Curing MS

C

How close are we to offering some people with MS a cure?

I am speaking at the Imperial College Neuroscience Society this morning on ‘how close we are to curing MS’. I think we are very close; in fact some of the longterm follow-up data of IRT (immune reconstitution therapies), in particular, alemtuzumab, non-myeloablative HSCT and myeloablative HSCT looks very promising. I suspect that when we complete our long-term follow-up of cladribine -treated patients we will find a similar story.

If you want to have any chance of potentially curing yourself of MS you have to be treated early, as early as possible, with an IRT preferably with one of the big guns. The problem you will have is finding a neurologist who agrees with this treatment strategy.

CoI: multiple

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.

63 comments

  • What would you say is the definition of early. Could EDSS 2.0 stable since diagnosis 4 years ago going for an IRT is early?

    • This a very good question which I have asked numerous times in the past. Yet not recieved single answer. I understand why in case it upsets those not at early stage of their disease. But if you want people to be treated early then please define early. Number of kession. Type of kession. Location kession. Edss level etc. You proud on telling it like it is. So why not answer this question or do a post! Or least have the honesty to say why you can’t answer the question.

    • Before you have any significant end-organ damage that disables you cognitively or physically and before the processes that drive smouldering MS get established.

  • How can this have such a high rise tintodometer when what your essentially saying is to stand a chance of firm remission you can’t be treated in the uk?

      • But when you say early – how’s that defined. They are available on the Nhs but not as early treatments. They are available after you have failed CIS and DMF, which takes years. By which stage you can’t turn it back… So it isn’t available.

  • Luckily cladribine was my first DMT, given to me straight after diagnosis. I love my no-bullshit country (Norway). Crossing my fingers, while at the same time try to keep an healthy assumption that more treatment will be required at some point.

    • I looked into the Norway healthcare system it sounds interesting. It is not free though and people aged over 16 years old need to pay each year the first 2,000 kr, which is about £170. This contibutes to any care, appointments and medicines. Then they are issued an exemption card to fund remainder costs for that year.

      • That is correct. Plus they prescribe high efficacy DMTs from the onset (if you want to). They do however some other stupid things, like taking Gilenya and Tysabri off the list, arguing they can be replaced by Rituximab and Mavenclad. IMO as many options as possible should be made available.

  • Hi Prof G,

    A nice set of slides for a presentation! Do you think you might be oversensationalising any aspects of it though? You argue a lot about smouldering MS and aspects of pathobiology that current DMTs may not appreciate, the real MS, that we need to investigate more. Do you think defining and measuring outcomes here might be important for the definition? My understanding of cure is stopping a disease process and any further damage it does, but then I’m not sure where the goal posts are going to be set?

    • Re: “Do you think defining and measuring outcomes here might be important for the definition?”

      Yes, the outcomes are very important and we should be deep phenotyping patients to make sure MS has been treated and has stayed in remission.

  • So why are so many newbies put on Avonex? I despair. These young people need the best chance. I’ve been on many DMDs. Possibly all a bit late. At 58 I have pneumonia I suspected from a choking fit on some food going the wrong way, I’m always told, no , this happens much later in disease. Well what is later in the disease, neurologists shouldn’t give it the chance. As with cancer, belt & braces job early on.

  • If the UK paid more into the NHS via contributions through income, would or could this in anyway change how NHS DMT’s are prescribed and are available ?

    • Maybe, maybe not! The neoliberal or Tory view is that the more you can shift healthcare expenditure privately the more healthcare will contribute to GDP and GDP growth. The latter does not automatically translate into the wider availability of high-cost drugs. At the end of the day, healthcare is too expensive for individuals and some form of insurance scheme will be necessary and the payers, or the insurance companies, will almost certainly have their own mechanisms to control high-cost drug prescribing.

  • Meantime I chip in £50 for the UK MS Society’s Stop MS appeal and return to reading something genuinely interesting.

    • I was diagnosed nearly 20 years ago. The MS society were saying we’re close to a cure. I kept, donating. I don’t now. I’d rather put my money into helping smaller charities working closely with MSers who need support. I worry that one of my children will develop MS and be given the cheapest drug not the best . My sister also has MS.

      • The UK MS Society funds physiotherapy with a proper neurophysiotherapist where I live. As well as other things such as transport to medical appointments for those unable to drive etc.

        • im Pleased it works well in your area. It’s clearly patchy, and depends how the group is run. I’ve tried to help and go forward but some people are set in very old ways.

    • Re: “So what about us? We with ppMS who were diagnosed late and now disabled – any cure or hope for a cure for us?”

      Yes, but a cure will look very different, i.e. it may stop new disease activity but it won’t necessarily reverse fixed deficits. In other words, you could remain disabled from previous damage.

  • I would like to ask Prof G, you state that early treatment is key, get a treatment ASAP. For someone diagnosed 6 mths ago with PPMS and no treatment being offered on NHS as ‘no fresh lesion activity’ what do you recommend?? From where I am sitting I now there are 2 options – 1. Do nothing except decline 2. Pay for myself somehow to go abroad for HSCT – would love to hear your opinion?

    • Re: “From where I am sitting I now there are 2 options – 1. Do nothing except decline 2. Pay for myself somehow to go abroad for HSCT – would love to hear your opinion?”

      What follows is not necessarily applicable to you, but someone in your situation. To give individual advice you need more information to hand.

      OPTION 1: Ask for a lumbar puncture to have your CSF neurofilaments measured; if raised you have active disease and ask for a treatment. Because NHS England doesn’t accept raised NFL levels as an activity marker you may need to ask for an off-label drug, e.g. subcutaneous cladribine.

      OPTION 2: Volunteer to participated in the ORATORIO-HAND study

      OPTION 3: Ask for a repeat MRI in 12 months time. If you have new lesions demand ocrelizumab under the NHS.

      OPTION 4: Ask for a second opinion.

      OPTION 5: Pay privately for treatment (my least preferred option)

      Please note I would not recommend HSCT; I am not convinced by the data that it makes any difference in patients with more advanced disease.

  • Agree with this, but not sure what patients can do with this.

    1) problem #1 as you stated, one has to find a neuro who believes this. So by the time most pwMS get past the shell shock of their diagnosis and find this, statistically most will already be on ocrevus or tysabri or gilenya (or worse a CRAB drug). So what do they do with this info? Are you suggesting they switch to an IRT asap, even if they are “doing well”?
    2) even if the answer to the above is yes, how do they know if they are “early” or if it’s too late for them to bother? If you’ve been on a dmd for 1, 2, 3 Years with no noticeable change is that still “early” Or is it too late? How do you know since end organ damage isn’t measured by most clinics?

    As a patient if this is your best shot at a cure, but most neurologists won’t treat you that way, it’s a big problem. It’s like telling a cancer patient “you might have beat this disease if you had known to find the one doctor who treated this way, but since instead your research led you to the “best” oncology center who you trusted and started the chemo they strongly recommended instead of the one that will cure you, you’ll probably die”.

    I realize your audience of Doctors needs to hear this message so maybe your post was more intended for them?

  • Raising expectations too high generally, in terms of the potential impact of the drugs available? I hope not. As for ability to access the IRTs in good time, it’s a different story (and I know this is one of ProfG’s main points.)
    I am now on cladribine as my first DMT, some 3 years after my initial CIS diagnosis, a full year after my MS diagnosis, and only after a request for referral to another neurologist, an MS specialist. at a different hospital, as only the CRAB drugs and Tec were options where I was originally. But I am able and motivated to self-advocate, I have a good support network and am fully mobile for travel. I wonder about the options and outcomes for those who are not so lucky.

  • I don’t want to be a killjoy, but a treatment that has potentially tumorous consequences and other known negative effects of many years of immunosuppressive therapy can’t be called a cure, in my opinion.

    You simply exchange one problem for another.

    Hopefully, current therapies will eventually lead researchers to develop a specific anti-EBV therapy for MS rather than shooting sparrows with cannons.

  • Natalizumab and been told I’m stable. Still suffering from bad fatigue and early symptoms before starting the drug. I don’t feel l’m cured.

  • “If you want to have any chance of potentially curing yourself of MS you have to be treated early, as early as possible, with an IRT preferably with one of the big guns.”

    There is no way that I would have chosen to be treated with something like Alemtuzumab, HSCT, or any “big gun” in the earliest days of my MS. Because of the side effects, (long term) risks. And because I felt so well.

    And even now, 20 years on, if I could wind the clock back and I knew everything I know now about my MS, I still wouldn’t want such treatments.

    These are treatments. Not cures. They will work better in some than others.

    To talk of a cure, you need to fully understand disease processes. We don’t know enough about MS yet by far. And part of the problem, in my humble opinion, is the fixation on the immune system’s response and anti-inflammatories.

    • “And part of the problem, in my humble opinion, is the fixation on the immune system’s response and anti-inflammatories.”

      That’s not part of the problem, that is the main problem.

      • Point taken but it would be fallacious to deny that the immune system is involved in MS. What we need are add-ons on top, neuroprotectants etc. Progress on this is far too slow.

        • I know that I personally would not cope with anti-inflammatory alone, never mind + neuroprotectant. I reacted badly even to low doses of biotin and lipoic acid! I do not think this approach of drug cocktail is realistic.

        • Absolutely – it is important to understand the immune system response in MS. I completely agree with you.

          But instead of focusing almost exclusively on different immune cells and their effects and getting lost in the action-reaction maze of the immune system, it would be much more useful to first find out why the immune system reacts the way it does in the first place. The urge to do so seems to have been lost somewhere along the DMD-paved road.

          The circumstantial evidence of possible (viral) causes is as clear as it’s going to get. This should be the focus of all further efforts.

  • Am I correct to suspect that the neurodegenerative phase of MS (what you call smouldering MS) is postponed or even halted when you successfully stop the active inflammatory component of MS at an early stage? It seems that quite some evidence is pointing to that, or has this already been (dis)proven?

    • RE: “Am I correct to suspect that the neurodegenerative phase of MS (what you call smouldering MS) is postponed or even halted when you successfully stop the active inflammatory component of MS at an early stage? It seems that quite some evidence is pointing to that, or has this already been (dis)proven?”

      This is a 25-40 year experiment that is currently been run. Let’s see what happens to the alemtuzumab/HSCT cohorts that have been rendered NEDA over time. Will they come back with their SPMS in the future? Has alemtuzumab/HSCT simply kicked smouldering MS into the long-grass by preventing too much early damage and hence the substrate that drives smouldering MS?

      This is a question keeps me up at night ruminating about how we can tackle this from a research perspective. This is why we need to get our deep phenotyping study funded and started ASAP.

      • “This is a 25-40 year experiment that is currently been run.”

        No so long ago it was a 15-20 year experiment. I’m guessing the answer is that it doesn’t (MS always wins in the end). But it will keep the next two generations of MS researchers fully employed.

        There must be some lessons from cancer research and research in the rheumatology field. MS is a devastating disease, particularly for people in their prime, but I find the almost casual attitude to addressing it (ie come back in 25-40 years time) almost heartless.

        Most research (not just medical) makes incremental advances (with the occasional eureka moment). Every year that passes should provide a greater understanding of the disease and be a step closer to tackling it properly. Unfortunately with MS it’s 1 step forward and 3 steps back. The MS researchers (across the world) with all the technology now at their disposal should take a look at themselves in the mirror. A story last year of a 46 year old woman being placed in an elderly care home really hit home. There is something seriously wrong with MS research. I’m sick of hearing that research / science is a slow process when young people are seeing their lives destroyed. Where is the urgency?

        • Sour as always. Compare the huge advances in treatments alone in MS over the last two decades and compare that with the situation in MND or Alzheimer’s to give but a couple of examples and think on.

          • Huge advances in profitable anti-inflammatories. Which don’t do much/anything for progressive disease. I am so disappointed by the advances and I could not blame anyone for being sour. Especially if they have PPMS like me.

          • I will point you in the direction of Ocrelizumab. Progress on add-on neuroprotectants is still far too slow though.

          • Yes but I for one am not eligible for Ocrelizumab – had PPMS too long, inactive disease etc. etc. And there are serious side effects with it too. So it doesn’t rock my boat. 😕

  • Hi ProfG, thanks for this rose-tinted post 🙂

    Would you say Natalizumab is one of the big gun you’re talking about?
    If not, (as long as NTZ is capable of preventing transition to smouldering MS, which I don’t know), is there a benefice to switch to an IRT, considering a JCV- or <0.9 JCV+ profile.
    (Keep those glasses, please!)

By Prof G

Translate

Categories

Recent Posts

Recent Comments

Archives