Professor & patients' paper on the solvable biological challenge of ME/CFS: reader-friendly version
Simon McGrath provides a patient-friendly version of a peer-reviewed paper which highlights some of the most promising biomedical research on ME/CFS ...
Discuss the article on the Forums.

EBV in bone marrow of rheumatoid arthritis patients predicts response to Rituximab

Discussion in 'Rituximab: News and Research' started by Marco, Nov 22, 2011.

  1. bel canto

    bel canto Senior Member

    Messages:
    218
    Likes:
    305
    Hi, Nielk - my immediate family has many autoimmune conditions, as well as me/cfs. Rheumatoid arthritis , primary biliary cirrhosis (pbc), scleraderma, multiple sclerosis, IBD/crohn's, pulmonary hypertension, vitilago, and an extremely rare form called castleman's disease.

    The liver enzymes can be elevated by the pbc, but we also have a case of long-term elevation of alkaline phosphatase, which can be related to the liver, or to bone.

    And diabetes can be the type 1 autoimmune form even when it begins in adulthood.

    Please feel free to contact me if you want to specifically discuss multiple autoimmune conditions. Hopefully, that will not be the case for you. Good luck!
     
    merylg and Nielk like this.
  2. Pyr2

    Pyr2

    Messages:
    55
    Likes:
    34
    I know this post is old, but the topic is still very current, at lest for me. I have a bone marrow cytogenetics test which showed a "lymphoproliferative disorder" and yet the actual bone marrow biopsy was fine as was flow cytometry.
    A more current PCR test for EBV on blood was negative.

    So its in my marrow but not in my blood by PCR. Yet on blood immunofixation it shows a polyclonal IgM, which is consisent with a chronic inflammation or infection.

    Given that, do I qualify for rituximab? I am going to a hem/onc next week to see.

    How did I get here? Mono 1986. Then weird neuro/cognitive/immune symptoms started in 1999. Went through exhaustive testing which showed the then unexplained cytogenetics test. Was told to go on with my life, its nothing. The symptoms subsided so I did. At the time I was not tested for ebv and no one considered the prior mono. Fast forward to 2013. Reactivated ebv and crash of symptoms (mostly neuro, cns, pain neuralgia- not to much fatigue) still here two years later. SOMETHING is going on. If only I could get myself to the right researcher!!!! Would love to hear from some of you scientific types!!!!

    It is interesting b/c you wonder if bone marrow analysis were standard, would they find more of us who had mono as a teen with these bone marrow abnormalities!
     
    snowathlete and heapsreal like this.
  3. Kati

    Kati Patient in training

    Messages:
    4,127
    Likes:
    9,924
    Hi @Pyr2 first I am sorry to hear about your current diagnosis.

    I wonder where you are from (which continent) and what precipitated I am interested to hear what the hematologist will tell you next week, please update us.

    As for whether Rituximab could be helpful, it would not hurt to ask with bringing relevant papers to the physician but only if they are open to that. It is possible they have a better treatment option for your specific condition.
    It is possible they could add Rituxan to that as well.

    Personally I would be all for getting a bone marrow biopsy and further invasive testing such as cerebro-spinal fluid analysis. We have the technology to get it done.

    Best wishes.
     
  4. Pyr2

    Pyr2

    Messages:
    55
    Likes:
    34
    Hi Kati. Well my current diagnosis is nothing more than a lot of you have - basically my dr says I am in the Lerner subset of patients who have a chronic case of EBV. I am in the US (NJ), near some of the best research universities and hospitals, someone should really take up my case, but so far no luck! She says that 30 years post mono and 15 yrs post bone marrow biopsy, if it were something more severe I would be in worse shape or not likely to be here at all. Im knocking on wood and crossing my fingers, and throwing more than a few prayers up to God that she's right.:)) I will definitely update. Thanks for answering.
     
  5. soofke

    soofke

    Messages:
    37
    Likes:
    20
    Dutchy
  6. anciendaze

    anciendaze Senior Member

    Messages:
    1,471
    Likes:
    3,201
    The question of other herpes viruses is quite reasonable. The non-EBV responders may have had different infections in which B-cells were involved.

    A different problem is that all EBV is not created equal, even beyond the major strains found in different parts of the globe. If you have any doubts about the ability of EBV to carry insertions in its genome I can supply references. The mechanism by which herpes viruses insert genetic material is about as selective as a shotgun blast.

    Much of the work dismissing the importance of EBV in autoimmune disease took place at a time when nobody knew it had three latent states, some of which could replicate DNA without causing lysis. If tests were based on antibodies to proteins present in lytic replication they could miss cases in which DNA replication would only be found by looking for antibodies to early enzymes.

    This becomes important when EBV infects B-cells undergoing clonal expansion in response to unrelated antigens. The number of infected cells can increase dramatically without much lysis. Increases in early proteins could get lost in the noise of immune response to an unrelated pathogen. In human terms we might say this is an example of a "false-flag recruitment". I doubt humans were the first to invent this form of deception.

    While dismissing studies of autoimmune disease with small sample sizes you might consider this study about MS and EBV. The incidence of MS in EBV-negative patients is so low you have to seriously consider false negatives. If this sample size is not enough, I doubt it is possible to conduct research on MS and viral infection that would meet your standards.

    The connection between EBV and Burkitt's lymphoma is well established, and so are connections with several other cancers. You can argue this in two ways: 1) that the strains of EBV causing cancer contain sequences not found in other EBV; 2) that the increased incidence is the result of a different kind of immune dysfunction, which we don't know much about. Interactions with other pathogens in the environment cause me to favor the latter. If the former alternative is true, then I believe dismissing connections with generic EBV in other diseases is bad research practice, and irresponsible. You could dismiss the connection between HPV and cervical cancer as very uncertain if you accidentally omitted the particular strains responsible, out of more than 100.

    Immune system response to EBV is a road to insight into how response to viral infections works in a number of pathological situations. If we really understood this I doubt we would have so much trouble treating viral infections. If depleting B-cells has significant benefits in some subset of patients it should be obvious that we need to find out what a subset of cells are actually doing in those cases where treatment works. Current levels of discourse on the subject are too often simply replays of past disputes.

    Many years of work on RA have done nothing to reduce incidence in the general population. How would you advise governments to reduce future costs associated with RA, assuming you don't favor euthanasia? Large sample sizes are necessarily tied to large funding, not innovation. Funding nine ideas with little chance of success to get one good idea would not be more expensive the last few decades of experience. (Ask Google about long shots.) If anyone wants to break out of the current stalemate I'd suggest they change current funding approaches.
     
    Ingrid88 and SOC like this.

See more popular forum discussions.

Share This Page