Alemtuzumab Epiphany

A

Prof G is in a melancholic mood. Why?

This week I am doing video consultations with all the volunteers who participated in the pivotal phase 3 and 10-year extension studies of the alemtuzumab clinical trials. My objectives are three-fold. Firstly, to make sure they are referred back into a routine NHS MS service and are not left floundering without follow-up. Secondly, to complete a few exit EDSS examinations of the last few subjects and thirdly, and most importantly, to thank them for their time and commitment to these trials. 

During my video consultations, it dawned on me that I have never seen a cohort of patients doing so well 10+ years into their MS disease course. The majority are NEDA (no disease activity) fully functional and participating fully in life. Yes, fully in life; married, in civil and other partnerships, working, with families, playing sports, participating in creative activities, volunteering and with very few symptomatic MS problems. Yes, a few of them have thyroid problems, but these are all being managed without a major impact on these patients lives.

I am convinced that some of these trial subjects may actually be cured of having MS. I am witnessing something extraordinary and at the same time something very sad. Why have we, the MS community, not adopted early alemtuzumab treatment as the standard of care? Why wouldn’t you want to take a chance on a treatment that maximises your chances of staying fully functional and may even offer a cure? 

The patients who are not doing so well, unfortunately, got onto alemtuzumab late and therein lies the epiphany; early highly-effective treatment is the only way to realistically slay this beast.  Knowing what I know, if I had MS I would have no hesitation being treated with alemtuzumab or even HSCT.

The tragedy is that the MS community and the regulators have killed alemtuzumab relegating it to a second or in most countries a third or fourth line agent. This is an international tragedy and I am not sure if we will ever get alemtuzumab back to its rightful place as a first-line treatment option for early active MS. 

Alastair Compston, his protege Alasdair Coles and the Cambridge team deserve all the plaudits for getting this innovation to the clinic. However, sometimes this is just not enough to get wide adoption of an extraordinary innovation.

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.

87 comments

  • Prof G,

    Thanks for this. I’ve done very well following two rounds of Alemtuzumab (14 years ago).

    “The tragedy is that the MS community and the regulators have killed alemtuzumab“ I do wonder if it was MS researchers who killed off Alemtuzumab with the trickle of bad news stories about very rare side effects. After a while the run of research papers on individual cases with rare side effects built up a steam and scared both potential patients and regulators. The papers didn’t provide any context in terms of patients who had done well or how many side effects can be picked up by monitoring and successfully treated. Also no context about what MS does. A piece in The Times yesterday highlighted the need to legalise assisted suicide – a 60 year old man with MS (35 years since diagnosis) who had lost all functions (couldn’t lift a teacup).

    If my children showed any signs of MS I would want them to have Alemtuzumab ASAP to give them the best possible chance. This might mean getting treated abroad as getting Alemtuzumab here will take too long. A bit like the demise of Concord – we seem to have gone backwards.

    • In the US, alemtuzumab has always been third line, so information from Cambridge generated during development and the trial data was sufficient to cause concern to the advisors to the regulators. The severe vascular pathologies triggering the severe black box warning. But whilst pointing the finger at MS researchers you could even point a finger at the manufacturer.

      Sanofi settles lawsuit with former Genzyme shareholders Nov 01, 2019 (https://www.pharmamanufacturing.com/industrynews/2019/sanofi-settles-lawsuit-with-former-genzyme-shareholders/)
      Sanofi has agreed to a $315 million payout in an lawsuit alleging that the drugmaker failed to use “diligent efforts” to advance development of a former Genezyme multiple sclerosis drug that would have resulted in payouts to shareholders. When Sanofi merged with Genzyme Corporation in 2011, Genzyme had been conducting clinical trials for the multiple sclerosis drug, Lemtrada. Per a Contingent Value Rights Agreement, Sanofi agreed to make up to approximately $3.8 billion in payments to former shareholders upon the completion of certain milestones relating to Lemtrada, including getting FDA approval of Lemtrada on or before March 31, 2014, and obtaining specific sales volumes in defined periods. The lawsuit, filed in 2015, claimed Sanofi submitted a poor application to the FDA that triggered an initial rejection — leading to the missed approval deadline — and then failed to support Lemtrada commercially so it would miss sales targets. Under the settlement agreement, Sanofi has agreed to fully and completely resolve the claims without any admission of liability or wrongdoing.

    • Inspiring !! Cases like your should be the standard!!
      Why do they kill Alemtuzumab? Prof G as done it all to save Alemtuzumab, even with a letter, a plea, to European Medicines Agency !! Who benefits? I think we know the answer! Patient associations should team up with doctors like prof G to provide the best treatment in early stages of the disease, before it gets to late !!

    • Inspiring !! Cases like yours should be the standard!!
      Why do they kill Alemtuzumab ? Prof G as done it all to save Alemtuzumab,even with a letter, a plea, to EMA (European Medicines Agency) !! Who benefit ? I think we Know the answer ! Patients, patients Association should team up with doctors like prof G to provide the best treatments in early stages of the disease, before it gets to late !!

    • My first choice when diagnosed 2 years ago was alemtuzimab. You are correct in that during my own research h the side effects and bad reports turned me off and I chose differently doing well but will i always wonder if I made the right decision for the long term

    • Perhaps if the manufacturers had been a little more forthcoming in acknowledging the “very rare” (50% or so is rare?) side effects, perhaps they would not have run into trouble with the regulators. Par for the course though this may be for pharma. Pointing out the negatives, with the aim of improving things for pwms for example don’t keep treating if you’re making a neutralising antibody response and alemtuzumab will no longer work and you’ll relapse and lose brain is a good thing, no? That said, undoubtedly for many it’s been a life-changing treatment.

  • Bless you !! if i was fortunate to have a doctor like you since the beginning, maybe (for sure) I would be far better today. There are a lot of pwMS, specially from UK, diagnosed with very active RRMS that were fortunet to have Alemtuzumab as the first DMT !! they are NEDA (cured) for as long as 15 years !!

      • Yes, if MS treated early. As a group, these patients have the lowest brain volume loss or brain atrophy rates of all the DMTs. In fact, the rate is arguably in the normal range. The same has been shown for HSCT.

        • Can you characterize early in this case? Or is there a paper coming up (soom) that gives some stats on the population and outcome?

          Also, is there a good, granularoverview of adverse effects of alemtemzumab (saying 30% develop a secondary autoimmune is not really helpful without break down of what it is)?

          I am trying to figure out next steps in my own treatments but I feel like data is far too aggregated in many cases…

          • I appreciate that your decisions and choices will quite rightly be your own. I also understand the search for more and more data, (I did exactly the same)

            Ultimately, my choice was an easy one. My previous DMT was Tysabri. When I started I was OK with my PML risk. But over time everything moved against me and when my PML risk was too great, I was given the choice of jumping to Lemtrada and did. Thank you Salford Royal for giving me a lifeline.

            So I had to balance a high risk of contracting a probably fatal brain disease or a Lem side effect that was treatable. I apologise if my opinion on the side effects might offend some, and I appreciate some side effects may be grimmer than others, but for me I weighted possible death against a different treatable condition. There was no choice for me.

          • That sounds like fairly obvious choice there. May I ask if you considered HSCT instead of alemtuzumab?

            Ultimately I am trying to get a nuanced picture mainly of those two options.

          • It depends on when you have HSCT or alemtuzumab; if it is too late it makes little difference.

      • The people in the alemtuzumab trial went on alemtuzumab shortly after diagnosis. At the moment I think that the inflammatory response conditions the smouldering MS, stop the disease early enough less mouldering

        • Ah thank you, that’s really interesting. Well you couldn’t get more positive than that! The people who have had it to success are very lucky. I guess the majority of us will be smouldering away, and not just in the 32 degrees!!

          • I agree with Hannah. With my early PPMS, I had probably had progressive MS many years before it became clinically apparent.

  • Is 10 years really long enough? With me and my slow, early onset PPMS with spinal lesions, I was still “participating fully” in life 10 years after symptoms started. If I hadn’t got spinal lesions, I’d probably still be doing pretty good. I’ve never had any DMT or medication for symptoms.

    • The original cohorts are now close to 20 years. I know of one patient treated in 2004 is NEDA and fully functional and plays professional golf. I consider him cured.

      Yes, 10 years is long enough. Within 10 years at least 30% and close to 50%, if you interrogate the nervous system by stressing, will have clinically apparent SPMS. In alemtuzumab-treated patients, this figure is well below 10%.

  • I couldn’t agree more, being one of the PwMS who first received alemtuzumab 18 years ago under Alastair Coles care very early in my disease course after only 2 relapses. It quickly restored my functioning although the fatigue took longer to resolve. My life returned to normal, allowing me to resume a professional business career involving frequent international travel, take adventurous holidays abroad, walk regularly including up Ben Nevis, ski, cycle, dance… To date, I haven’t suffered any of the rare side effects. It’s a tragedy that this opportunity is not available to everyone newly diagnosed with MS.

        • More scaremongering from the mice. Thyroid issues are the main side effect and can be picked up and treated effectively (as was mine). You achieved your aim and scared potential patients and regulators off this highly effective therapy. Patients could go on a CRAB drug but you have written these off as next to useless. Ocriluzimab is another option, but you’ll be pointing out all the risks with this drug. If you knew someone with MS for 20-30 years you’d know how awful this disease is. What therapy should patients take that are highly effective and relatively safe? I know the risk that comes with having MS, I’d rather take my chance with Alemtuzumab than sit in a nappy in an electric wheelchair in 20 years time. I’m glad you don’t face such a decision.

          • Whatever happened to Trent? He sounded rather more agreeable. Please explain what is scaremongering about stating the facts? Having met hundreds of pwms (and personally having a family memeber with MS, along with two former colleagues who developed MS) over the years we are well aware of how awful the disease can be and also how the situation is much, much better than it was when I started researching on MS. I firmly believe that useful and undoubtedly effective as alemtuzumab has been for many, we can still strive to do better and your carping (check out the replies to your “Mike” posts yesterday to see how popular they are) will not deter us from that.

          • What happened to moaning Mike (David Icke)….Give him some neuroprotection study and what does he have to say NADA

          • Dear Kev,
            I dont recall talking to any regulators so not sure the mice scared anyone. Would we scare you to have a name change? Thyroid issues are 60-70%

          • Hey mouse doctor’s, you have your numbers confused. The rates are not nearly that bad. Many, not all, who experience thyroid trouble return to normal thyroid function in time. Especially those who suffer from the hypo to hyperactive pendulum swing. Most of those will find that the pendulum will swing less each time and gradually find a new normal. I’m not saying it’s pleasant, and thankfully I have been spared. By the way, have you been through Lemtrada treatment? Do you even have MS? If you can’t answer yes to both of those questions your comments lack credibility.

          • Thyroid disease is about 60-70% of the autoimmunities that occur in 5 years after alemtuzumab about 30% get thyroid issues, apparently by 12 years this is about 50% (published last week) at 5 years about 50% of people get autoimmune problems Tuohy et al. 2015, e.g. see data from Cardiff. Which rates do you want me to check and retract?

            “Have you been through XXXXXX treatment? Do you even have MS? If you can’t answer yes to both of those questions your comments lack credibility”.
            Please expand…What comments are you specifically talking about? “they are not all trivial”? Maybe we should not comment on anything

  • I could not agree more. For the right patient, this treatment has produced excellent results. In our hands the only thing better has been AHSCT.

  • I agree wholeheartedly, but I’m wondering: how early would you start with a highly-effective treatment? Would you start right after a definite RRMS diagnosis?

      • Alemtuzumab has some non-negligible side effects. Would you just ignore them and treat all newly diagnosed people with Lemtrada?

        • Yes and no. I will recruit them into an adaptive multi-arm trial to test different therapeutic strategies to prevent secondary autoimmunity. Can you imagine what a game-changer it would be if we could derisk alemtuzumab and prevent secondary autoimmunity?

    • Absolutely. The brain volume loss with alemtuzumab is less than 0.2% per year compared to natalizumab at about -0.24% per year and for ocrelizumab ~0.35% per annum. In addition, the disability improvement rates with alemtuzumab is superior to both natalizumab and ocrelizumab.

      • It would be instructive to see how the CARE MS 1 study patients on Rebif did over the long term. You’ll recall there was no difference in disability outcomes for patients on alemtuzumab or interferon beta 1a after two years. And remember these were ‘early’ RMS patients. There are multiple confounding issues with such a post-hoc analysis, but it might get to the heart of the matter in terms of long term efficacy of alemtuzumab

        • Just a note, there most definitely are cases where disability improves within two years of treatment with alemtuzumab. I am one of them. I put my cane down shortly after round one. Haven’t used in it 3.5+ years except maybe for a prop to get early boarding on the plane!

          • We happy for this. A can is also useful to fast track through immigration control
            The biology we need to understand (a) Does alemtuzumab promote repair or (b) does it stop damage and allow the natural repair agents to work

      • Im so grateful for having had lemtrada. Diagnosed in April 2016 (huge shock as I had no idea what ms was at that point) told I had highly active rrms. After a few tests (and a chicken pox vaccine) i recived my first dose weeks after. Followed by second dose 2017. And I’ve been great since. And knowing what I know now I’d still jump at the chance to slow/stop any further relapses. I’ve brrn relapse free since. Gutted for all the people that now have to fail other drugs to thenn be considered for lem. Time is the biggest issue in ms. Treat fast first.

  • Can you quickly say something positive about Mavenclad for those of us on that? That’s a good drug, right? I was offerred Alemtuzumab, which at the time seemed a drastic action. But the few months after diagnosis are mentally challenging to say the least, and i wonder if i was in the right ‘space’ to make amn informed decision. I hope that tunring it down is not something i live to regret.

    • I suspect if we use cladribine as early as alemtuzumab was used in the CARE-MS1 trial we may get similar results. I still have concerns that we are under-dosing on cladribine at the licensed dose. So yes cladribine as an IRT is a good drug.

  • Re. ‘ Yes, fully in life; married…..’. It’s perhaps a generation and cultural thing but I don’t see those who are not married particapting less in life.

      • I assume you are aware that pwMS are much more likely to separate from their partners or get divorced; in the order of 4x more likely.

        • I don’t know but I look at my friends and cousins and many are seperated or divorced and they don’t have MS.

          One friend is onto their second marriage and they are in their early 30’s.

          Apparently 42% of marriages end in divorce in the UK. If a person gets married early in life, the more likely they are to divorce.

          So perhaps this partly the reason why??, that people who marry at a young age, then get MS are more likely to divorce?

          It would be interesting to see the age range of the pwMS, who got divorced.

          • There needs to be up to date, UK new research on divorce and MS . All I can find is UK research from 13 years ago, and more recent research, 2018 but from Sweden.

            Times have changed from 13 years ago and Sweden is different to the UK.

            Attitudes to divorce have changed and it’s much more acceptable these days to get divorced and more than once.

          • Very interesting and I wonder if in medicine, some doctors take on a traditionalist view about marriage and that if a patient is not married they do not tick a box of some kind. With regards to social stability.

            I get the feeling they do, and its quite out of date. It’s not that long ago, that women in the UK had to give up work if they got married !! Bonkers to think that now.

          • Much higher. MS is a disease that shreds the brain and causes dementia and personality changes. This does not happen with other diseases.

          • I think that part of it is that having MS sorts wheat from the chaff to some degree. It’s very hard to posture in an empty facade of a relationship when you have fatigue, have lost your career and skills acquired over a lifetime etc. Someone has to truly love you, and you have to love yourself, despite all. Speaking personally, with my progressive MS, I have been honest and felt that I should tell my partner to run, that I should turn them away for their own good. But my partner always said that none of us know what may happen to our health in time.

  • It is amazing to see your email and so massively disappointing to read your closing sentences.

    I was diagnosed back in 2000 when beta-interferon was the wonder drug. I was offered Lemtrada back in December 2017 when my risk rating associated with my then DMT moved too close for comfort. I’ve been wheelchair living since 2016, so I knew Lemtrada could never give me back what I’d already lost, (and this was made abundantly clear to me at the time), but my MRI’s have been stable since Feb 2018.

    Unfortunately, my mobility etc continues on a, (hopefully slow) downward trajectory, but I have accepted this is a combination of age – I am an old fart – and wear and tear on existing damaged nerves. However, I am sure that had Lemtrada been a frontline choice in 2000, I’d still be running around.

    Clearly Lemtrada wasn’t available in 2000, that’s just the progress of medicine. But, it does appear to be a major travesty that it’s available to be used now, if you are newly diagnosed, yet it won’t be utilised.

    We shouldn’t be letting others have modern day versions of my story, when we now have the tools to prevent this from happening.

      • It is a shame indeed. But, unfortunately, that’s life. I’m not bitter, as I can’t see the point. And I hope you are likewise. Be strong and keep adapting.

    • Re
      Clearly Lemtrada wasn’t available in 2000
      No, but not long after Campath 1H was. Anyone remember prescribing or having this off-label? Before the 2012 (?) fiasco…

      The hospital I attended when first diagnosed in 2006 were offering off-label Campath for those lucky enough to relapse on Rebif. Sadly not me.

  • Late onset MS is massively on the increase.
    I was diagnosed in my 50s with highly active RRMS.
    My brain and my spine were riddled with lesions, including a ‘black hole’ on my spine.
    Fortunately my then neuro agreed to me having Alemtuzumab.
    That was nearly three years ago and at age 56 I have NEDA, and have no progression in my disability/symptoms.
    Even for those of us who are not young and who have evidence of accumulated disease activity Alemtuzumab can be a boon.

    The key point you make ProfG is heart wrenching! The lack of access to this DMT on a first line basis, even with its potential for nasty side effects, is criminal!

  • Hi Prof G,

    I am wondering if you would have the same advice for patients (to go hard and heavy with treatment options) who have had mild and stable MS (measured by MRI and lack of relapses/symptoms/progression) over a 10 year period. For example after my first mild attack I went untreated for 8 years until I had a second mild attack 2 years ago and then started Plegridy, no further activity since. Neuro says my MRI is barely a 1 out of 10 for severity, and EDSS of 0. Would you still recommend a HSCT/Alemtuzumab/Cladribine in what has proven to be a very mild case so far over the first decade? Are there cases where you might think that the benefits of “the good stuff” might not actually outweigh the risks? Of course here in Ireland I couldn’t get access to “the good stuff” that would prevent a severe attack that will cause disability until I have a severe attack that causes disability, which seems perversely ironic!

    • It is always a risk: benefit decision. As long as you are being monitored your treatment can always be escalated later.

  • I was diagnosed in September last year and was told that Copaxone was a good choice because my MS is mild. This post doesn’t make me feel melancholy, it makes me feel bloody angry. I want to be able to make informed decisions about my treatment choices and have a frank, open discussion about my options and their risks and benefits. Instead I feel powerless. Thank you Barts MS Team for doing what you do. Even though I don’t live in the UK, it reassures me that there are professionals out there who are willing to kick ass for PwMS.

    • There is no such thing as Mild MS. Just the lession has not appeared on area of the brain to manifest with physical symptoms. You should change your neurologist.

    • Jo – challenge your MS team and shout loudly. My MS was, in my opinion, relatively ‘mild’ for the first 10 years. The next 10 were a rollercoaster. I’m writing this now from my electric wheelchair having just emptied my catheter bag. Sorry if I offend anyone’s gentle nature with these comments. Lemtrada IS a wonder drug, (I believe Ocrevus to be similarly wonderful). If I had my time again, I would treat my MS aggressively while it was supposedly ‘mild’ and probably have it wrestled into a corner never to resurface again. Yes there are potential side effects with Lemtrada, but in my opinion, they’re all preferable to where I am now. You have a right to feel ‘bloody angry.’ Use your anger wisely.

  • I have never seen a cohort of patients doing so well 10+ years into their MS disease course.

    Does that include patients from HSCT patients? Or are you saying alemtuzumab is more effective than HSCT?

  • I’ve asked this question number of times but no answer. I understand why not to depress those already in advanced stages of MS. But surely in order for patient to take the big guns they need to have a baseline to measure from? What is early MS ? 5 lessons, brain lessons? SPINAL Lessions? How may and where is called early stages of MS? What if your ms is undiagnosed for years? Then you re diagnosed and go straight to Alemtuzimab. Isnthat clossed as early stages? Given pros and cons of answering this question I feel pros outweigh the cons.

  • I’d like to thank Dr Coles for all his work. I received excellent care at Cambridge. I hope Alemtuzumab has a second life as the outcomes can be life changing. There are risks (mostly manageable), but some of us are happy to accept them after careful consideration of the potential benefits v potential risks (and the strategies for reducing the risks / minimising the impact if the risks materialise). 15 years since diagnosis (aggressive RRMS) and 12 years since my second and last Alemtuzumab infusion, I’ve been able to participate fully in the lives of my children (now at University) and not have any more disabling relapses where I was confined to bed for weeks. Priceless. It was once said by a smart ass that economists see something working in practice and wonder if it will work in theory. Sounds like some MS researchers – lots of percentages thrown about, lots of potential risks identified…. but MSers have to deal with reality not theory. Do you do nothing and watch your brain shrink, go for the Lidl option and still see it shrink, or go out blazing with one of the big guns (riskier but greater potential rewards)? Each to their own.

  • I was recommended Ocrelizumab when I had my second relapse last year (first one 10 years prior and no DMT in between and EDSS 0). Even my second relapse was mild and my EDSS remains 0.

    I accepted the ocrelizumab as I’d never heard of any DMT and just wanted to ‘get sorted’. Is it as good an option as a ‘big gun’ as Alemtuzumab?

    • No not when it comes to brain volume loss. According to Stephen Hauses most of his patients on rituximab end up with SPMS; I am not sure ocrelizumab will be any different. PIRA is still a problem with ocrelizumab. The real MS is not relapses and/or focal MRI activity it is the end-organ damage that continues at double the rate on ocrelizumab when compared to alemtuzumab.

      • Hi Prof G. I am pretty confused right now with this answer. Everywhere on this blog I have read during the last year that, in order to avoid end-organ damage and SPMS, you need to “start highly effective DMTs as soon as possible”.

        Thanks to these pieces of information I managed to go for ocrelizumab (I have been diagnosed 16 months ago) witch, you said in previous blog posts, is “a game-changer” and a highly effective DMT. Do I have to understand now that having ocrelizumab is not really useful?

        What about what you said on this blog post? (https://multiple-sclerosis-research.org/2019/12/killjoys-peddle-fake-news/) : “One message that is loud and clear with this data is that the earlier you treat the better and you have a much better outcome if you flip the pyramid and start on high-efficacy DMTs first-line”.

          • Yes but is it its long term efficacy as good as alemtuzumab (or HSCT)? We obviously do not know but looking at rituximab as its closest relatives I have my doubts.

            It definitely has a better side effect profile than those two, though.

          • “Ocrelizumab is a highly effective DMT for MS.”

            There are no effective DMT.
            DMT is totally different from IRT.

            Don’t drink the Ritux/Ocrevus kool aid…says G….from March 2019…and yet still asked here in June 2020.

            “Why is everyone drinking anti-CD20 kool-aid?”

            https://multiple-sclerosis-research.org/2019/03/why-is-everyone-drunk-on-anti-cd20-kool-aid/

            “I included in my presentation on why I think anti-CD20 is not good enough to treat MS in the long term and why we need to think beyond NEDA. I presented data, mainly from ocrelizumab, that shows MS continues to smoulder away on ocrelizumab despite patients being NEDA. ”

            “Stephen Hauser implied two year’s ago in a response to a question at ECTRIMS that anti-CD20 was not the panacea everyone wants it to be and that a lot of his long-term rituximab-treated patients were now secondary progressive, i.e. they had smouldering MS. ”

            Sad to see so many here on Ocrevus. And they have no idea about any of this. And so ask is Ocrevus a highly effective DMT. It is not.

            https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5221476/

  • Why do dome comments have a reply facility and some don’t? Is it a way of controlling the thread and conversation ultimately, by the person posting the page?

  • Prof G,

    Just finished watching your recent Youtube video further explaining your smoldering MS theory, and you presented a couple of studies where anti-CD20 drugs (rituximab and teriflunomide) showed the best evidence of fighting the underlying disease. After an IRT such as alemtuzumab or HSCT, would you suggest patients immediately begin an anti-CD20 drug, despite currently experiencing NEDA?

    Thank you

  • The list of activities you give are fundamental to health: “Yes, fully in life; [married, in civil and other partnerships], working, with families, playing sports, participating in creative activities, volunteering.”
    As an aside, I left off “marriage etc” since it’s a value judgement but moving on…
    Physical activity is not a sign or symptom that some other force is good (drug or therapy) but rather that the decision has been made to be active. If the drug or therapy serves as a catalyst to feel confident or hopeful enough to make the decision to undertake physical activity then it’s okay in my book. Of course, the catalyst should be as benign as possible.

  • Knowing what I know, if I had MS I would have no hesitation being treated with alemtuzumab or even HSCT.

    Professor G, I thought a lot of people on HSCT do not have their disease halted when I last asked about it at your clinic. Can you please confirm what chance you think people have of curing their MS or are we just shooting in the dark?

    • We need to start off by defining what we mean by a cure. I have been trying to get consensus on this for over 5 years without success.

      • I guess that is a difficult question to ask given that we would have to observe people for the majority of their lives to get a definitive answer. But I think I, and probably most others, would be happy to get 10 years stability following HSCT.

        Do you think a significant enough proportion of people on HSCT would be free of disability for 10 years post treatment?

        Do you think this proportion changes significantly if you are already 10-15 years into your disease?

        Hope you are well and enjoying summertime 🙂

  • This makes for very reassuring reading. I feel so lucky to have been treated by a forward thinking neurologist. Despite being told I have mild MS and being diagnosed so early on that the diagnosing neurologist demanded a second opinion I was able to have Lemtrada – I snuck in a few before the review. My thyroid might be giving me grief but I’ll take that over disease progression any day. I would be absolutely distraught if I was diagnosed now and knew I wasn’t getting the best treatment option

  • I agree with Prof G whole heartedly.
    My son, who died last year aged 50 was in Alisdair Coles clinical trial. He was already in a relapsing remitting stage but Campath (as it was called then) stabilised him and he went on to work and live a fairly productive life. I think if he had it when he was first diagnosed he would still be alive today.

    • Dear Kamalini, I am very sorry to hear about your son and I am sure the other readers will join me for thanking you for sharing your story. Your experience supports the ‘treat early’ or ‘treat very early’ and ‘effectively’ paradigm to protect the brain and spinal cord. Why? We don’t have any therapies to repair the damage and unlike rheumatologists and nephrologists, who can do joint replacements and kidney transplants, respectively, we can only watch and contemplate how different things could have be.

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