Unrelated Comments & Questions – October 2017

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Sometimes you want to say something unrelated to the thread or ask a clinical question or some other MS-related question that has not been answered in past. This is the place for you.


About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.

114 comments

  • Can Alemtuzumab cause gaot? Given the debris caused by the dead lymphocytes circulating in the blood. Surely this is one side effect that's not been documented? I am 3 weeks post treatment and wondered my symptoms are coincidental or Due to treatment?

    • Yes, it can. Gout is due to crystals of raised uric acid forming in the joints. When alemtuzumab lyses cells the DNA that is released has to broken down and this leads to increased uric acid levels. In general this is really only a problem when alemtuzumab is used to treat lymphomas with a high cell or tumour burden. In MS the cell burden is much lower and gout is uncommon. However, some pwMS who are predisposed to develop gout may develop gout after alemtuzumab and other cell depleters. Please note this is only likely to happen in the first few days after being treated with alemtuzumab; at 3 weeks this is likely to be due to another cause. I have seen joint pains and arthralgias in several patients post alemtuzumab. It is usually self-limiting and clears spontaneously.

    • Hmmm strange. My first and only gout attack was 9 years. I decided with a heavy heart to stop beer. Instead took up wine. Been alcohol free for 4 weeks. On Alemtuzumab diet free of meat. Eat a lot peanuts though. Some reason get a yearning for them. On the plus side isn't high uric acid indication of no ms activity! If so will take it even if the foot pain is unbearable!

    • Is TB something else that should be flagged up with Alemtuzumab.
      Saw MS nurse Friday who mentioned they've had four patients test positive for TB between 1st and 2nd round of infusions. Consequently I was tested for it Friday, alongside everything else.

  • Is it possible/common for onset of cognitive fatigue/issues to occur as long as a decade before other clinical signs of MS? Mental activities got more draining/hard over the years, where now I can't even read a book without it being taxing. But 10 years before just seems so implausible and I'm hesitant to bring it up with my neuro as to not come across as crazy

  • MS newbie here! What is considered "inadequate response to the treatment" given that NEDA is not achievable over long term? Consequently, how is the decision to switch from one DMD to another made?

  • Does Ocrelizumab really cause Breast Cancer? How big of a risk is there? Where can more information be found on this? Is it something I should be worried about? (Typing breast cancer and ocrelizumab is proving to be unhelpful as I don't know who to believe) I'm told by my neurologist that I may be able to start once it's available on the NHS but hearing about the cancer risk is putting me off. I know there was a post on rituximab on the blog but I couldn't find anything on Ocrelizumab itself.

  • Was reading the Wikipedia page for DMF, and found it states "Phase III clinical trials found that DMF (BG-12) successfully reduced relapse rate and increased time to progression of disability in multiple sclerosis (trade name Tecfidera).[5][6]" (https://en.wikipedia.org/wiki/Dimethyl_fumarate)

    As I know you are interested in MS nomenclature and untruths on the internet,
    I thought Id mention it, particularly as the reference is your paper.

  • At Team Barts, what do you currently offer to any of your progressive patients as treatment plan in terms of Dr. G's treatment pyramid?

    How do you follow these patients along over time to know if your treatment plan is effective as course of progression in individual patients is so variable. IE. MRIs of grey matter/atrophy, clinically (9 PEG, EDSS, 25 foot walk test) and NFLs on LP?

    • In terms of of progression and the pyramid there is nothing licenced for progressive MS (in EU) that can go on the bottom. In our PROXIMUS trial it is any DMT

  • I am currently taking Copaxone but recent MRI has shown disease activity. Having read your posts on Cladribine, I am very keen to take this as the off-label injectable and I'm prepared to pay for it if necessary. Would I have to be referred by my own GP to your team at Barts and travel to London to access this treatment if my own consultant says it is not available where I live? Do you think the oral equivalent will be available in 2018 or later? Thank you for your time and best wishes to all at Barts.

    • DrK may be able to answer your question.

      Apparently the oral version can already be a private prescription in UK according to the people from Merck.I don't know the cost.

      As for the NHS there will be the haggle with NICE it's label is only for highly active…

    • Drug should be available privately, there was an advert in Practical Neurology for the UK market. Current price tag is £2,047.24 per 10mg tablet; pack of 4 costs £8,188.97; pack of 6 costs £12,283.46. As the dose is weight adjusted (https://www.medicines.org.uk/emc/medicine/34044) the cost for a 70-80kg person would be £28,661.36/year; double that (£57,322.82) for the complete course (28 tablets). I don't know whether the NHS will pay that much, or get a (usually undisclosed) discount.

    • Anon 7.28
      If you're RRMS ask your neuro if you qualify for escalating treatment? Eg to fingolimod or dmf?Off-label cladribine inj sounds great doesn't it? If you are RRMS and qualify for something else your neuro would have to justify use of off-label (assuming willing to prescribe it).

      Crikey, look at the cost of those tablets! Crazy money.

    • So the cheaper off-label subcutaneous Cladribine would not really be an option for me/not currently accessible at all in the UK? Would 'highly active' MS be classed as having a heavy lesion load on MRI and having failed more than two DMT's?

    • Anon 5.56
      Go to the web version of the blog, click on the tab about cladribine. There's a Barts MS NHS document that explains about off-label cladribine injections. Print it out and take to your neuro for discussion if you're interested.

      Re highly active MS, there are criteria to meet. Try searching the blog or MS Trust website.

      Re off-label cladribine inj accessible in UK, no real reason why it shouldn't be but in practice places don't seem keen. Might be different when Ravenclad licensed for those 'lucky' enough to qualify for it, why shouldn't those who don't qualify not have equally effective off-label injections?

  • It would be great if you could do a future post on treatment options after an MSer has received their two initial cycles of alemtuzumab in an induction approach to treating to relapsing MS. How do you decide whether to initiate a maintenance drug versus waiting for evidence of disease activity before initiating a third cycle of treatment? Do you have any preferences with respect to the different maintenance drugs that should be initiated after the first two cycles of treatment with alemtuzumab? Can you anticipate that ocrelizumab might be an appropriate or safe maintenance drug to use after alemtuzumab? Could ocrelizumab help avert the onset of secondary auto-immunities that can emerge after alemtuzumab?

    • ProfG may respond as it is something he has been thinking about.

      I think the situation is that we can only prescribe the two infusions as NHS England won't pay for any more. This is daft as we know that about 50percent of people will need a third dose. The data from Cambridge seem to indicate that three doses will sort out about 85percent of people so it is crazy that people don't get third dose. If you go maintainence afterwards what is best.

      We proposed a number of things to try and reduce the autoimmunities a
      .One proposal was to use rituximab. There was no interest in doing this at the time it was proposed. Maybe things are different now.

  • The role of T follicular regulatory cells at how autoimmune disease develops

    IL-2 promotes FoxP3+ regulatory T (Treg) cell responses, but inhibits the differentiation of T follicular helper (Tfh) cells. However, it is not clear how IL-2 affects T follicular regulatory (Tfr) cells, a cell type with properties of both Treg and Tfh cells. Here we show that IL-2 prevents, rather than promotes, the development of Tfr cells. Using an influenza infection model, we found that Tfr cells were barely detectable at the peak of the infection, but accumulated as the immune response resolved. High levels of IL-2 at the peak of the infection promoted the expression of Blimp-1 in Treg cells, which suppressed Bcl6 expression and thereby precluded Tfr cell development. However, as IL-2 levels declined some CD25+ Treg cells down-regulated CD25, up-regulated Bcl6 and differentiated into Tfr cells, which prevented the accumulation of self-reactive antibody-secreting cells. Thus, unlike its effects on conventional Treg cells, IL-2 inhibits Tfr cell responses.

    http://www.jimmunol.org/content/198/1_Supplement/152.8

    https://medicalxpress.com/news/2017-10-autoimmune-disease-viral-infection.html

    • This simplified…

      "The team discovered that about a week after the infection, levels of an immune regulator called the IL-2 protein increased. This triggered the multiplication of common regulatory T-cells, or Tregs. When this phase of the immune reaction was fading, TFR cells started multiplying, reaching peak numbers about a month after infection.
      The formation of the TFR cells was therefore tightly linked to the processes controlling Treg production, researchers said, with falling levels of IL-2 allowing the new phase of the immune response.

      The TFR cells migrated to the lymph nodes — the headquarters of antibody-producing B-cells. Here, B-cells proliferate and change their antibody-producing genes to create new, stronger antibodies. But sometimes the gene changes, or mutations, give rise to an antibody that attacks the body, instead of invaders.

      Researchers discovered that TFR cells prevented B-cells, which gave rise to autoantibodies, from accumulating in the lymph nodes. Importantly, the TFR cells had no impact on the immune processes targeting the influenza virus.

      When researchers prevented TFR cells from forming or removed them from mice, the animals started producing autoantibodies, they explained."

  • This seems important

    By scanning the brains of healthy volunteers, researchers at the National Institutes of Health saw the first, long-sought evidence that our brains may drain some waste out through lymphatic vessels, the body’s sewer system. The results further suggest the vessels could act as a pipeline between the brain and the immune system.
    Dr. Reich’s team plans to investigate whether the lymphatic system works differently in patients who have multiple sclerosis or other neuroinflammatory disorders.

    “For years we knew how fluid entered the brain. Now we may finally see that, like other organs in the body, brain fluid can drain out through the lymphatic system,” said Dr. Reich.

    https://www.technologynetworks.com/neuroscience/news/the-brains-meninges-harbour-its-lymphatic-system

  • Does BMI, gender and following the OMS diet affect Gilenya. I have many days sick and thought maybe it could become too effective because of BMI of 19 and the other above mentioned factors?

  • Why is ocrelizumab taking so long to be approved by EMA? Their more than 6 months behind FDA. Surely they must have sla? Not to mention patient lives to consider.

  • Fast Forward, a non-profit subsidiary of the National Multiple Sclerosis Society, will give financial support to TG Therapeutics to advance TGR-1202 (umbralisib) into preclinical testing as a potential oral therapy for progressive forms of multiple sclerosis.

    TGR-1202 (umbralisib) is an orally available PI3K delta inhibitor, targeting the delta isoform with nanomolar potency and several fold selectivity over the alpha, beta, and gamma isoforms of PI3K. The delta isoform of PI3K is strongly expressed in cells of hematopoietic origin and is believed to be important in the proliferation and survival of B-cell lymphocytes. Inhibition of PI3K delta signaling with TGR-1202 has demonstrated robust activity in numerous pre-clinical models and primary cells from patients with hematologic malignancies.

    Umbralisib has been successfully combined with TG-1101 (ublituximab), an engineered antibody that targets a specific sequence on the CD20 protein found on immune B-cells, on cancer.

    http://www.tgtherapeutics.com/publications.cfm

    • Fastforward are ace and saved us when we were about down and out.
      However if it is preclinical it is years away for being an ms drug.

    • Yes, and the money they donated are far from being enough to support a trial. If the company has no interest in running it, it can take a long time. TG-1101 is close to be released but I dont know what extra can offer with Ocrevus and -soon- Arzerra around.
      It is interesting as a combination therapy though and I am wondering if FF chose it for progressive forms to fill the drug gap or there is some extra benefit on progression to it.

  • I am diagnosed with PPMS. As a child, I regularly developed severe wheezing with viral infections. But as an adult, I never develop full blown colds or coughs. I can't remember the last time I had a cold requiring a box of tissues. At most, I am just tired and briefly have a mild sore throat (usually in the early hours of the morning, before I get up). What does this say about my immune system?

  • I have been reading today that "Almost half (45%) of people with MS feel they have experienced mistreatment or stigma because of their symptoms, according to our most recent survey. " (MS Society 2016).

    I have MS and experienced discrimination recently about my MS. This was from someone who should know better.

  • Do you know more about the patients who had breast cancer in the ocrevus trial. I recently found out that one of them had tested positive for brca gene. Do we know much about the others?

    • Had thought their ages would have been all over 50 which is a risk factor but no some were early 40's. Other risk factor is breast tissue density..they really should have screened for these risk factors.

  • There are quite a few posts on this blog about clemastine – type clemastine in the "Search this blog" box next the top of the page on the left – and then ponder why this promising treatment hasn't been further investigated (and I'm not having a go at Team G here, so please don't misinterpret me about that)

    • Simple reason…we do not work on remyelination at present and therefore it is not on our radar.

      It is a old drug and so there is no pharma interest in old drugs…they take the surprising approach of using antibodies that are 99.9% excluded from the CNS:-(

      However, the study poses questions and surely this deserves more study to get answers. A lovely piece of basic science leading to useful clinical outcomes

    • We don't work on remyelination…should we have a go and see what it does to chronic EAE. Does this mean we should start prescribing this? Pharam wont be interested, unless they get can make money out of this, so let's see what happens. Why haven't we reported on this…Ari Green has been asked to do a guest post, however profG has been slacking with a response,as I am sure you are all asking why can''t we have this drug now.

    • Exactly, anonymous, there is no profit in this for the pharma companies. So should we be asking more of our MS Societies, to fund research into drugs that pharma will never consider? Would this work? (That is a genuine question, by the way, I would appreciate your thoughts, everyone)

    • You have had MS Societies funding CCSVI, sem cells, statins why not?

      However how good are the results, are they clinically meaningful?

    • So how do we get clinically meaningful results? (Again, genuine question) – all these promising old drugs just seem to go nowhere after the first brief flurry of interest – it's very frustrating for pwPPMS, the answer could be out there, but no-one looks….

    • The Italian face of stuff done in China. Mice rats and now dogs. Not of the faint hearted…just as well they don't live in UK they would need protection from the anti-vivisections and quite a few others.

      "Dr Canavero managed to reconnect the severely damaged spinal cords using a chemical called polyethylene glycol, or PEG"

      PEG is commonly known as anti-freeze.

      It is is used as a glue when making antibodies and as a carrier of interferon beta.

      https://www.ncbi.nlm.nih.gov/pubmed/28612398
      Polyethylene glycol-induced motor recovery after total spinal transection in rats. Ren S, Liu ZH, Wu Q, Fu K, Wu J, Hou LT, Li M, Zhao X, Miao Q, Zhao YL, Wang SY, Xue Y, Xue Z, Guo YS, Canavero S, Ren XP.CNS Neurosci Ther. 2017 Aug;23(8):680-685

      I note the lead authors are all from China

      Immunohistochemical evidence of axonal regrowth across polyethylene glycol-fused cervical cords in mice. Kim CY, Oh H, Ren X, Canavero S.
      Neural Regen Res. 2017;12(1):149-150

  • http://www.foxnews.com/health/2017/10/16/why-americans-with-ms-are-going-to-russia-for-treatment.html
    stumbled across this on the internet. "Broadly speaking there are two types of MS: RRMS and progressive MS"
    Bruce Bebo, the head of research for the NMSS of the U.S. still stratifies MS into relapsing and progressive MS. The one thing that needs to happen is for MS to be considered one disease as Prof G has been harping on. Hopefully ECTRIMS 2017 will unify neuros on this point. Lastly, you can read between the lines that HSCT is facing serious head-winds from pharma and insurance companies.

    • It is company stuff so I am not going to comment or post on this, but it is stem cells that have been engineered to make growth factors, the phase iii trial has started this month, so lets hope it is positive

    • "The beginning of the end of MS as neurodegenerative disease?"

      Maybe for mice..people???

      “These stromal stem cells are more flexible, and that’s why, although they represent less than 0.1% of those cells in the bone marrow, we take them, we expand and purify them, we produce tens of millions of those, and then we try to inject them. First we tried in the mice models of multiple sclerosis and it was fantastic.”..“We saw that paralyzed mice regained their walking and jumping abilities, so this means that these cells induce recovery and prevent damage to the nerves.”

      Not sure about this but there's a ppms patient claiming to
      have restored 7 years of progression with the stem cells.

      "Now in his late 40s, the dual Israeli-British passport holder and a former marathon runner had sought help from many sources to fight MS, but had been told in Britain that “they had nothing at all to offer” other than a little help from speech and physical therapists or cholesterol tablets."

      https://www.jpost.com/Jerusalem-Report/Opening-a-door-to-regenerative-medicine-459639

  • Programmed death 1 is highly expressed on CD8+ CD57+ T cells in patients with stable multiple sclerosis and inhibits their cytotoxic response to Epstein–Barr virus

    Growing evidence points to a deregulated response to Epstein–Barr virus (EBV) in the central nervous system of patients with multiple sclerosis (MS) as a possible cause of disease. We have investigated the response of a subpopulation of effector CD8+ T cells to EBV in 36 healthy donors and in 35 patients with MS in active and inactive disease. We have measured the expression of markers of degranulation, the release of cytokines, cytotoxicity and the regulation of effector functions by inhibitory receptors, such as programmed death 1 (PD-1) and human inhibitor receptor immunoglobulin-like transcript 2 (ILT2). We demonstrate that polyfunctional cytotoxic CD8+ CD57+ T cells are able to kill EBV-infected cells in healthy donors. In contrast, an anergic exhaustion-like phenotype of CD8+ CD57+ T cells with high expression of PD-1 was observed in inactive patients with MS compared with active patients with MS or healthy donors. Detection of CD8+ CD57+ T cells in meningeal inflammatory infiltrates from post-mortem MS tissue confirmed the association of this cell phenotype with the disease pathological process. The overall results suggest that ineffective immune control of EBV in patietns with MS during remission may be one factor preceding and enabling the reactivation of the virus in the central nervous system and may cause exacerbation of the disease.

    http://onlinelibrary.wiley.com/doi/10.1111/imm.12808/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER

  • A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis

    Highlights

    •HDAC1 has a novel pathophysiological role in EAE.
    •Mice with a T cell-specific deletion of HDAC1 are completely resistant to EAE.
    •Selective inhibition of HDAC1 might be a promising strategy for the treatment of multiple sclerosis.

    Eighteen HDACs take part in the epigenetic process of turning genes on or off. In addition to regulating gene activity, they can change the activity and function of proteins. The bottom line is that they play a major role in regulating a cell’s behavior.

    http://www.sciencedirect.com/science/article/pii/S0896841117305954?via%3Dihub

    • Thanks for this but I generally do not post on EAE cures of the week because their are too many and because even if they are amazing it is light years away from MS.

      Importantly I come across as a grumpy old geezer (person) when all around is saying amazing.

      Get rid of T cell function and you get rid of EAE, but if MS is not T cell driven then is it relevent.

    • It's true about the mice and EAE, but till we have a solid theory that doesn't leaves holes behind (which we don't), we need to be open to any possibility. Not only as a real prospect, but as food for imagination. When you constantly look at one image, it begins to appear blurry.

  • Just watched the Taubman Prize lecture by Dr. Hauser. Wonderful journey on how B-cells came to be the driving force in MS and development of Ocrevus.

    Would be great to post on the Blog. I have no idea how to get the lecture. As Dr. G was mentioned in the credits, maybe you can reach out.

    Debbie

    • I,ll have a look. Was it mentioned that anti CD20 was shown to be active in rheumatoid years before the studies in MS.

    • Yes. He was recognized for his 20 year achievement in pursuing where the science led him. It was very compelling and for many of us not in the thick of the research very informative. And so hard to think that for so long he/others were told it could not be B cell driven.

      Just wanted to share.

    • Thanks, we will see him at the burning debate, if you find a youtube link if it was filmed post the link.

      I hear he is writing a book, maybe that is why profG went to meditation.

    • Hope you've had chance to listen to it MD, especially the questions at the end 'why does atacicept make MS worse?' Hope he's read your paper by now 😉

    • Yes I heard the last bit and it was a pathetic attempt that could have bee ########################################################' '''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''n so easy

  • Hi. Just finished my first course of ale.tuzumab. Just wondering can drinking alcohol affect the outcome or efficacy of the drug? In absence of advise. How long should one abstain from drinking alcohol to ensure full efficacy of drug?

  • Dear Anon 15.07

    Clonal Evolution of Autoreactive Germinal Centers (24 August 2017)
    I have put your comment in SPAM and have created a Guest Post which should get launched this week

    Do you want to identify yourself as you imply, it is your work?
    Well done getting it into Cell.

    If you do…Send us a picture of yourself, a Biography and report any Conflict of Interests

    If you do I will send you the post, so you can edit it as I have added some links to help the readers,

  • Question on co-morbidities. It has been shown that people diagnosed with Ehlers-Danlos Syndrome are 10 times more likely to develop MS. But I can't find anything on this site about EDS and MS. But there is info on the EDS sites about MS. Is there any chance you could cover this topic please? Why do the 2 seemingly unrelated illnesses have an increased link?

  • I've been really curious about the user of fasting in MS patients. While the MS clinical results are totally provisional, what we know from other fasting studies is that it's one of the best ways to induce autophagy in the immune system. What they've seen in animal and mouse studies is that during a fast the patient's white blood cell count goes way down and then rebounds afterwards as naive immune cells repopulate the immune system. This seems to fit well with the EBV and memory B cell explanation of MS. Do you know anyone who's been doing work on this in the MS field?

  • Could such vaccines work on MS too?

    "…combining the tetanus vaccine with a viral particle that normally affects cucumbers can be used to treat psoriasis and allergies, and may even protect against Alzheimer's disease.

    …"For chronic diseases, these antibodies are specially made against one of the body's own proteins. By blocking that single protein, the disease gets better. To use the example of psoriasis, a protein called Interleukin 17 needs to be active for the disease to progress. By creating a vaccine that stimulates the body to make antibodies against Interleukin 17 itself we can replace the need for frequent and expensive injections and make this type of treatment much more affordable and accessible to patients who could otherwise not afford specially made antibodies."

    https://medicalxpress.com/news/2017-10-vaccinating-psoriasis-allergies-alzheimer-possibility.html

  • This is for Md

    Conclusions: CD20+ B-lymphocytes, but not CD3+ T-cells, are associated with more aggressive MS, as reflected by a younger age at death. B- and CD3+ T-cell levels are associated in different brain compartments, and are associated with microglia/astrocyte activation in WM lesions. These results support the recent focus on medications targeting B-cells

    https://onlinelibrary.ectrims-congress.eu/ectrims/2017/ACTRIMS-ECTRIMS2017/200606/marcello.moccia.association.between.cd202B.b-cells.and.age.at.death.in.multiple.html?f=menu=6*ce_id=1278*ot_id=18221*media=3

    Sharing is caring

    Obrigado

    • Thanks I will try and read, I appreciate you reading for thanks for bringing this to my attention, I didn't get to see it

  • According to what I saw in this ECTRIMS and regarding the diagnostic criterion of MS without evidence of dissemination in time?
    Now is that definitive redefinition of the McDonald's criterion?

  • A question for a neurologist.

    Is it normal to be asked about ones sex life (a female patient), more specifically how many times one has sex each week? An appointment with a male neuropsychiatrist.

    No discussion before hand prompting this question.

  • The statin trial for MS how does this relate to the following study?

    J Neurosci. 2008 Dec 10;28(50):13609-14. doi: 10.1523/JNEUROSCI.2765-08.2008.
    Negative impact of statins on oligodendrocytes and myelin formation in vitro and in vivo.

    Klopfleisch S1, Merkler D, Schmitz M, Klöppner S, Schedensack M, Jeserich G, Althaus HH, Brück W.
    Author information

    " Statins are thus considered as potential therapeutic drug for the inflammatory demyelinating disease multiple sclerosis (MS). However, little is known about the effects of statins on myelin-forming oligodendrocytes. Here, we show that statins hamper process and myelin formation in vitro by interfering with Ras and Rho signaling in mature oligodendrocytes and provide evidence that statins impair ongoing remyelination in vivo. Our findings may have significant implications for the application of statins in MS patients and in other demyelinating diseases of the CNS."

    • thanks for your reply.
      is the off label intravenous cladabrine available at any NHS hospital even if a hospital tends to favour Mitox?
      Also, if you had both Mavenclad and Ocrelizumab at your disposal for both RRMS and progressive MS which would you favour in each case?

    • IV CLAD and sub cut CLAD are both available, we use Sub cut because it is easier.

      Maven v Ocrelizumab they are both good drugs. You talk to the pwMS to find out what suits them, I personally think their MOA is the similar.

    • hi again.
      Sorry what is MOA?

      I know you offer off label clad , but should any hospital be able to access off label clad?

      Also is the strength and overall treatment comparable in both Mavenclad and the sub cut version you use?

      Finally, which has better outcome data for progressive MS cladabrine or ocrelizumab? Is there a direct head-to-head comparison somewhere?

      many thanks

    • Sorry MOA = mechanism of action
      Yes any hospital could off label clad…I believe on clad clad will be available in the UK very, soon.

      Mavenclad v sub cut the doses are similar, but we have been monitoring the influence on white cell depletion to determine how many doses and we have been treating with anti-virals.

      Maven v ocrelizumab head to head….at the moment not likely because maven not available in US, and ocrelizumab not available in Europe. In time it will be tested maybe by real life experience with MSbase. Ocelizumab will keep B cells at none-existent levels for ever and so may be more effective but that may carry the risk of a death due to serious infection as occurred in SLE and arthritis.

    • hi me again
      so would I be right to say that off label clad could be secured for someone who probably won't fit the the usual restricted criteria which will accompany mavenclad but who would still benefit?

  • Any thoughts on the paper by Green et al. (2017) in the Lancet "Clemastine fumarate as a remyelinating therapy for multiple sclerosis (ReBUILD): a randomised, controlled, double-blind, crossover trial" that leads to interpretations that
    "To our knowledge, this is the first randomised controlled trial to document efficacy of a remyelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis. Our findings suggest that myelin repair
    can be achieved even following prolonged damage."

    For those of us with MS, this is uplifting that an over the counter anti-histamine could help repair myelin damage with minimal side effects, but am somewhat frustrated as this has been on the market for >20 years but only just coming to light.

    Could Prof. G or Mousedoctor give us an update on this?

    Thanks, our man in Brum –

  • Having just listened to your Ascend summary on you Tube as someone who had three years of Tysabri then having had the now ill advised drug holiday followed by Cyclo then Lemtrada would it be a bad idea to request to restart TySabri in order to halt my upper limb deterioration? I am JC virus positive or at least I was when I was on TySabri. Will these results mean that more people will be pushed towards Tysabri again even though there is the problem of PML?
    Also, do you think that cladribrine is as effective in the protection of upper limb function as Tysabri hence its selection for the pending chariot trial?

    • Hopefully Dr K or Prof G will answer your questions. Being JC positive indicates that Tysabri is no longer an option given the PML risk i think. We don't know about cladribine and protection of upper limb function as far as I'm aware as yet.

    • We think blocking the inflammation will have the benefit and so other highly active agents should do the same thing and the data with ocrelizumab was even better

  • Hello, I wonder if you can interview Prof Pender on how things are going with the EBV work he's doing? There doesn't seem to be an update that I've seen.
    Thanks

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