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Mark Berry, Acting CEO of Phoenix Rising, presents the Board of Directors’ open letter to Queen Mary University of London (QMUL) urging them to release the PACE trial data, and hopes that other non-UK organisations will join British charities in the same request...
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Stats on PWCFS and other autoimmune conditions

Discussion in 'General ME/CFS Discussion' started by knackers323, Sep 1, 2014.

  1. knackers323

    knackers323 Senior Member

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    Anyone know if any numbers have been taken on this and where to find them?

    I believe it is said that once you have one autoimmune condition, you have an incresed risk of developing another.

    So these numbers may be able to tell us a bit about whether cfs is an autoimmune condition or not.

    My brother and grandmother have crohns and lupus respectively and I have a history of psoriasis.
     
  2. minkeygirl

    minkeygirl But I Look So Good.

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    @knackers323 My dad has all sorts of autoimmune stuff on his side including psoriasis, (which I have, thanks dad) crohns', diabetes, a bunch more I can't remember.
     
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  3. knackers323

    knackers323 Senior Member

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    Also does anyone know what the prevalence ratio is for cfs between the sexes?

    Is it similar to the known autoimmune diseases?
     
  4. redrachel76

    redrachel76 Senior Member

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    http://phoenixrising.me/archives/6190

    Yes it is. This link has the stats.

    I think ME is autoimmune.

    The CFIDS Foundation official position is that this is autoimmune. http://www.ncf-net.org/faq-home.htm
    FAQ
    "Who gets ME/CFS?
    ...As with most autoimmune illnesses, it affects women in higher numbers than men although, in children, it is nearly equal."
    There is a paper by CFIDS Foundation about anticardiolipin antibodies in CFS which the CFIDS Foundation says proves autoimmunity. Sorry if this post is not clear, I am a bit brainfogged.

    It annoys me Invest in ME and all the other groups ignored that anticardiolipin paper. I think there is definite autoimmunity in this.
     
  5. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Do you have any more details about this paper redrachel? I could find a paper by Hokama et al in 2009 but it does not give enough information to be useful (no control data, inadequate information on co-morbidity etc.). It would be interesting to see if there is anything more substantial. I could suggest some cases are tested at UCL.
     
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  6. Forbin

    Forbin Senior Member

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    FWIW, I found this 1991 report of a study that found anticardiolipin antibodies in 51% of fibromyalgia patients and in none of the controls (100 patients/20 controls). I'm not sure if there is a more detailed paper or if this is all there is.

    From the report:
     
    Last edited: Sep 4, 2014
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  7. redrachel76

    redrachel76 Senior Member

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    I did not know that it did not give enough information to be useful.
    Here is the paper
    http://www.ncf-net.org/pdf/AnticardiolipinAntibodies.pdf

    There is an interpretation for lay people like me.
    http://niceguidelines.blogspot.co.il/2011/10/study-demonstrates-that-95-of-mecfs.html

    I wish that more were tested at UCL.
     
  8. Jonathan Edwards

    Jonathan Edwards Senior Member

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    The reason I say it does not give enough information is that in order to know what the results mean we need to know results from normal people to compare. We would also need to know that the ME group had no other illnesses that might be linked to the antibodies - and in fact they did have other illnesses and we are not told much about this.

    The real problem here is that there is no agreed standard for what a 'positive test' is for anticardiolipin antibodies. It is difficult for lay people to appreciate that these tests give no definite answer. The ELISA test is a bit like making toast. If you cook it long enough it will always go brown. So you have to do a comparison. To see if one type of bread made toast easier than another you would have to set a fixed time and try slices of each and see which gave a good brown in a shorter time. You would also have to be careful you kept the breads the same way to ensure that one had not dried out more than the other earlier.

    Anticardiolipin tests are notoriously variable from lab to lab and day to day. So to be any use you would need to store all your patient samples at -80 degrees and store a good number of normal people's samples at -80 degrees and then do the test on all samples on the same day on the same set of plates with patient and normal samples in a random order with a blind code so that there was an even chance of which plate they were tested on. Researchers who understand these problems report the fact that they have been this careful to show to other scientists that they know what they are doing. If a paper gives no control values for healthy people using the same test runs, I am afraid that tends to be an indication that the researchers are not familiar with how tricky the test is to interpret.

    If the results in this study were reproducible and different from normals it would have been noticed long ago I think. I very much agree that some forms of ME are likely to be autoimmune but we need more reliable evidence.
     
  9. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Just to go back to the original question, it is worth pointing out that psoriasis is not as far as we know an autoimmune condition. Crohn's disease is probably not primarily autoimmune either, although a proportion of patients have odd antibodies to sugar chains. There is no association between psoriasis and conditions like lupus and rheumatoid arthritis, which are truly autoimmune in the sense of having an immune response to self in the form of autoantibodies.

    I strongly suspect that some forms of ME are autoimmune and we may see associations with antinuclear antibodies or antithyroid antibodies and we may find new types of antibody, but I suspect there are other forms of ME that are not related to autoimmunity at all. The higher incidence in women does perhaps suggest that as many as 50-60% of ME cases may be linked to autoimmunity, as does the apparent response to rituximab.
     
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  10. Kati

    Kati Patient in training

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    Would you actually say, @Jonathan Edwards that the auto-immunity subgroup, those with antibodies are most likely to respond to Rituximab, because this was not my case at all. High titers ANA, no response to 6 doses.

    We know that Rituxan kills cd-20 surface antigen cells ( the B-cells) so are we absolutely sure we are attacking the right group of cells/ the reservoir? What about the T cells?
     
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  11. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Good point Kati. I think we have an idea of the problem here.

    The 'right cells' are in a sense plasma cells, because they are the ones that make the antibodies, not the B cells in fact. B cells are really just training squad kids. Some get to play in the A team, some in the B team and some never get to play. The problem with certain types of ANA, and particularly the speckled ones, is that they are made by very long lived plasma cells (at least that is the simplest explanation) and so after rituximab they do not go down much. On the other hand rheumatoid factors seem to be made by short lived plasma cells, so after rituximab the A team dies off within 6 months and because the rituximab has wiped out the training squad there is nobody to make antibodies. Trouble is that in some cases the B team, which are in fact mostly retired stars like David Beckham who don't actually die off, can train up a new squad in no time once the rituximab has worn off.

    So I think it is all B cells and their daughter plasma cells. Nobody has ever found anything wrong with a T cell in RA in forty years as far as I know. You might not think that from reading the ideas in the popular journals but I have yet to hear of an autoreactive T cell in RA. What we need is a drug that gets rid of long lived autoreactive plasma cells without getting rid of long lived useful plasma cells. That is tough, but one day it will be possible.
     
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  12. Kati

    Kati Patient in training

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    Thank you @Jonathan Edwards. I have seen rituximab working wonders in lymphoma patients, with some patients litterally coming back from the dead.

    It is my hope that patients with ME can experience the same kind of effect from good and effective treatment from big pharma. i am convinced it is totally possible, if we break down the barriers to good research and breakthrough.
     
    NK17 likes this.

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