July Q & A 2019

J

You know the drill, if a question pops up that doesn’t fit with a post, this is the place for you.

About the author

MouseDoctor2

102 comments

  • What are a few medical advances in MS treatment can patients and their families realistically expect within the next, say, 5-10 years? What are you most excited about?

    I know, really general question… hope it’s fine.

    I love your work and it has been immensely helpful to me and my family.

    • If you get the glass half full story from ProfG there will be more choice, but remember if the phase II trials haven’t begun on a treatment then unless you are in a trial it will be at least 5 years before the treatment materialises.

      You never no what is round the corner so hard to predict.

  • So what should people with MS do about the live shingles vaccine. I am fed up with professionals sitting on the fence over it …viz MS nurse.. take a considered approach rather than all this up to you stuff .

  • Hi Mousedoctor,

    Thanks for this. What is your prognosis for someone diagnosed with MS in 2019 on the basis of:

    Type of MS

    Gender

    DMD drug categories

    And can I also ask why, when is it a more effective category drug and not highly efficacious, Mavenclad is indiacted for highly active RRMS.

    Thank you for reading!

    • Prognois for someone in 2019

      Much better than someone in 1995 (Pre-DMT era)…that is as long as your Neurologist is not still living under a rock and has read, understands and impliments the concepts in http://www.MSbrainhealth.org.
      There are still many laggards out there.

      Being on an effective DMD is better than being on an ineffective DMD or nothing and young white,female and young is probably better than being male and old and non-white buuut there are no hard and fast rules.

      Why indicated for highly active RRMS…….The regulators. Merck were going back to the regulators without doing more work and they clearly did not have the Cahonies to challenge the view that its licence should have been as liberal as alemtuzumab….A big mistake in my opion, but I guess the risk of getting a license by not rocking the boat or not getting a license.

  • What do you advise patients taken off reasonably successful Tysabri due to PML risk, then unsuccessful Cladribrine. Yet another DMD? If HSCT is so successful for some, why is it not the treatment of choice as all DMDs have side effects?

    • Yep…another DMD or maybe another cladribine dose…I don’t advise patients.

      HSCT please read the blog for some reasons of why not. Many neuros are weirded out at the risks of anything more risky than a CRABdrug..need I say more

      • Thanks, this blog is so helpful. Are you generally avoiding Tysabri for JC positive patients or ever putting patients back on it who did well and failed subsequent drugs eg Cladribrine?
        What do you do with people with low lymphocytes of only 0.7? Drug choice is restricted presumably.

    • ” If HSCT is so successful for some, why is it not the treatment of choice as all DMDs have side effects?”

      Many have it done now wthin 3 months of diagnosis.
      check out facebook india…russia…mexico…hsct

  • Can you tell me the total percentage of patients that are NEDA 3 (ie in complete remission) after 8 years in the original care-ms trials (Alemtuzumab trial). I can find the data on each year of percentage that are NEDA, but not cumulative data.

    • That is the fudge. The data always appears hidden rather than being simple to find…it makes me wonder what is being hidden

  • Similar to Bernie’s question, is there any information on how the original oral cladribine trialists fared since 2010 (?)

    • What would be a good-ish ALC 2 months after first cladribine dose? Should it be < 1 x 10^9/L or is any reduction OK?

  • Was Prof G the “man sunbathing in his Clapham garden” when the passenger from the Kenyan Airlines flight landed 1 metre away from him? I’m guessing not as Prof G spends most of his time at international conferences.

    • No but the person who was sunbathing is known by the Giovannonis…a very very near misss…A case for PTSD I suspect

  • What is internal tremor and how common is it in MS? I have looked at the interwebs and have found little on it and mostly it’s associated with PD.
    Love the blog, it rocks the house!

  • I am starting plegridy on Monday. I was only offered first line treatments due to ms activity. What is your opinion on going on infusions and hitting ms hard straight away? (Given the side effects for infusions appear quite severe) thanks

  • A shame you had to take that post down – We all agree with you in silence:

    “But Switch to What? Ocrelizumab?/Siponimod?
    Do we honestly believe that these current DMT are good enough to halt progression. ”

    Now this may sound like Pascal’s wager, but if we do know that (i) natalizumab and alemtuzumab (albeit with less history) do NOT prevent a conversion to SPMS (let’s call it thatfor now) and that (ii) Ocrelizumab/Siponimod have not shown evidence in either direction yet.

    Aren’t we better off switching to Ocrelizumab with the hope (however finite) that Ocrelizumab may turn out to be better that the existing DMTs in 10 ys time?
    What would be the downside to this logic if all DMTs are on an equal footing today and Ocrel/Siponimode offer this tiny optionality?

    Tony

      • Maybe you will get a chance to address the point I am making then 🙂 it is the only real thing than matters in the decision making algorithm in the absence of perfect information:

        Does the fact that Ocrel works in PPMS when Alem and Natal don’t gives it a 1% potential (i.e. probability) of having a better primary outcome regarding BVL over the next 10ys?
        If not, what is the clinical cost (i.e. efficacy / inflammation / etc…) for NEDA 3 patients on a maintenance therapy to switch to ocrelizumab and expose themselves to this unknown potentiality? Would it cost anything in efficacy?

        (cost is not monetary here but clinical: the cost of shifting from chemeo to paracetamol for a stage-3 cancer patient is huge, when the cost of shifting from ibuprofen to paracetamol for someone with a slight headache minimal)

        • In my opinion you are probably deluding yourself that you say ocrel works when Alem and Natal do not. Alem and Natal have not been tested in PPMS and if the population was selected as occurred in the ocrelizumab trials, I am pretty sure that they would work (or not work) in a similar way. Ocrelizumab is a maintainence therapy…but with a long interdose frequency.

          If you are on a weak maintainence agent you can pay the price in lost brain volume the ocrelizumab extension studies show this. I am sure similar data would be obtained with alemtuzumab for example

          I think NEDA-3 is a problematic term as it involves progression which probably due to two central processes that both may not respond to therapy

          • asking for a 1% upside is not the slightest deluding in my view (think Team Sky) – but thanks for your thoughts on this.

  • First Treatment for Neuromyelitis Optica Spectrum Disorder Approved

    https://www.neurologyadvisor.com/topics/neuro-ophthalmology/first-treatment-for-neuromyelitis-optica-spectrum-disorder-approved/?utm_source=newsletter&utm_medium=email&utm_campaign=na-update-hay-20190705&cpn=&hmSubId=&hmEmail=VHU0u6r2Q_Y1&NID=&email_hash=88dcf3bd84ab18b95096dd9b5aa1a8cd&mpweb=1323-60486-10917

    In 2010 Alexion priced Soliris as the most expensive drug in the world,[10] at approximately US$409,500 a year in the United States (2010),[10] €430,000 per year for ongoing treatment in the UK,[11][12] and $500,000 a year in Canada (2014).[9] Alexion started selling Soliris in 2008, making $295 million in 2007 with its stock price rising to 130% in 2010.

    https://en.wikipedia.org/wiki/Eculizumab

  • Discovery reveals prolific ability of Schwann cells to generate myelin

    https://medicalxpress.com/news/2019-07-discovery-reveals-prolific-ability-schwann.html

    By contrast, remyelination in the central nervous system tended to be an evolutionary dead end since few would have survived a severe whack to the brain or spine.

    “There’s no selective pressure in repairing myelin damage in the central nervous system, because you’re probably going to die,” Monk said.

    Violence

    • An interescting approach. Neural bridging to by pass areas of damage to promote limb function following spinal injury is an emerging science. Following traumatic injurgy the are of damage is fixed but in MS the target is moving and worsening, so unless MS is stopped your repair for today could be a target for MS tomorrow.
      Maybe ProfG will do a post on this

  • 2 questions

    Sorry if an obvious question but what has happened since rituximab has become off patent? I thought there was hope that a cheaper version could be offered to Ms patients i.e. ocrelizumab through a backdoor

    Second question if everyone says cladribine is so inferior why are you wanting to use it for those in wheelchairs?

    Hope these questions particularly the second is not ignored just because of the pending trial

  • A quick question for the doctors and anyone who has received alemtuzumab: How common are elevations in liver enzymes during and post treatment (ALT / AST)? I’ve had a look at the phase 3 data and it looks around 4% but I’m sure this is higher in clinical practice.

  • So, I’ve just spent a week in the chemo ward with my wife as she received her year 1 alemtuzumab. During this time, I met a number of wonderful people receiving treatment for MS. What struck me the most was the difference between those that received a high efficacy drug first line (typically Tysabri) versus those that started on a low efficacy drug and escalated treatment as the disease worsened. The later group were in a far worse condition than the earlier (time from diagnosis was roughly the same). Moreover, two of the people I spoke with regretted their decision not to start on the high efficacy drugs sooner (in Australia, all DMTs are available first line). I appreciate this is anacdotal but it really cemented our decision to hit the disease hard and early.

    I appreciate this isn’t a question but I thought i’d share as our experience is largely in accordance with the treatment opinions captured in this blog.

      • Even in svelte adults, cutting about 300 calories daily protects the heart

        (6 Oreo cookies)

        Fasting
        Caloric restriction

        Is good for you (not just your ms)

        The trial, part of an ongoing project with the National Institutes of Health called CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy) continues to build on the researchers’ hypothesis that it’s not just weight loss that leads to these improvements, but some more complex metabolic change triggered by eating fewer calories than what’s expended

        “This shows that even a modification that is not as severe as what we used in this study could reduce the burden of diabetes and cardiovascular disease that we have in this country,” Kraus said. “People can do this fairly easily by simply watching their little indiscretions here and there, or maybe reducing the amount of them, like not snacking after dinner.

        ( Mark mattson advice)

        “There’s something about caloric restriction, some mechanism we don’t yet understand that results in these improvements,” said the study’s lead author William E. Kraus, M.D., a cardiologist and distinguished professor of medicine at Duke. “We have collected blood, muscle and other samples from these participants and will continue to explore what this metabolic signal or magic molecule might be.”

        Ps: Md are you listening???

        🙂

        • No I’m reading.
          Are you saying loose weight or look for the magic bullet
          You will have to wait for the Cambridge study on calorie restriction

          • “Magic bullet”

            Is pharma territory

            Fasting ,calory restriction is adptation to the Environment
            Phylogenetic conserved in every living organism

            😉

  • Is Alemtuzumab worth the risks?

    If a young, white female with EDSS of 1, one year into RRMS with symptoms/MRI activity decently well controlled on Ocrelizumab were given the opportunity to ‘upgrade’ to Alemtuzumab with full coverage, should she bite the bullet swallow her fears and do it?

    Lemtrada is a scary drug. MS is scary too. Which dark tunnel does one walk down?

    • Young white female – I feel your anguish. My wife was in this situation less than 2 weeks ago. Lemtrada is a scary drug but progressive MS is scarier. After much research and reviewing the data on end organ damage (provided courtesy of this website), my wife went for Lemtrada, finishing her last year 1 infusion on Friday. I’m not gonna lie, it was a rough week for her. However, Lemtrada is the only treatment (other than HSCT) that has the potential to bring brain atrophy back to within normal ageing limits. For her (and me) this treatment potential outweighed all the risks associated with the drug. We’ll deal with these risks if and when they arise.

      The other reason we didn’t go for Ocrevus was her JC titre (3+). Although there hasn’t been an index case of PML with Ocrevus, her neurologist believes it’s only a matter of time before we start to see cases (PML is a realised risk with rituximab). So, she didn’t want the spectre of PML hanging over her head (no matter how small the risk).

      It’s early days and we just don’t know if ‘it’s worth it’. We won’t know this for another 2-3 years. What we do know is she hit it with what we believe to be the most effective treatment that was available to us. So, we won’t be left thinking ‘if only’…..

      It’s a very hard decision to make. Talk to your neurologist, educate yourself, and most importantly, live and love to the best of your ability. Best of luck with your journey. Stay strong and keep the bastards honest.

      • I think you did the right thing, for what it’s worth. Hit it as hard as you can. The end stages of SPMS are horrible. I just lost my mum to it through the associated complications and I have relapsing MS. It’s a fxxking awful, sxxt disease.

      • Mighty Mouse, can I just add how fortunate your wife is to have your knowledge, advocacy and compassionate presence through this process. She is blessed indeed. Wishing you both strength for the journey. And thanks again for the helpful insight into the decision making process.
        Anjali

    • Age 55yrs I’m definitely an old (er😆) white female, EDSS 2.

      I received Lemtrada 2016/17 and like MM recommends, did a lot heap of research first, mainly on this Blog. I also think Aaron Boster Lemtrada vids on YouTube are useful.

      You’ll hear some success stories and other accounts of people having disease breakthrough. Of course no treatment is guaranteed to stop MS in its tracks.
      Thus far I’ve no disease activity and have remained stable, though with the limited walking capacity and neuropathic pain largely unabated, with a degree of fatigue.

      If I may, I’d like to recommend starting by seeing this as a positive – that you’ve given the option – that this in itself is a bonus. Being given the option allows you, if you so choose, to become a more informed and potentially empowered patient – this site provides heaps of valuable information.

      I am persuaded by the prospect of Lemtrada reducing brain volume loss, as well as reduction in relapses, and I also have the mindset I’d rather address the scary I know I have than the scary that may happen.

      BUT we are all unique individuals and our MS can feel almost as unique at times, so you must obviously, go with what is best for you. Wishing you all the best

      • `Thank you both for your compassionate, informative answers. I do feel like I am in an extremely privileged position to have these options. I have followed this blog for the past year and do have awareness of the challenge so many face of accessing the dmd’s that would be most beneficial to them.

        It really feels like a gift to have the option of Lemtrada. Its just a scary move to make at this stage, not having a crystal ball of the future. I have a significant lesion load in my brain and recent activity in my spinal cord so I think Lemtrada is most likely a smart move. I am in the thick of parenting a 2year old and a 4 year old without extended family support or even much emotional support from my partners, so the practical aspects of getting through the week of infusions/month of recovery feels daunting to say the least.

        My neurologist is supportive of whatever I decide but I dont feel like I always get honest, informative answers from him. I do feel grateful that he takes me seriously. Sounds like that’s not the case for so many. I am very, very lucky.

        One thing I am frustrated about is that we do not have/use technology to assess brain atrophy rates. I realize that this (atrophy/silent symptoms) are the ugly monster we are all up against in the long run and it sounds like Ocrevus doesn’t hold a candle in that respect.

        I also have no idea whether I am JC virus positive. Is this something every person receiving treatment for MS should know? My neurologist has said nothing about testing for it. Again I just wish I understood so much more than I do.

        Ive read through the B verses T cell debates much earlier this year and it was helpful information to work with. I wish I had someone I could talk through all these things with as it seems making informed decisions with MS requires an extensive education in Neurology/immunology/pharmacology amongst other sciences.
        This blog is the best thing I’ve found, though talking it all through with someone is definitely the missing piece for me.

        I’ve checked out a few of the Aaron Bolster vids and will continue to do so.

        Thanks again for your incredibly kind input and feedback as I fumble blindly forward deeper into this ominous jungle of questions.

      • `Thank you both for your compassionate, informative answers. I do feel like I am in an extremely privileged position to have these options. I have followed this blog for the past year and do have awareness of the challenge so many face of accessing the dmd’s that would be most beneficial to them.

        It really feels like a gift to have the option of Lemtrada. Its just a scary move to make at this stage, not having a crystal ball of the future. I have a significant lesion load in my brain and recent activity in my spinal cord so I think Lemtrada is most likely a smart move. I am in the thick of parenting a 2year old and a 4 year old without extended family support or even much emotional support from my partner, so the practical aspects of getting through the week of infusions/months of recovery feels daunting to say the least.

        My neurologist is supportive of whatever I decide but I dont feel like I always get honest, informative answers from him. I do feel grateful that he takes me seriously. Sounds like that’s not the case for so many. I am very, very lucky.

        One thing I am frustrated about is that we do not have/use technology to assess brain atrophy rates. I realize that this (atrophy/silent symptoms) are the ugly monster we are all up against in the long run and it sounds like Ocrevus doesn’t hold a candle in that respect.

        I also have no idea whether I am JC virus positive. Is this something every person receiving treatment for MS should know? My neurologist has said nothing about testing for it. Again I just wish I understood so much more than I do.

        Ive read through the B verses T cell debates much earlier this year and it was helpful information to work with. I wish I had someone I could talk through all these things with as it seems making informed decisions with MS requires an extensive education in Neurology/immunology/pharmacology amongst other sciences.
        This blog is the best thing I’ve found, though talking it all through with someone is definitely the missing piece for me.

        I’ve checked out a few of the Aaron Bolster vids and will continue to do so.

        Thanks again for your incredibly kind input and feedback as I fumble blindly forward deeper into this ominous jungle of questions.

        • JC virus assay is provided globally by Biogen (Manufactures of Tysabri). Given my wife was treatment naive, all treatment options were on the table including Tysabri. However, given her JC status and titre level, her time on Tysabri would have been time limited to about 6 months. We didn’t see the logic in starting a drug we knew she’d have to transition off (and risk rebound).

          Your neurologist could still test your JC status if you want to. However, to my knowledge, there has only been 1 reported case of PML on Ocrevus and that was a patient who was previously on Tysabri. Similarly, there has been a case of PML on Lemtrada but again, this was not an index case (e.g. the patient had prior exposure to DMTs). We decided against Ocrevus because the data suggests it isn’t as effective in controlling end organ damage as Lemtrada (although no head to head studies have been done so this is debatable) and the risk of PML on rituximab (indicating a risk with Ocrevus). My wife and I also hope she responds well to Lemtrada and will go into long term remission following year 2 treatment. This means no more treatment for 5-10 years (unless the risk of secondary autoimmunity is realised).

          So yeah, we rolled the dice with Lemtrada. We thought the odds were better than gambling in the disease (she too has a high MRI burden of disease but no disability).

          I too have no idea about whether brain volume is routinely measured. This is on this list of questions to ask her neurologist. If it isn’t, we’ll try find a way to get it done (paying for the scans if we have to).

          YWF – you don’t sound like our stumbling your way through anything. Your on a highly effective treatment, engaging with the research and educating yourself about the disease. Keep reading and keep asking questions. Make a nuisance of yourself if you have to and question anything you are not happy with or don’t understand.

  • Question regarding female MS patients having Lemtrada.
    I keep reading online that female MS patients taking Lemtrada must have a HPV test each year.
    The Pap test/ smear test in the UK doesn’t include a HPV test, it’s only if abnormal cells are found, then a HPV test is done later on – according to the NHS website.

    Please advise do Barts offer both tests? For female Lemtrada patients? Should all female lemtrada patients be offered both tests, the Pap and HPV?

    There is a HPV self test, which has been NHS trialled, including at Barts but not specifically for MS.

    • I found the Lemtrada Healthcare Professional Check List by the Lemtrada drug makers online. It states to have a HPV test prior to the first round of Lemtrada and a HPV test annually after. It doesn’t mention that an annual pap test is required to check for cell changes.

    • My wife was tested for HPV prior to starting Lemtrada. It’s standard in Australia for woman to have a cervical screen yearly from the age of 25 with costs covered by Medicare (Australia’s approximation of the NHS). Definitely get it checked prior to starting treatment.

      • Thanks Mighty Mouse. That is different to the UK. Here are the details of the standard cervical screening, from the NHS website.

        ” When you’ll be invited for cervical screening:
        Age When you’re invited

        under 25 up to 6 months before you turn 25
        25 to 49 every 3 years
        50 to 64 every 5 years
        65 or older only if 1 of your last 3 tests was abnormal ”

        https://www.nhs.uk/conditions/cervical-screening/

          • It’s a bit conflicting the information.
            The drug company produced Lemtrada documents advise a HPV test is required annually.
            But UK hospitals seem to be advising for a cervical smear test annually to a check for cell changes, rather than a HPV positive or negative test result.

            In the UK the two tests are not the same thing currently.

            I’ve been reading the Shift MS website comments and people assume a smear test already includes a HPV test.

            So this needs to be clarified ASAP.

      • The UK smear test was going to change according to the Independent, they were going to introduce a HPV test as part of the smear test.
        However, there have been delays in adding the HPV test to the smear/pap test. The following published in October 2018, so I don’t know if it is still up to date?

        Gavin do you know?

        “Public Health England and the NHS, who are responsible for the screening programme in England, have until recently aimed to switch to the HPV test in April 2019, but are now working towards a deadline of December 2019. Introducing HPV testing into existing screening programmes has been much more complicated than expected. ”

        https://www.independent.co.uk/life-style/health-and-families/features/cervical-cancer-test-smear-accurate-delay-new-hpv-nhs-public-health-england-a8568916.html

        • I have not had a HPV test before and I’ve already had Lemtrada round one. I’ve only had a smear test and in England.

          Is this the same for any other female MS patients, having Lemtrada in England?

          • I was told by the nurse who talked me through having Lemtrada (London centre/not Bart’s) that they’d asked NHS England to start offering annual smears to women who received it, but that this was refused.

            As I’m over 50 I’m in the every 5yrs group and this isn’t ideal as someone who has had three abnormal smears in the past and needed treatment for a couple of those (presumed to be caused by the HPV)

            Fortunately I’m able to pay and the gynaecologist I’ve been under previously was so angry that women having Lemtrada aren’t being given this screening that he’s got the local private hospital to provide a cheaper price for his conducting the smear and for analysing the cell sample.

            Whilst I’m very grateful for this, it’s another awkward reminder that money talks – what of those women who can’t use lots of cash on a private smear each year?!

          • I am tempted to buy the self test HPV test for females, from a well-known online chemist. If the NHS don’t offer it.

  • I would like to see more on microglia from the blog, especially from MD who does not seem so interested in them 😉

    Microglia Linked to Brain Atrophy in Progressive MS

    Using a novel tracer molecule known as [F-18]PBR06 and Positron Emission Tomography (PET) imaging, the team detected widespread and abnormal activation of microglia in MS patients and a link to brain atrophy, physical disability, and progressive MS.

    “There’s evidence of inflammation in the brain’s grey matter, not just the white matter. Here we have a technique to detect it and a path to develop this technique for use in the clinic in looking for early signs of progression and the effects of treatments.”

    They found more grey matter microglial activation in the MS patients as compared to healthy controls, particularly in hippocampus, parahippocampus, cingulate gyrus and amygdala regions of the brain.
    Brain structures in the deep grey matter, particularly the thalamus, showed higher microglial activation in secondary progressive MS than in the relapsing remitting MS patients and healthy controls. This correlated significantly with physical disability and brain atrophy.

    https://www.technologynetworks.com/neuroscience/news/microglia-linked-to-brain-atrophy-in-progressive-ms-321342?fbclid=IwAR3FSB7dTZGQ-on8x79EkLi29go7guQgxM0Ln2wt_tcrPRVL9zEN6yjB5uU

    Singhal, T et al. “Grey Matter Microglial Activation in Relapsing versus Progressive Multiple Sclerosis: An Initial Experience using [F-18]PBR06-PET” Neurology: Neuroimmunology & Neuroinflammation. DOI: 10.1212/NXI.0000000000000587

    • I don’t see why you say this. I am interested in microglia.

      Dr Love has a project on microglia.
      However I must say I am no longer convinced that PET agents like PBR06 are simply detecting hot.microglia. It picks up astrocytes and neurons. The imagers need to come clean.
      The thalamus is getting damage so you would expect.microglia to be there. Damage and atrophy is not good so surely finding microglia in areas of damage is not.surprising.As to correlation and any MRI outcome they are not worth reporting if they are r less than 0.8. However I will have a read of the paper and come back to you on this one

  • Are newly diagnosed making a mistake going on Ocrevus? Newly diagnosed female, age 40. RRMS, low to no disability. Doing well on Ocrevus, traveling, working full time, living life. Hoping she stays controlled a few more years until research provides a better options. Is she doing the right thing or should she be pushing for HSCT or Lemtrada?

    • NEWTOMS – In is my understanding that accessing Lemtrada and HSCT first line in the UK isn’t an option. So, Ocrevus (or Tysabri) is about aggressive as you can go. A mistake would be to accept a CRAB.

  • Big Ph€rm$$$$$$$$$$$$$$$$$$$$$

    The drug industry extort us

    They take any price, that they think politicians are willing to acept

    It has absolutely nothing to do with research and development costs

    The drug industry is more criminal than any other industry

    Which is very shocking because these crimes lead to manny deaths

    That could have been avoided and its also a fact that our prescription drugs

    Are the thrid leading cause of death after heart disease and cancer

    And manny of these people who die because of the drugs they take,

    They did´nt even need them

    Which make the tragedy even wrost

    Who make the drug trials?

    Thats primarily the drug industry

    And we know generaly that this trials are not reliable

    Not even the randomised trials where half of the patients get a placebo and the other half get the

    drug

    They are bias in all sort of ways

    So doctors generaly have a to much naive idea that ,if a drug trial has been publish in a prestigious

    journal like New england journal of medicine or Lancet

    Then its probably reliable

    It is not

    We must demand drug trials to be made by independent parties with no commercial interesses

    whatsoever in the outcome of the trial

    Casper H J van Eijck
    Erasmus MC | Erasmus MC · Department of Surgery

    Speciality Pancreactic cancer

    By now every scientist .be it in the Netherlandsor the Us ,is convinced that all form of cancer are curable in mice

    For our patients that´s not the case unfortunately so at Erasmus Medical centre our emphasis is

    on so called clinical research research in patients ,thats expensive but yu need to facilitate it

    Because it brings progress and you end up with so much expertise in hospital that pharma

    companies can never claim their development costs are very high

    As all the work will be done in hospital that´s a way to keep the price of medication low

    It has been my principle to keep the industry at a distance to avoid the danger of becoming dependent on them concerning the prescription of drugs or whatever

    I DONT LIKE THAT AT ALL

    Whenever pharma companies approached me i said:

    I rather get funding for research than expensive trips for dinners

    Those are really a waste of money

    A lot of people have personal motivations in most cases they have lost relatives to cancer

    My father died from it at a very young age,that gives you a certain drive to try to achieve something

    with your team

    Why do we continue to pay so much money for cancer drugs that are ineffective for so manny patients?

    The system as it operates now is very agreeable to them

    They sell drugs that are ineffective in 70-80% o f patients it´s close to incredible

    So for a very large group of patients who get chemo therapy it´s useless

    Big pharma couldn´t careless that most patiente don´t benefit from it

    And that should really be stopped

    • The drug development industry is broken in many ways and I agree with much of what you say above. However, drug development is expensive with around 1 in 100 molecules hitting the market. I’ve lost count of the projects I’ve worked on that fell over at phase 2 ( I recall two that fell over st phase 1). So, the costs of approved drugs have to cover these failures within the patient window before computing it’s the market (including the manufacture and pre-clinical costs). The average cost of a phase 2 study runs to about 6 million USD when GMP manufacture and assay validation is factored in. These costs increase significantly for phase 3 studies. So drug development isn’t cheap. It’s no wonder that pharma churns out ‘me too’ drugs as their probability of failure is much less than drugs with a new and novel mechanism of action.

      Governments and public institutions just don’t have the money (and in many instances, expertise) to successfully develop a new drug through to market. So, unless caps are placed on drugs costs, or governments start subsiding the drug development process, the prices of new drugs will continue to rise.

      Do I believe new treatments hitting the market are worth the price-tag. No I don’t. But tell that to someone who has a family member with advanced lung cancer. The extra months of overall survival these drugs deliver means the world to these patients.

  • Selma Blair today tweeted she is getting sicker with her MS. Given her personal wealth and access to the best treatments. And we now have treatments that effectively shutdown ms in rrms. Also given she has had plasma exchange. My question is why is she getting sicker?

      • What about your prior emphasis that despite achieving NEDA we can all deteriorate? Also, of course, despite treatments such as Alemtuzumab and HSCT there are those who fail on whatever it is they have received.

        • I you missed the point of Prof G’s response. The vast majority of patients who have MS do worsen with time, especially if treatment was implemented late. This is the reality of MS for most patients. I’d hazard a guess that Selma very much has MS and her disease is worsening despite receiving treatment (see all posts about disease worsening despite being NEDA and / or all posts on progressive disease and limited treatment options).

  • Everybody should see this even the “Mavens” 😉

    A Brief History of Fat, and Why We Hate It

    Min 1.45 “When i think of mamals the word that came to mind is adaptation”

    Min; 2.06 “we (humans) can go quite a long time without food must longer than some other animals
    fat gave us a big advantage in terms of beginning to colonise hostile environments

  • Another “Maven” another award 😉

    Professor Catherine Lubetzki picks up the mantle for prestigious MS Charcot Award!

    Professor Lubetzki is professor of Neurology at Pierre and Marie Curie University and head of the department of neurological diseases in Salpêtrière Hospital. She coordinates the Salpêtrière Multiple Sclerosis clinical research centre. Her research focuses on the pathophysiology of MS, notably uncovering the interactions between myelin and axons, showing that the electrical activity of axons induces myelin formation , and that positive or negative axonal signalling can impact the repair mechanism.

    (Nice did´nt know that that why we need to move …Alot.. 🙂

    https://thefemalescientist.com/portrait/multiple-sclerosis-international-federation/2264/professor-catherine-lubetzki-picks-up-the-mantle-for-prestigious-ms-charcot-award/?fbclid=IwAR2gnZTs9Bi6StKs6Qrt6DzT31WzNrYj8tDSns9_KKe0V0TiiRZ_8J75Ea4

    Obrigado

  • When I was an inpatient having my Lemtrada I was disturbed at night by a HCA video phoning relatives. As the staff room was near to my bed.

    I was then moved to different bed, near a storage room on day 2. The staff kept letting storage room doors slam at night.

    I wondered could hospitals introduce a ‘ quiet time’? At night and for staff to be mindful of the noise they make?

    I know nighttime checks are often necessary on many patients. But this would be appreciated.

    • I had the same problem for both courses of lemtrada despite having complained following the first course
      I have always said that the stress from the hospital ward and the lack of sleep made me feel worse than the lemtrada itself

      • Lemtrada is given in an outpatient setting in Australia. No overnight stays unless you experience multiple cock-ups and end up being admitted like my wife was. Those cock-ups and the nights in hospital were terrible but that’s a story for a different day. She said the same, the lack of sleep made her feel 100 times worse. The night’s she was at home we’re much easier for her.

    • Akkermansia muciniphila treats mice with ALS, so this is good news as this microbiome agent that is associated with MS…is it doing good?

      This is a paper in Nature (https://www.nature.com/articles/s41586-019-1443-5) on my fovourite subject. You know what I think. So before you get your new feacal Akkermansia transplant read this. In this experiment all mice were dead by day 160 but after the microbiome addition they were all dead by about day171. This was not a cure in the mice. This was associated with enhanced nicotinomide….so would nictinomide do the trick. We have done one unpublished experiment with this and I will simply say if I rememebr properly…Don’t hold your breathe. I’ve seen other stuff

      • Thanks MD. I’d not do a transplant (perish the thought 😳), but maybe if this beneficial bacterium could be increased through healthy diet then that could be considered something for brain health.

  • In the BBC link posted by Anonymous July 25, 2019 at 5:32 pm:

    “And early spinal cord damage was also an indication that a patient would go on to develop the secondary progressive form of MS, which currently has no treatment and is where disability gets steadily worse.”

    That doesn’t make sense to me. Effects from a spinal cord lesion are much more likely to be obvious than a brain lesion in a “non-vital” area. But a person could have multiple clinically silent brain lesions and yet already have progressive disease, without knowing it?

  • Could the following help pwMS, with their MS symptoms in any way?

    The BBC website today:
    ‘Tickling the ear with a small electric current could rebalance the nervous system in over-55s and help them age more healthily, research suggests.

    Stimulation of the vagus nerve, which connects to the heart, lungs and gut, led to improvements in body, sleep and mood, a small study found.’

    https://www.bbc.co.uk/news/health-49157343

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