Making MS is a rare event

Zhu TH, Nakamura M, Abrouk M, Farahnik B, Koo J, Bhutani T.
Demyelinating disorders secondary to TNF-inhibitor therapy for the treatment of psoriasis: A review.J Dermatolog Treat. 2016 Feb :1-8. [Epub ahead of print]

BACKGROUND:Tumor necrosis factor-α inhibitors (TNFi) are the most widely used systemic treatments for patients with psoriasis and psoriatic arthritis. There currently exists a U.S. Food and Drug Administration issued warning label on all TNFi for “rare cases of new onset or exacerbation of central nervous system demyelinating disorders.” The aim of this review was to update the incidence of TNFi-induced demyelinating diseases.
METHODS:Pubmed database was searched for safety data regarding demyelinating disease secondary to TNFi therapy prescribed for psoriasis.
RESULTS:In clinical trials: 6990 patients had received treatment with etanercept with one reported case of multiple sclerosis; 5204 patients were treated with adalimumab with no cases identified and 2322 patients were treated with infliximab with one case of demyelinating polyneuropathy. Outside of clinical trials: 19 individual cases of demyelinating disorders from TNFi treatment have been reported.
CONCLUSION:Although there is potential for TNF blockade to lead to demyelination of the central and peripheral nervous systems, the results of the present review suggest that demyelinating diseases associated with TNFi are extremely rare. TNFi are not recommended for use in patients with a personal history of demyelinating disease. However, with clinical vigilance and individualized treatment regimen, TNFi may be safe for use in other patients.

Tumour necrosis factor is a cytokine that is involved in the control of infection. It is also is a major target in rheumatoid arthritis, However a side-effect of this drug is that it induces MS. In this study thet looked in psoriasis and found that the MS-like condition is a rare event.  It shows that you cant jump from one autoimmune disease and jump to the next on and expect everything to work.Sadly because we filed a patent on this with the guy who filed the patent on the treatment of arthritis.

You loose some can we win any?

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  • I also always wanted to understand why treatment with alemtuzumab, for example, causes autoimmunity to the thyroid, and that daclizumab can lead to liver autoimundade and perhaps psoriasis…
    But the same thought can be taken to why blocking of TNF-a pathway may lead to treatments for MS in rheumatoid arthritis.
    Perhaps even if they are autoimmune diseases, ie, they share similarities, they share differences, and to move on a path towards a determined vis suppressing an autoimmune end arousing another…

    Perhaps MD can give an explanation …

    • with Daclizumab you can perhaps argue that you are blocking Tregs Blocking Interleukin2 function leads to a variety of autoimmune conditions including gut disease. Likewise CD25 deficiency leads to autoimmune disease.

      I believe alemtuzumab causes autoimmunity because of the way it does or doesn't deplete B cells and other types of regulatory cell. We will submit paper soon.

      Interleukin-2-deficient mice (IL-2-/-) generated by targeted mutagenesis proved to be an excellent system to study the function of this lymphokine in the context of whole immune system. In addition, they provide an animal model of a primary immunodeficiency caused by a single-gene defect. Our results indicate that the essential degect in IL-2-/- mice is the lack of a negative regulatory function, which leads to breakdown of self tolerance. The development of autoimmune diseases in IL-2-deficient mice stresses the link between autoimmunity and primary immunodeficiencies.

  • always loved abstracts like this
    > METHODS:Pubmed database was searched
    such science much authors so research nice funding wow

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