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Research: blockade of TNF can trigger the onset of MS

Discussion in 'Other Health News and Research' started by Ecoclimber, Jan 29, 2013.

  1. Ecoclimber

    Ecoclimber Senior Member

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    http://multiple-sclerosis-research.blogspot.com/2013/01/research-blockade-of-tnfgives-you-ms.html

    Objective. To determine the pattern of demyelinating disorders (DDs) occurring during anti-TNF-α therapy.
    Methods. Between June 2005 and April 2008, 1800 French rheumatologists and internists were contacted to report cases of DDs occurring in patients treated with anti-TNF-α.
    Results. After a median of 10.2 (1.5-39.9) months of treatment, 33 patients developed DDs: 22 had CNS and 11 peripheral nervous system (PNS) involvement. Underlying diseases were RA (n = 16), AS (n = 11), PsA (n = 4), JIA (n = 1) and PM (n = 1). Anti-TNF-α was infliximab (n = 15), etanercept (n = 12) or adalimumab (n = 6). CNS involvement was encephalic lesions (n = 16), transverse myelitis (n = 8) or retrobulbar optic neuritis (n = 5). Cerebrospinal fluid (CSF) analysis in 16 patients and MRI in 20 patients were abnormal. All patients discontinued anti-TNF-α. Fifteen patients required steroids. Twenty patients initially improved. Five patients developed multiple sclerosis. PNS involvement was chronic (n = 9) or acute inflammatory demyelinating polyneuropathy (n = 2). CSF analysis revealed an increased protein level in nine patients. Nerve conduction studies confirmed DD in all these patients. Anti-TNF-α was discontinued in 10 patients and 8 received i.v. immunoglobulins. Two patients relapsed after introduction of another anti-TNF-α. Overall, a causal relationship between anti-TNF-α and DD was considered as probable in 31 patients and definite in 2 who had positive rechallenge.
    Conclusion. Causal relationship between anti-TNF-α and induction of DD remains unclear, but in some cases the chronology of clinical events is suggestive. Nevertheless, DD might persist despite treatment discontinuation, suggesting that anti-TNF-α could trigger the demyelinating process, which further evolves independently.
    [​IMG]

    People treated with Lemtrada can develop autoimmune thyroid disease, it appears that people with arthritis treated with anti-tumour necrosis factor develop demyelinating disease and multiple sclerosis. This is further evidence that overall blockade of TNF is not a good idea in MS. Most experimental data may suggest that TNF blockade could be good, however I think this shows that TNF does lots of different things some could be good and others bad and balance is that its removal at least from the peripheral compartment is bad news. This can tell us something about biology. Following Lemtrda administration there is a cytokine storm, quelled by steroids, that reactive old demylinated lesions
    Eco
     
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  2. Enid

    Enid Senior Member

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    Marvellous research findings you have brought together today Eco - yes demyelisation suspect on my own scans etc. too.
     
  3. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    Please pay attention to pde4, with respect to ME. I suspect it is elevated, and its also elevated in disorders involving mast cells. pde4 is phosphodiesterase 4 and it degrades cAMP. This will affect sleep and memory as well as immune issues.

    PS This implies that resveratrol is a BAD thing for MS.
     
  4. lampkld2

    lampkld2

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    Is this why bosweillia and paradoxically fish oil worsens my inflammatory neuropathy??! Any suggestions? My body is literally eating every nerve I have and it feels terrible. Methylation treatment and zinc started teh cascade two years ago....

    How do I raise TNF-a? I think mine was really low...
     
  5. lampkld2

    lampkld2

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    http://www.jci.org/articles/view/45262



    Can TNF-α boost regulatory T cells?

    Angelina M. Bilate and Juan J. Lafaille
    Molecular Pathogenesis Program, Kimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, New York, USA.
    Address correspondence to: Juan J. Lafaille, Molecular Pathogenesis Program, Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA. Phone: 212.263.1489; Fax: 212.263.1171; E-mail:juan.lafaille@med.nyu.edu.
    First published November 22, 2010
    Deleterious immune responses that cause autoimmune diseases such as type 1 diabetes are normally kept in check by a myriad of mechanisms. Among these, protection mediated by CD4+Foxp3+ Tregs constitutes an essential pathway. Much work over the past decade aimed to understand how Tregs affect immune responses triggered by effector T cells (Teffs), but less is known about how Teffs affect Tregs. In this issue of the JCI, Grinberg-Bleyer et al. report the clearest example thus far regarding this important aspect of Treg biology. They find that in mice, sustained protection from diabetes by Tregs is dependent on Teffs and partially dependent on TNF-α, a cytokine traditionally considered proinflammatory.
     
    alex3619 likes this.
  6. ramakentesh

    ramakentesh Senior Member

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    This is definately true. happens in a small percentage of patients who are treated with TNF alpha blockade for Ankylosing Spondylitis.

    that being said I wouldnt use this as a reason not to consider TNF alpha blockade in other illnesses but with the potential risk of MS (although this is actually rare)/
     
  7. Enid

    Enid Senior Member

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    Gee whiskers - can't any scientist put all the research findings together yet.
     

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