Unrelated Blogger Comment March

Abit slow today, but if you have an unrelated comment this is the place for you.

Theres lovely:-)

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  • Mouse Doc & Co.

    have you heard about the possibility of one autoimmune disease getting worse/ relapsing but AT THE SAME TIME another autoimmune disease going into remission?

    So psoriasis relapse (really bad) but MS remission AT THE SAME TIME in the same person?

    How would you explain?

    My psoriasis is going bonkers (really bad) since this simvastatin thing BUT my MS is kinda "silent" at the same time – this different is really evident now after 6 months. WHY?

    My ignorant explanation is kinda of: the statin kind of REDIRECTED the attack site to the skin instead of the brain……???

    • Statins seem to have some anti-inflammatory effect, it is not very strong, though. And yes, it is perfectly possible to have one autoimmune monster thriving while another monster is sleeping: look at what happens after alemtuzumab (Lemtrada). MS + other autoimmune disease, no MS + no other disease, no MS + other autoimmune disease.
      But in the case of MS and psoriasis … psoriasis shows up, in MS not everything is clinically apparent. Have you had an MRI recently and know that all is well there?

    • The statins flamed up my psoriasis really horribly. I've stopped statins long ago but the skin is still going crazy.

      No, no MRI but I compare the clinical outcomes from before the skin outbreak last year and now.

      I would even talk of improvement in MS (very little vertigo, can walk for 2 kilometres, climb stairs etc.). Without stress it looks even better.

      Psoriasis lesions increase now after stress. before they were very few and stable over years.

  • Cinara wrote;

    I was scared today to discover that in September 2016, the Anvisa (national sanitary surveillance agency here um Brazil) authorized the distribution and commercialization of the generic Fingolimod. In other words, from what I learned, Brazil broke the Fingo patent and the EMS pharmaceltical laboratory will produce and distribute generic in the country. It remains to be seen whether quality will be maintained and whether this will actually force the price of the drug to fall in the country. Now I just don't understand why not take drugs that are already generic and has several studies indicating guaranteed efficacy in the control and reduction of MS, as in the case Rituximab and Cladribine, they are already "available" there, without the need to create a "legal dispute".

    • Thank you MD2.

      The patent issue is very delicate.
      At the same time as of should respect the innovation exorbitant prices and the exclusivity of the patent unfortunately has forced to extreme measures, such as the breaking of patents mainly in poorer countries, as in the case of Brazil.
      I just think that they could also look first for the reuse of already generic drugs that have studies and proven effectiveness against a certain disease, as in the case of Cladribine.
      From there it seems a strange "game": for example in the case of Cladribine, if then Merck would re-launch it in the market as a drug for MS in the oral version, then some time later resolve to break the patent of something that was once generic…

    • Don't know if this is true but profG has maintained the Australian fingolimod patent has expired. In the US an extension was granted to 2019 so I suspect Brazil may not be breaking patent override Novartis would be suing the Brazilian government. Maybe this is the year that the ms gravy train begins to crumble. Ultimately it may mean no new drugs if the price plummets if pharma can't make a buck they will be off..

    • Oral cladribine may be arriving soon but that would not stop one using the generic off label.

      What will stop people using rituximab when ocrelizumab arrives.

    • pharma will always make a buck, because there will always be people who have gone through a lot of treatments over a decade or so and still have active disease /do not tolerate drugs they have tried /are jc virus positive etc.

    • They are trying to in Sweden after what I heard…but I don´t think they will get lucky, we have thousands of people using it (rituximab. intersteintg though because I always thought how are they going to act now when ocrelizumab is on the table..

    • The Swedish Government was taken to Court and they put the finger up to pharma.

      However once ocrelizumab arrives we will see what they do? Also what will Roche do they make both rituximab and ocrelizumab.

      What will happen when cladribine comes back to the party?

      Will they start with generic cladribine, it will save them even more money than using rituximab?

      Exciting times

    • Rituximab is coming off patent, so some Celltrion or other Korean Samsung-like creature will happily produce a nice biosimilar. I am sure there are enough people around the world waiting for their chance to get some treatment.
      BTW, if Gisela K. was right UK is one of those places where people do not get treatment.

    • Me no I don't have opinions ProfG might but he is very busy he doesn't even reply to me. So don't hold your breath sorry.:-(

  • Prof. G. et al.

    Befuddled by steroids. How do they work or not work?

    I’ve read Prof. G’s risk/reward concern with use of high dose steroids for all relapses in this 2013 blog: http://multiple-sclerosis-research.blogspot.com/2013/09/clinic-speak-how-good-are-steroids-for.html. We’ve also been told by the MS nurse that steroids do not prevent damage or aid in repair; it just gets a person to the new baseline faster.

    (Now this first bit still confuses me since my understanding is that the steroids are used to reduce inflammation. So why doesn’t reduced inflammation result in less damage?)

    However, if steroids do not reduce damage, should they be used in an early relapse? My pwMS has been treated with two 3-day courses of high-dose oral steroids for optic neuritis—the first just the day after vision change and the second course two weeks later when vision improvements started to reverse.

    The neuro strongly advised steroids and said that the relatively mild vision impairment could decline much more without it to reduce inflammation.

    So we’re confused and would like to sort out steroids—it’s hard to argue in the moment with, “your vision may well get much worse.” Is there something about steroids for early ON that doesn’t fit the, “steroids don’t reduce damage” line? Or is my pwMS racking up risk without any change in outcome? What’s the practice at Barts MS?

  • I would definitely take a course of i.v. steroids if the problem has not resolved in 5 days or so.
    Do not demonise steroids, they deliver when needed and do it quick and effectively. 3 days i.v. does less damage than slowly slowly taper taper dragging on for many months.

  • Hi team. What would you recommend for tracking active demyelination in a patient who is allergic to contrast dye? I have read some articles on your site that show that neurofilament light chain levels in the cerebrospinal fluid are a good marker of active damage/inflammation in the brain but no neurologist seems to want to go down this route. Any other options?

    • Dyslexic DNG = NeuroDocG
      She is the Biomarker Queen and may suggests things mine was soluble CD27 a marker of T cell activation or is that B cell activation. When the cells are activiated they shed CD27. However there may be better ones like osteopontin. It is not my field.

      However we do test for neurofilaments as a service (whether there is enough sensitivitiy in blood) maybe NDG can comment

  • Hi,I have heard that MS lesions can disappear (especially in the early days). Can you shed a bit of light on this please?

    • MS lesions based on frequent MRI scanning are thought to last 2-4 weeks before they start to disappear. In animals the defaiult mechanism is repair

  • Can myoclonus in MS present itself as tiny singular bodywide twitches that are invisible to the eye (such as on the arm)?

    From what I read myoclonus is more jerk like movements. thanks

    • I'll have a look once I get access to paper. I had never heard of 14-3-3 the outhebrides football team formation against Germany. Not sure why you couldnt apply to larger animals

    • I meant if the axon regrowth approach itself is feasible to pursue in large animals?
      I've read somewhere else that natural growth rate is incredible slow

  • Question to MD and MD2 :-). Is it true that one can induce visible signs of brain aging in mice by injecting them with D-galactose?

    • Apparently yes
      "Chronic administration of d-galactose has been reported to cause deterioration of cognitive and motor skills that are similar to symptoms of aging and, therefore, is regarded as a model of accelerated aging"

    • It has been replicated many times by different groups so this one is real. I suspect the salt water one will never be repeated as the company won't let the "compound" out for an independent assessment. All the studies (Alzheimers, Parkinsons, MS etc) seem to originate from the same group.

    • Right. And how do you induce neurodegeneration/senescence in mice/rats? or do you just buy old ones and try to remyelinise them? (MD was sulking today at people preferring clinical data to rodents … go on, here is your chance, I like your style :-).

    • You can do both. When I looked for galactose and aging I got over 700 papers. We know old animals dont remyelinate as well as their macrophages do not clear up the debris as well as young mice. Likewise old mice dont sprout nerves as well as you animals

    • Shoot… if it is true that galactose ages rodents, what does it do to my brain? ( do you remember my ramble about Japs not having so much MS and not having gazzilions of galactose in their diet from age 1 to age 101?). I would actually like to write a paper on this and publish it in some "Medical Hypothesis" journal nobody reads. MD and MD2 invited as co-authors ;-).

    • Reading through masses of papers and a funny thread emerges, I'll keep you posted on the progress 🙂

    • We are not organising it it is UCL's turn, I don't think they have done e much organising yet I am not sure…

  • Regulatory T cells promote myelin regeneration in the CNS.

    This is the headline from an article published in Nature. (See link below.)
    It relates to experiments in mice, but how does it fit in with the many T v. B cell articles that are now appearing in this blog?

    Thank you.

    • I'll cast a beady eye. Treg = regenerative. Like it , as everything immunology increases T regs it sounds great…As to T and B cell articles it makes little impact for most but could be bad news some e.g. daclizumab that kills of Tregs. So we are back into protective autoimmunity mode again….yeah my favourite:-).

    • The Nature article above is similar to the BBC article posted by Anonymous March 16 2:36am.
      The Nature article explains that myelin repair involves differentiation of oligodendrocytes from oligodendrocyte progenitor cells, and that in multiple sclerosis this differentiation fails.
      The article investigates how Treg cells promote oligodendrocyte differentiation, which might be through a mediator protein produced by Treg cells called CCN3.
      As MD suggests, a "Regenerative" effect.

      Current DMT's work sometimes by affecting B memory cells, other times by T cells. This research suggests (I think) that DMT's inhibiting T cells might reduce relapses, and keep axonal loss at bay for longer, but will not stop axonal loss because the myelin sheath will not be repaired.

      The same probably applies to B cell modulators,(e.g. Cladribine) because if the Treg cells are not producing CCN3 protein properly, then re-myelination will not occur.

      So perhaps we need B memory cell inhibitors, with Treg/CCN3 enhancers to be given together.

    • Yes the research has been done at Queens University in Belfast. I agree it needs more discussion please.

    • To be quite honest… sounds like another "BBC cure for MS". A few weeks ago a Norwegian National Broadcaster (NRK) had one, too.That one was supposed to cure rheumatoid arthritis, MS and psoriasis – magic :-).

  • I know a few pwMS discussed communication problems in the NHS before. I think this is very important in MS care.

    I came across this:
    "Communication errors behind third of hospital complaints. Poor communication, treatment and errors in diagnosis have once again topped the list of causes of hospital complaints investigated by the Parliamentary and Health Service Ombudsman. " Nursing Times Sept 2015.

    I have experienced poor communication and wondered if (more) research would help?
    How can hospitals improve communication without it costing more money?

    I know NHS hospitals are facing funding challenges.

  • CBD balm for MS neuropathic pain, can this be researched please?, people are reporting this helps. (Not the balm with THC).

    I have neuropathic pain and not many spasms and would like to know more about this.

    • Evidence of CBD on pain is weak, the THC acts via CB1, if you don't have spasms that does not matter on where it will work in neuropathic pain. if the CBD balm has THC in it it may.
      Sativex THC/CBD is licenced for neuropathic pain iun Canada

    • Could it be the CBD balm contains a small amount of THC anyway, even though it's marketed as just CBD balm and that's why people report it helps?

  • I have new activity on my latest MRI scan, I'm on a tablet DMT.
    How do I know when it's time to switch DMT, if my neurologist is conservative and doesn't treat MS aggressively?
    How many new lesions and signs of deterioration does it take to switch to a more effective DMT?
    I know I need to have this discussion with my neurologist but I want to be informed about this subject before the discussion.

    • Anon – don't know if this will be helpful or whether you already have this information, but I used the Association of British Neurologists Guidelines 2015 and their definition of 'more active' MS and the eligibility therefore for category two treatments. I found the guidelines via a google search easily enough. The guidelines state that evidence of more active is via frequent clinical relapses and/or MRI activity, either untreated or while on a category one drug. It then reads 'We recommend that with patients with more active disease, use of one of the category two treatments' Best wishes for your treatment

  • Platelet level has decreased since receiving Alemtuzumab in November '16 and my test from two weeks ago is now showing that it has moved from the normal range to just below normal at 143.
    I have experienced petechia since the beginning of February but no other signs of ITP.
    Thrombocytopenia? Do I worry or not worry??? Seeing neurologist next week and will, of course, raise with her. However, I don't follow the pattern highlighted in the post a few days ago 'Not All Low Platelet Counts Are Due To ITP' so that's somewhat disconcerting. This is especially on top of realising last night that I'd returned to gardening when perhaps I shouldn't have!
    If any of you super busy Bart's team can advise I'd appreciate it.

  • MD

    Just noticed denim jacket with Iron Maiden back on a young lady with a midlands English accent. skull with cork screw out of right ear over a water bed with a couple of rocks. What album was that?

    • Eddie (skull) and corkscrew is "Can I play with madness" single from "Seventh son of a seventh son" albumn 1988 not sure about the water bed? A spoon scooping out the brain

  • Is there information on the web about doctor grading? I am interested to know at what level registrars join NHS neurology teams. If I see a registrar are they supposed to introduce themselves as neurology registrar rather than neurologist?

    I am keen to know this as it would help me ascertain how much medical training the registrar has had. thanks.

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