but often the disease will return later, there are forum members here who have reported up to 10 year remissions, then a return of ME/CFS. Perhaps the placebo remission was just like that.

    But I think the first point you mention is the most important, the improvement fades over time, perhaps as the B cells are replenished. Does that happen in the autoimmune conditions treated with Rituximab? (anyone read that lit yet?)

    This does not sound like a good long-term treatment for ME/CFS. We have other immune problems already, do we really want to continually be taking out our B cells? I don't like the idea of losing any WBCs. But definitely a great clue. In fact this makes me wonder about Lyme Disease in ME/CFS, as there can be WBC involvement in that disease. And there was a recent study showing b.B (Lyme) hides in the lymphatic system.
     
  3. Snow Leopard

    Snow Leopard Senior Member

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    In RA for example, patients are to be treated every 6 months as the B cells are replenished.

    With regards to ANA, this doesn't show up in all autoimmune conditions. Those with Diabetes mellitus (Type 1) for example, only a minority (say 15%) have positive ANA at any one time.
     
  4. Kati

    Kati Patient in training

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    Personally I am not quite buying into the auto-immune stuff either, however if Rituximab can work even just alleviate symptoms for a period of time, so I can recover some quality of life, I am cool with this drug.

    No drug so far have been helpful. Ampligen's side effects sound horrendous. It sounds like it doesn't offer a cure to people. It is quite pricey and you have to move out of your area and close to a doctor that offers it in order to get it.

    Until we have better options, this is what we got. And it sounds like very promising to me- in the meantime. Waiting for science to figure it out and waiting for our government to give the money to research (is it going to happen?)

    To me it sounds like a very appealing option. All I got to do is to convince someone, anyone, to push it into my veins.
     
  5. Lily

    Lily *Believe*

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    I agree and would be willing to try this as well. It's well known with safe protocols (relatively speaking). I'd do it in a heartbeat.
     
  6. sandralee

    sandralee

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    Hi all,

    I have a question regarding the mechanism of action of Rituximab versus some of the immune modulators used by some ME/CFS patients.

    My understanding is that Rituximabs effectiveness is through the depletion of B cells. Do any of the modulators like LDN, GcMAF, Nexavir, Cycloferon, etc. work on B cells, and if so, do they enhance or deplete the B cells?

    This is certainly the most exciting study Ive ever come across, and it would be interesting to know whether there were any patient profile differences between the 10 responders and the 5 non responders.

    All the best,

    Sandra
     
  7. Sasha

    Sasha Fine, thank you

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    Hi urban - I've been googling on "Rituximab CFS" to see what's coming up on the net and now this thread's edited title is coming up prominently entitled "Crazy Norwegian research..." which makes it sound as though someone thinks the research is crazy. I realise this is an unintended consequence but we shouldn't have something on the net that appears to disparage the research.

    I hadn't thought about the internet search angle on this and personally I'd avoid putting the word "crazy" with this thread at all. I didn't understand the humorous reference of the original title (maybe because it's a US one? From a TV show or something? Or maybe just a US figure of speech?) and perhaps neither will a lot of people on the net who are just googling (sorry, urban, it is horrible to make a joke and for people not to get it!).

    I'm black triangling this post to get a moderator's attention and hope they will fix this right away!
     
    taniaaust1 likes this.
  8. globalpilot

    globalpilot Senior Member

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    Hi Rich,
    Great response. You are just the best in my view. I have some comments and questions which I'll insert into your text preceded by GP.

    Hi, all.

    I think this is a very interesting development, and I want to suggest what I think is going on when Rituximab is used to treat ME/CFS.

    It will probably come as no surprise to those familiar with my history here that I will propose a mechanism that fits with the GD-MCB hypothesis for the pathophysiology of ME/CFS.

    O.K., here it goes:

    Based on the body of immunological studies that have been done in ME/CFS over quite a few years, we know that the immune system is dysfunctional in this disorder. In particular, it has a pronounced shift to the Th2 type of response, away from cell-mediated immunity.

    The NK cells and the cytotoxic (CD8) killer-T cells are ineffective, partly because they are unable to produce enough perforin to punch holes in cells that are infected with viruses. Since this is the main mechanism normally used to knock out viral infections, these infections cannot be knocked out.

    The immune system is forced to use its fall-back mechanisms, which are the humoral immune response (antibodies produced in Th2 by the B cells, which become plasma cells, and the interferon-induced mechanisms, including RNase-L).

    GP: Are these really fallback mechanisms or rather normal important parts of the immune response that continue because the infection is not resolved due to the problems with cell mediated immunity ?


    These are less effective and are not able to completely knock out viral infections (The cell-mediated cavalry never arrives). This is the reason for the ongoing guerrilla war in the person's body, with both the reactivated viruses which have been in the body in the latent state, and with new ones that come along and infect the person after the onset of ME/CFS

    As has been noted, the B cells do produce proinflammatory cytokines, which of course promote inflammation. Because most PWCs also have a dysfunctional HPA axis, cortisol tends to be low, and the inflammation is allowed to intensify to a higher level than normal.

    GP: Recently I sent you an email regarding some information on the function of beta-endorphins in the body. The book I found stated in part The most relevant immunostimulatory action of beta endorphin would consist of the stimulation of t lymphocyte proliferation, probably by acting in part on NLX insensitive receptors and activation of natural killer cell cytotoxicity. On the contrary, he most evident immunosuppressive effect of beta endorphin is represented by the stimulation of IL-10 secretion from TH2 lymphcytes, by acting on specific mu-opioid receptors, which is antagonized by NTX. Perhaps this is how LDN is helping some patients, by stimulating IL-10 which downregulates the immune system which would result in less antibody production ?

    Note that one of the main features of inflammation is oxidative stress, because cells of the immune system produce oxidizing species to attack the body's enemies. Oxidative stress is well-documented in ME/CFS, with perhaps 20 published papers reporting evidence of it now.

    GP: Just wonderng then if antioxidant therapy would interfere with the immune systems attempts to elinatinate an infection ?

    And those familiar with the body's antioxidant system will know that when a state of oxidative stress is present, the antioxidant system is losing the battle between oxidants and antioxidants.

    Those familiar will also know that glutathione is the basis of the antioxidant enzyme system in the body. So now we come to realize that in the subset of PWMEs/PWCs in whose bodies infection is a major aspect of their illness, we can expect that a major part of the oxidative stress, and hence a major part of the demand on glutathione, will be due to inflammation, which is being stimulated by the B cells in the overactive Th2 immune response.

    O.K., so now we put in Rituximab, which kills the B cells. What happens?

    Well, the inflammatory cytokines drop down, as does inflammation. This lowers the oxidative stress, taking a big demand off glutathione, which is then able to rise to at least some degree.

    GP: When the glutathione rises, shouldnt the cell mediated immune response reactivate again resulting in oxidative stress ? Or do only B cells produce inflammation ?

    The autoantibody theory makes a lot of sense too. They mentioned testing ANA and thyroid autoantibodies. I wonder about the ones commonly found ui autism: myelin basic protein and neurofilament.

    Aficionados of the GD-MCB hypothesis will immediately suspect that a big part of the symptomatology of ME/CFS will diminish, since the causes of a large fraction, perhaps the majority, of ME/CFS symptoms can be traced directly to the depletion of glutathione.

    So voila! The patient feels better, until her/his B cells grow back, and the whole process repeats itself, making her/him miserable again. So we hit the patient with another dose of Rituximab, and she/he bounces back up, and so on. If we do succeed in permanently devastating the B cells, what happens in the longer term? Certainly they were there for a purpose. Will the body be adequately defended against its enemies in the future? I think that's a big question.

    GP: Yes, thats my concern and especially since seeing the picture of my stomach with > 50% dsRNA enterovirus.

    The main point I want to make is that this treatment, like many others that have been used or proposed for ME/CFS, addresses a down-stream issue in the pathophysiology, and does not get to the root of the problem, which I believe (and have evidence to support this belief) is a vicious circle mechanism that includes glutathione depletion, a functional deficiency of vitamin B12, a partial block of methionine synthase in the methylation cycle, and draining of folates from the cells. So far, the only way it seems to be possible to break this vicious cycle is to lift the partial block in the methylation cycle with appropriate treatment that includes simultaneous use of active forms of folate and high dosage of forms of vitamin B12. Among other effects, this should rebalance the immune system, so that the B cells as well as the other components of the immune system will return to their normal functions. I do need to add that some other things will likely need to be done as well to help this process along, and which things will depend on the details of each case. But lifting the partial methylation cycle block is the fundamental thing that needs to be done.

    I would welcome any criticisms of this proposed mechanism. As far as I can tell, everything fits together well.

    GP: It makes sense to me but the autoantibody does too. Maybe both are occurring.

    If anyone wants to get more information on the GD-MCB hypothesis, I recommend watching the video at

    http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

    The slides from the talk are available there too, if you don't want to hang in for the whole 3-plus hours.

    Best regards,

    Rich
     
  9. taniaaust1

    taniaaust1

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    Im excited to hear about all this :)

    thou that wouldnt be a full underlaying answer, it still would be a big step in the right direction as "autoimmune" diseases at least get decent funding for good studies to be done.
     
  10. globalpilot

    globalpilot Senior Member

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    Hi Rich,

    What you've written below about autoantibodies provoked a question I've been thinking about. If the production of autoantibodies rises when cells are dying more than usual and releasing fragments, what does this mean for myelin autoantibodies where the antibody is directed towards a protein that is extracellular. Would this be more a case of molecular mimicry from an infection ? and the thyroid antibodies that are sometimes seen in CFS - would excess cell death in the thyroid be necessary for these autoantibodies to be produced ?

    Regards,
    GP
     
  11. taniaaust1

    taniaaust1

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    I wouldnt be surprised if they are already getting onto doing that :p . They were real fast off the mark with disproving XMRV. Look out for the Rituximab study done by S. Weaselly being published in 2-3 mths to disprove it. :p .

    Get ready to for the heightened campain to try to knock this news out of news headlines. Wondering what he will come up with this time to get the news focus on himself and his so called issues rather then on us and the new discovery. Maybe he can incite a patient so much that someone tries to shoot him.. yeah that would grab the headline to himself again. (His stories must be starting to wear thin so he'll need something big).
     
    LaurieM and Enid like this.
  12. LaurieM

    LaurieM

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    Tania - It wouldn't surprise me either, and he would get instant wall to wall news coverage, which unlike this ground-breaking discovery has not been seen outside Norway as far as I can see. :(
     
  13. Sasha

    Sasha Fine, thank you

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    In the paper (p. 8) the authors say that they retrospectively applied the CCC (they'd used the Fukuda 1994 criteria to select patients) and one of the two placebo responders didn't fit the CCC. They don't say (can't see it now, anyway!) whether that was the one who had been the big responder.
     
  14. Sasha

    Sasha Fine, thank you

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    I've been googling away but can't find any coverage in the UK media (or anybody's media except Norway). I'm surprised - there have been loads of, "ooh, look, ME is real after all" stories in the UK press at least over the decades, only to be swamped later by garbage but news is news and it sells papers. We have papers such as the Independent and Daily Mail that I would normally expect to cover this stuff without an anti-ME agenda.
     
  15. taniaaust1

    taniaaust1

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    I hope if anyone does this and manages to get the drug to try it, I really hope they will start up a thread like Daffodil did with those other drug,s where everyone can follow their process with the drug. This kind of info is invaluable to us.
     
  16. taniaaust1

    taniaaust1

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    Im feeling the same way about the title of this thread.. It isnt encouragement for researchers and others. This is serious research and its like its being made fun of by the title of the thread.


    We are a patient group who so many have called us crazy. (We all do have different sense of humour.. but I dont find this at all humourous but not at all right.. Im finding it upsetting that someone is calling new researchers valuable work to CFS crazy).
     
  17. Boule de feu

    Boule de feu Senior Member

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    I was wondering about the same thing.
    WebMD did pick it up, so it shouldn't be too long now.

    http://www.webmd.com/chronic-fatigu...-drug-may-also-treat-chronic-fatigue-syndrome

    On the French side, Psychomedia is a big player. =-)
    http://www.psychomedia.qc.ca/syndro...011-10-20/efficacite-mabthera-rituximab-cause
     
  18. Sasha

    Sasha Fine, thank you

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    Thanks, Boule, that's good - still nothing coming up on google, though. Maybe by the end of the day! I wonder if the study authors put a press release out internationally?
     
  19. Sasha

    Sasha Fine, thank you

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    Hi tania - please don't be upset, I'm sure this is just something that has been lost in translation - in the US "crazy" probably can mean something like "bold and daring" rather than the UK/Oz "we have an urgent need for some straightjackets". I'm sure a moderator will be on it soon (I don't think we can edit our own titles).
     
  20. kheopz

    kheopz

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    The study is very well done. I saw the slides. These guys are oncologists, not crystal wielding naturopaths. (not that theres anything wrong with those)
    They went straight for a large double blind study which is expensive and resource demanding. Their methology seems very good. They wanted to do this
    to convince the medical community they were on to something.
    Some say they take credit... I say they take patients with cfs seriously.

    If you dont buy into the auto immune theory.. you are closing your eyes and ears. There have been many speculations through the years regarding auto-immunity in cfs. Heres the evidence. If its not that then Retuximab must be doing something very strange that no medical scientist are yet able to explain.

    The patients tend to improve in all symptoms, this indicate the medicine touch upon a central disease mechanism says Fluge.

    There could still be connections to HHV viruses and EBV, to oxidative stress and gut health, however these studies and these oncologists experiences
    point to something definite going on regarding the bcells.

    Some people dont improve, the authors are looking into treating them more aggresively but they also have applied for permission to remove plasma, and maybe they have other ideas aswell. Because the patients relapse they are now doing maintenance therapy and my impression was that they are happy about those
    results so far.

    I say more auto immunity studies... now
     

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