New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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Chronic lymphoproliferative disorders

Discussion in 'General ME/CFS News' started by heapsreal, Jul 29, 2011.

  1. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    australia (brisbane)
    Reading about this disorder really seems alot like cfs, dysfunctional cd lymphocytes, b-cells and nk cells.

    Possible causes:
    Altered immunity
    3.3.1. Inherited syndromes and susceptibility via individual inherited genetic sequences. Several studies have suggested a slight excess of cases occurring in blood relatives. There is a range of rare but well defined and usually simply inherited conditions that have an excess of lymphoproliferative disease as part of the syndrome, for example, ataxia telangiectasia, Wiskott-Aldrich syndrome and common variable immunodeficiency. The potential underlying genetic defects in heterozygotes could represent a major initiating cause of a lymphoproliferative disorder although it would be unlikely to be the only step required to manifest the disease in this population.
    3.3.2. Immunodeficiency due to past medical history. There is a higher risk of developing chronic lymphoproliferative disorders in individuals receiving long-term immunosuppressive drug therapy such as transplant recipients and patients with autoimmune diseases. An increased risk is also seen in patients suffering from a variety of autoimmune conditions, for example, rheumatoid arthritis, Sjgrens syndrome and coeliac disease, independent of immunosuppressive treatments.
    3.3.3. Infections. Human immunodeficiency virus (HIV), human T-cell lymphotrophic virus type 1 (HTLV-1), human herpes virus-8 (HHV8) and Epstein-Barr virus are all associated with an increased risk of certain types of lymphoproliferative disease, most probably by causing immunosuppression. HTLV is a retrovirus that is endemic in southern Japan and the Caribbean basin. Infection with HTLV-1, especially in early childhood, is strongly related to the development of adult T-cell leukaemia/lymphoma with an estimated cumulative lifetime risk of approximately 5%. HTLV can be transmitted both sexually and by blood transfusion. Unlike HTLV-1, EBV infection is a highly prevalent
    5
    infection in the adult population (approximately 90% of individuals in developed countries having evidence of previous infection by the age of 40). The association between EBV and lymphoma is well described for both Burkitts lymphoma and immunodeficiency-associated lymphoma. Nearly all cases of endemic Burkitts lymphoma (in Africa) can be shown to contain EBV viral genomic DNA, but the frequency is less than 20% in sporadic cases in developed countries. Natural killer (NK) cell lymphoma is an aggressive and refractory form of lymphoma which is strongly associated with EBV and although rare in the west has a relatively high incidence in south-east Asia. In addition, the Gram negative bacterium, Helicobacter pylori, is associated with the development of gastric non-Hodgkins lymphoma (NHL) of B-cell origin arising from the mucosa-associated lymphoid tissue (MALT).

    Prognosis:
    4.1. It is impossible to generalise regarding the outcome of chronic lymphoproliferative disorders due to the heterogeneity of the group and the different behaviour of each disease entity. Furthermore, within each entity there is a wide variation in potential outcomes, although it can be stated that in the majority of cases survival is measured in terms of years rather than months.
    4.2. Many patients do not require any treatment when first diagnosed, with an expectant or watch and wait approach employed. In very indolent disease patients may never require treatment for their lymphoproliferative disease and remain asymptomatic during their lifetime. The aims of treatment are to control symptoms or other effects of the tumours.
    4.3. Chronic lymphoproliferative disorders are incurable using conventional treatments and tend to run an indolent course with treatment being required when there is symptomatic disease progression. Treatment modalities include chemotherapy and radiotherapy with varying degrees of response and remission. Newer agents, such as monoclonal antibodies, can improve the response rates for some tumours and achieve responses in patients refractory to other forms of chemotherapy.
    4.4. The only potential curative treatment for these disorders is through allogeneic haemopoietic stem cell transplantation. However, this approach is only suitable for the minority of younger and fitter patients and is associated with a high mortality and morbidity. Therefore, it is still considered as an experimental treatment in chronic lymphoproliferative disorders and should only be performed in the setting of a well designed clinical trial in younger patients with aggressive or poorer risk disease.

    http://www.veterans-uk.info/publications/chronic_lymphoproliferative_disorders.pdf
    It all sounds familiar, mmm cfs/me and this document is from the UK.

    cheers!!!
     
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  2. Pyr2

    Pyr2

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    Hi there. I have become a recent poster and this applies to me. I had a bone marrow biopsy done a 15 yrs ago and bone marrow normal but cytogenetic results showed an acquired mutation of a lymphoproliferative disorder. Doctors could not explain the result and told me to move on with my life. The bone marrow was done in response to a "flare of symptoms" that eventually died down so I took their advice. Little did I know that was probably an ebv reactivation (funny how they did a bone marrow biopsy but not a simple ebv test!) Would happen occasionally over the next decade with no real problems. Then 2 years ago, the "flare" started again and never left. I am going back to the hem/onc this week. Interesting, but my bone marrow could have reflected cfs/me would happen years before it ever did.

    Heaps I see that you have lots of knowledge and are posting interesting stuff. Thanks, very intriguing!
     
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  3. Violeta

    Violeta Senior Member

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    What type of symptoms did you have your doctor decided to do a bone marrow biopsy? And do you mind listing your current flare symptoms.

    I know nothing about this but I do think it's important.

    And may I ask, does it have something to do with EBNA 2, because I just found this:

    https://books.google.com/books?id=t...h3RzwNF#v=onepage&q=naringenin ebna 2&f=false
     
    Last edited: Oct 3, 2015
  4. Pyr2

    Pyr2

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    So the only way I can describe it was like a switch turned in my brain. Very similar to what CFS/ME patients describe. With both major occurrences, I can tell you exactly where I was when I said "oh this isn't right." Like an immediate attack. For me, in enormous increase in anxiety, OCD, feeling of being unwell, depersonalization, depression, etc. All very CFS/ME, but the rest not. I had a lot of neuro issues. Tingling and aching limbs, shooting pains, especially at night. Cranial issues - burning mouth, tongue pulling sensations, all types of head neuralgia patterns - trigeminal, occipital, glossopharangyeal. Also, yes I did lose a lot of weight and had giant bruises on my body which made the hem/onc nervous and he did the bone marrow. So nothing that would make people say, hey I think she has a reactivated infection (no night sweats, no fatigue, no lymph nodes no sore throat etc.) That flare lasted 6 months. I had mini flares in between and now, over a decade later, have a nonstop 2 yr flare.

    Over the years I have ALWAYS been suspected of having autoimmune disease. Low titers of positive ANA and also positive for low levels of anticardiolipin antibodies. But never diagnosed with any autoimmune disease or antiphospholid disease. And my MRIs of brain show microhemmorhages, consistent with an inflammatory response or infection. Vasculitis has also been suspected but never shown. And every time I have a flare, it is usually after taking antibotics or amoxicillian for something, which is why Lyme was suspected (herx). I have specific lyme titers (like band 39, 23, 93. etc indeterminate) but my dr says while I definitely had Lyme exposure, she is not sure if I had lyme disease- whatever that means). I did treat for a while for Lyme. But now we are really thrown by the way Im (nt responding). Seems like its something deeper.

    So its definitely an autoimmune reaction or weirdness going on all along in response to ebv in my body. I am going to hem/onc next week and an ID dr later in the month at Upenn. I have to get this straightened out!!!!
     
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  5. Violeta

    Violeta Senior Member

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    I'm sorry, that's quite a bit to deal with!

    The only thing I can think of at the moment is that antibiotics make viruses worse, so that would make sense that it is EBV made worse by the antibiotics. I realize that's no help, but for what it's worth.

    Also, I can see there might be some dots that connect this to endoplasmic reticulum stress, well more so a straight line pointing in this direction but I don't know what the dot in the brain would be. The line heading in this direction would be that ebv causes endoplasmic reticulum stress, just saw that the phosphatidylserine/choline connection to mitochondria/microglial function.

    Ah, maybe ROS, as viruses cause ROS. So oxidative stress in the brain.
     
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  6. Violeta

    Violeta Senior Member

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    I'm not yet sure if this is applicable, but see what you think, @Pyr2 and @heapsreal :

    http://www.ncbi.nlm.nih.gov/pubmed/25675483

    I realize we aren't mice, lol, nor do we have AD. Not yet, anyway.

    Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice.
     
  7. Violeta

    Violeta Senior Member

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    This is strange to me! ROS mediates activation of EBV! What a turn of events.

    http://www.ncbi.nlm.nih.gov/pubmed/24376853

    Reactive oxygen species mediate Epstein-Barr virus reactivation by N-methyl-N'-nitro-N-nitrosoguanidine.
     
  8. Violeta

    Violeta Senior Member

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  9. Research 1st

    Research 1st Severe ME, Severe POTS

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    Hi I have a little pet project on this topic regards to ME, vs Severe ME.

    One method (indirect) to show something is really wrong in my vie, is to go looking at the effects of infection and autoimmunity in ME:

    Multiple oxidative stress markers, cytokines (IL-2,4,6,8,10,12) chemokines (MCP1, MIP-1a, MIP1b) with IFN-gamma, PGE2/VEGF/TGF-B1/RANTES/ and finally PrPC levels, this my theory, not an official ME test I should add. Also I run a Lymphocyte subset test. This can show evidence of B Cell, T Cell, NK Cell activation. Sometimes I have B,T,NK very high all at once (If chronic this is very bad), but I always have NK Cell activated no matter what.

    The problem with ME really, is it fluctuates, it's rare you're going to have consistent evidence of something understood and well known and it's unlikely we're going to be in a flair up during a blood draw. (Shame we aren't allowed to go to a hospital when this happens).

    Get the full house above as I did and you've got undeniable evidence of microglial activation/inflammation, and via IFN-gamma, possible infection None of this should happen in people without infection alleged to have a 'CFS', so some of us do have an infection it just hasn't been tested for (Lyme) or is a stealth pathogen (Tissue bound Lyme, retrovirus etc) or is not seen by the immune system (inability to make antibodies due to white blood cell infection). The last point I think it the key. I am convinced we don't have a correct immune response, and I think there was paper published somewhere last year or so, about EBV being negative,but actually positive:

    I found this:

    EBV I: A Deficient Immune Response, Increased Levels of Epstein-Barr Virus Opens Up EBV Question in Chronic Fatigue Syndrome Again
    http://simmaronresearch.com/2014/03/1591/

    And this from a German paper:

    Going away from specific infection back to related oxidative stress. As PrPC is protective of oxidative stress in the brain, I have a theory the lower it is, the more severe the ROS will be. There is no test yet for misfolding prions and this to me is the holy grail of ME research (if the person with ME has very low PrPC and presence of misfolding). That's an entire other discussion though and probably ventures into the realms of dementia.

    Either way, if anyone's interesting you can get an experimental prion protein estimation level test at REDLABS in Belgium. It's only 75 euro ($84).

    I've heard from a few cases on here and myself, of very low PrPC in people very sick, but less so in less severe. I've also got very high levels of oxidative stress at rest and the inflammatory/immune brain cell markers above.

    So it all correlates what you're saying and in ME. Infection based massive ROS, damages your brain and other tissues and artificially ages you over time more than 'healthy' people without this chronic inflammation.

    There must be pathogens behind this (immunosupressive defect in ME) and no wonder we can display signs of a Chronic Lymphoproliferative disorder.
     
    Last edited: Oct 3, 2015
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  10. lansbergen

    lansbergen Senior Member

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    I still wish some severe ME patients would be tested for PrPc antibodies.

    Anyway the immunemodulator I use is a superoxide scavenger and there was a paper on SOD2 dislocation and depletion in TSE.
     
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  11. Violeta

    Violeta Senior Member

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    What is this? PrPsC? I should probably ask about it with a better question, but right now I don't know what to ask.

    "Prion diseases result from conversion of a normal, cell-surface glycoprotein (PrPC) into a conformationally altered isoform (PrPSc) that is infectious in the absence of nucleic acids.'
     
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  12. Violeta

    Violeta Senior Member

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    @lansbergen , what is the superoxide scavenger you use?
     
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  13. lansbergen

    lansbergen Senior Member

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    Levamisole
     
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  14. lansbergen

    lansbergen Senior Member

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    Is it? I do not doubt PrPsc is part of the TSE disease process but I never was impressed by the arguments used by the protein only hypothese fans.
     
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  15. Violeta

    Violeta Senior Member

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    Okay, that would be part of the protein only hypothesis. If one were to get their PrPC measured would PrPsC actually fall into the measurement?

    I had to look up levamisole, how are you doing with it?

    For antioxidants, I am using ionized water, beta alanine, coenzymated B2, and most recently added in a good amount of reishi. Coenzymated B2 (FMN) was shown in another thread to be a precursor to thioredoxin, an endogenous antioxidant. I try to take some antiviral herbs, too, lomatium and olive leaf extract. For immune system improvement I take an astragalus formula and colostrum. Sometimes, like today, I still feel as though I'm losing the battle.

    http://www.lifeextension.com/magazine/2013/2/how-reishi-combats-aging/page-01
     
  16. lansbergen

    lansbergen Senior Member

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    The jury is still out on that one but some say they can differentiate it.
     
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  17. lansbergen

    lansbergen Senior Member

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    Much better.
     
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  18. Violeta

    Violeta Senior Member

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    U of Penn, do you live near Philadelphia?
     
  19. Violeta

    Violeta Senior Member

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  20. Pyr2

    Pyr2

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    Wow. These studies are telling. THank you all so much for the links. But I must say its all making me very depressed! Yes, I do live near UPenn. Violeta are you local?
     

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