Review: 'Through the Shadowlands’ describes Julie Rehmeyer's ME/CFS Odyssey
I should note at the outset that this review is based on an audio version of the galleys and the epilogue from the finished work. Julie Rehmeyer sent me the final version as a PDF, but for some reason my text to voice software (Kurzweil) had issues with it. I understand that it is...
Discuss the article on the Forums.

CRPS with dysautonomia patient treated with plasma exchange and rituximab

Discussion in 'Rituximab: News and Research' started by voner, May 27, 2015.

  1. voner

    voner Senior Member

    Messages:
    531
    Likes:
    790
    http://www.ncbi.nlm.nih.gov/pubmed/26011726

    I did not know These auto antibody tests existed.


    The plasma exchange success prompted them to start rituximab.

    if someone would like a copy of this paper, they can request it from me over in the "Request a paper" thread.

    comments?
     
    Sidereal, RL_sparky, Hutan and 7 others like this.
  2. Jonathan Edwards

    Jonathan Edwards Senior Member

    Messages:
    5,019
    Likes:
    29,099
    This is an interesting case.

    This is what I call algodystrophy, because CRPS seems to me to add unnecessary assumptions to a well defined clinical and pathological entity. A useful feature of algodystrophy is that it is objectively measurable - by isotope bone scan or thermography. Moreover, it is completely impossible to conceive of any way in which conscious beliefs about anything, or even unconscious beliefs about anything should induce the regional colour changes, osteopenia and hair and nail growth changes that occur. To treat something like this with CBT is pretty much equivalent to faith healing for cancer I think.

    The next point is that the algodystrophic response looks superficially a bit like inflammation but it is unrelated. The limb is cold, perfusion is reduced. Osteopenia is gross and localised to clear embryological domains (not nerve trunk domains) such as carpus or foot or patella. What is intriguing is that there is no known situation in which this response is thought to be useful - unlike inflammation. In that sense it might be a bit like epilepsy - a purely useless byproduct of the way regulatory systems are set up. And the fact that it clearly involves lot of signalling, but without inflammatory markers going up, makes it seem as if it might be a clue to some of the pathways in ME.

    I think the crucial factor in interpreting this case and the related cases is the interpretation of the antibody assays. These seem to be reported from several centres and we may be close to a situation where a standard reproducible assay recipe is available for use by regional centres in all developed health care systems. But there are words of caution. Some other autoantibodies that have got popular in a similar way have now begun to look doubtful - to the extent that the physician who invented the assay no longer uses it. Autoantibody tests are easily over-egged. Nevertheless, I am hoping these ones will pan out. They seem to turn up in rather a lot of diseases and different antibodies seem to co-occur in a lot of patients (antibodies to several receptors in one case). This is not quite the picture we see with traditional autoantibodies, but then I am all in favour of considering non-traditional autoantibodies.

    What I find most encouraging about this case report is that the patient actually seems to have got better. In my own experience I have never been around when this sort of algodystrophy went away. My understanding is that it can, but that it is unpredictable and many have chronic changes.

    Interesting.
     
    zzz, nandixon, Sidereal and 2 others like this.
  3. Hutan

    Hutan Senior Member

    Messages:
    1,008
    Likes:
    5,588
    New Zealand
    So potentially plasma exchange could be used to wash out the putative problematic antibodies in MECFS patients so that there isn't a 7 month wait for the rituximab to kick in?

    What's involved in finding the autoantibodies? The excerpts above make it sound routine for those two labs. Did the labs know what auto antibodies they were looking for (ie were the antibodies already known to be present in this particular illness?) or did they just fish about until they found something?

    Is there any point in looking for these particular auto antibodies in MECFS patients? Is there any point in individual MECFS patients finding a good immunologist with a research capability and trying to get tested for these auto antibodies?
     
    nandixon and Valentijn like this.
  4. Jonathan Edwards

    Jonathan Edwards Senior Member

    Messages:
    5,019
    Likes:
    29,099
    Plasma exchange might help. It is a laborious procedure and not without risk but it is used in autoimmune neurological diseases. The downside is that the effect only lasts a few weeks from each course.

    These autoantibodies are measured using novel assays developed in labs in the US and Germany. Some of the assays are very fiddly because they involve testing samples on live beating rat cardiomyocytes in culture. However, there now appear to be ELISA versions for at least some of them. These particular antibodies were looked for because people are finding them in autonomic syndromes of various sorts. So this was not fishing around to find something.

    These antibodies are being studied in ME but I am not able to give details. We will hear about them fairly soon I think. But I do not think there is any point in individuals going to have blood tested. We need well defined cohorts compared to controls in the labs that developed the assays and then getting other labs to reproduce that.
     
  5. voner

    voner Senior Member

    Messages:
    531
    Likes:
    790
    it is good to hear that these antibodies are being studied in ME/CFS. I have certainly always been struck by the prevalence of autonomic dysfunction across these syndromes of ME/CFS, fibromyalgia and CRPS (algodystrophy - I had to look up that definition). it sure would help in defining a subset of ME/CFS.

    if the autonomic dysfunction is not caused by inflammation, @Jonathan Edwards does it possibly have to do with Brain dysfunction that you described last week...

    but then, how does that fit in with autoantibodies? I am confused, as usual.
     
    Last edited: Jun 4, 2015
    Hutan likes this.
  6. Jonathan Edwards

    Jonathan Edwards Senior Member

    Messages:
    5,019
    Likes:
    29,099
    I think we are all a bit confused. Certainly all the researchers at IiME were a bit confused. Maybe the point about fitting with autoantibodies is that an autoantibody can cause any physiological change you like. It does not have to cause inflammation. It can cause hyperthyroidism or B12 deficiency or paralysis of muscle or whatever. And whatever might be something that never normally occurs - like a leg going blue and cold and nails not growing.
     
    Marky90, Valentijn and voner like this.
  7. voner

    voner Senior Member

    Messages:
    531
    Likes:
    790
    so, theoretically, could it be a causative factor of pain, also?
     
  8. Jonathan Edwards

    Jonathan Edwards Senior Member

    Messages:
    5,019
    Likes:
    29,099
    I don't see why not. Antibodies to spinothalamic nociceptors might logically produce burning pain all over.
     
    Marky90 and Valentijn like this.
  9. jimells

    jimells Senior Member

    Messages:
    1,996
    Likes:
    6,075
    northern Maine
    A very interesting thread. Thanks for posting it.
     

See more popular forum discussions.

Share This Page