Can you give some advice on what is the recommended treatment for pregnant MS patients postpartum? What are their options if they want to breastfeed?
We typically recommend 4-6 weeks of breast-feeding before recommencing DMTs. However, there is data that IFNbeta, GA and natalizumab are safe whilst breast-feeding. DMF, based in its MOA, is also very likely to be safe. Most of the other monoclonals are likely to be safe; they will get across into breast milk in very low concentrations and are unlikely to be absorbed to any degree in the gut of the neonate. The low concentrations that do get across in the milk are likely to be denatured by acid in the stomach and digested by enzymes in the intestines.
I have recently been diagnosed with RRMS and I have been advised to take Tecfidera. I am however anxious about this as I know I have EBV in my system as I had Glandular Fever as a child and I don't want the EBV to be able to cause more damage by using a drug that suppresses my immune system. Ocrelizumad sounds very promising, I hope that the EMA doee licence this drug. In the mean time I would really appreciate hearing your advice on if EBV can effect MS when taking disease modifying drugs such as Tecfidera. My neurologist and the MS nurses have said they cannot comment on this. Best wishes and thank you for providing this platform, your work is inspirational.
Prof G,What dose of Rituximab do you believe would be sufficient to dampen the B-cell overshoot 6 months post Lem? Also, would you base administration on the B-cell counts (wait for them to rise) or would you just administer it at the 6 month mark?
ProfG proposed a study We have submitted a paper that may shed some light on your questions
Using rituximab 6-months post-alemtuzumb may be too late. In our proposal we wanted to administer it within the first 4 weeks.
Thank you. At what dose? I am having Lemtrada round #2 soon and am asking my neurologist for that small dose of Rituximab. For me though I feel that the overshoot flared my disease at 7 months post round #1. I want to dampen the b-cell hyper proliferation so that it doesn't happen again. My neurologist is concerned about suppressing my immune system too much, but I don't think he realises how small the dose of Rituximab would be.
We think the overshoot may relate to the chances of secondary autoimmunity, which run around 50%. As to re-curence of MS, if Genzyme supply the data we want then we can address this.
Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Diseasehttp://dx.doi.org.sci-hub.io/10.3390/pathogens6010002Charcot 2? Much Ado about Nothing?
Prof G,could you please clarify.(1) For a long time you are saying that RRMS, SPMS and PPMS are the same disease.(2) Yet, you are advocating early aggressive treatment of RRMS as it may benefit long-term. May be my logic is flawed, but I can’t see how both this statements could be true at the same time.Isn’t it strange to expect aggressive treatments to have any long term benefits in RRMS when there are PPMSers in whom progrssion kicks in at the age of ~40 after a period of subtle focal inflammation , subtle enough not to be noticed (do RRMSers treated with alemz/tysabri early accumulate less damage?)
Yes, this is a very good question... does alemtuzumab/natalizumab early stop the progression to SPMS?Because ( as mentioned a few days ago on this blog), rituximab started at a low level of disability did not deliver and the patient progressed anyway with new spinal cord lesions. So, do people treated with Lemtrada/Tysabri develop SPMS anyway? (Relapses do not bother me that much, they are mostly sensory in nature and go over in a matter of weeks. If I am to go on Lem/Tys I want to know it is actually going to help in the long run).
We won't know for at least 10 if not another 25/30/50 years. A whole generation of people with MS (generation from the date of diagnosis, not birth) are participating in this experiment. Which will know then, when some neuro with access to some database extrapulates by reference to the natural history of MS.What's the suggestions in the meantime?
> We won't know for at least 10 if not another 25/30/50 years. This is well known and reiterated many times in this blog and I'm ok with that.But this two ideas:1. PPMS is the same as RRMS; and 2. highly active treatment could influence long-term outcomes in RRMSare contradictory by their nature and could not be both true at the same time.And its very strange to find Prof G to be proponent of both."Hey lets treat everyone to NEDA... look at the PPMSers, thy have the same disease! They are NEDA most time of their lifetime and then they do progress...ooops!"
Vasy - yes, I struggle to understand this too.
There are not NEDA because they (PPMS) are progressing
So a PPMSer just progresses - or plateaus - with maybe some "blips" of systemic (?) inflammatory activity.And other people - with supposedly the same disease - have big flares, that get noticed (and treated). But they are also progressing from the beginning - probably.We can treat the flares. But we do not yet know for sure about the progression - whether stopping the flares halts all of it. Maybe it depends on how early on in their MS the person had the noticeable flares. And there is as yet nothing for PPMSers. Because progression is something else altogether. (And it probably involves a lot more than B-cells.)
1. PPMS is the same as RRMS; and 2. highly active treatment could influence long-term outcomes in RRMS The heart of that idea, as I understand it, is not that PPMS and RRMS are identical... but that they have their common ground in focal inflammation that is relevant at some point in the history of both PPMS and RRMS. Is this right? - When I was looking at the issue in 2015, I wondered if this was the case. My wonderings were independent of this blog as the blog wasn't publicly consistently propagating the idea then. As I said in some other comment somewhere here, I had always wondered if true PPMS consists of those with a lot of disability and only very few visible lesions - and even then, are they just unlucky that their lesions are in grey matter where they can't be seen or is there a reason if they have lesions, they are more hidden away (such as a different pathological process).What percentage of disability is caused in an individual by focal inflammation and what percentage by other processes immune from DMTs? Until we figure this out the two ideas you postulate are going to be true and contradictory at the same time, depending on the perspective.... Perspective is not very scientific, I do accept that. There is a very vocal person with PPMS who had HSCT a few years ago and who says it has worked for her... I cannot comment on anecdotal experiences of course, but if do believe that this person has not continued to progress after HSCT for whatever reason... then you start to wonder how many PPMS diagnosis out there are correct. It's all a big puddle of mud (or dogma), really.
> There are not NEDA because they (PPMS) are progressingProf Mouse, you know what I mean, they _were_ NEDA for their lifetime before start of progression.Well you can say about MRI.. we don't know, I agree, but I have idea how this could be tested.I.e one way you can show this is not the case is to observe series of active RIS cases being transitioned to PPMS directly without any clinical manifestations before worsening starts.As RIS is pretty common finding nowadays and PPMS is not so uncommon I would imagine there should be cases described but I can't google/pubmed any such.
Does air pollution have nothing to do with MS?This study suggests that living near major roads increased the risk of developing dementia, but did not present an apparent risk of developing MS or Parkinson's disease.Http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)32399-6/abstract
An interesting publication:Cocapture of cognate and bystander antigens can activate autoreactive B cellshttp://www.pnas.org/content/early/2017/01/04/1614472114This is not molecular mimicry, rather lack of precision in localizing membrane-embedded antigens. Any comments?
On this blog I read promising studies on Ocrelizumab. My neuro has said that it is all hype and not get to get my hopes up and it is just pharma changing the name of an old drug Rituximab so that they will make more money. He says it will just do the same as Rituximab. To be honest I feel that I trust more of what is said on this site compared to what I am told by my neurologist.
Re: "Ocrelizumab ..... is just Pharma changing the name of an old drug Rituximab."This is not correct, ocleriluzmab is a more humanised monoclonal antibody. It binds to a different part of the CD20 molecule on B-cells and its so called Fc portion is different to Rituxumab. All these properties make ocrelizumab a different drug and some of these properties arguably make it better than Rituximab. We will only know if it is better than rituximab if we do a head-to-head study. This is something that we the MS community should consider doing as soon as ocrelizumab is launched.
Pharma are developin gcerlizumab so they can make money, rituximab is coming out of patent life, however as ProfG says it is humanised rather than chimeric and so is better suited to repeated injections
If I were to do a trial, I would suggest rituximab against alemtuzumab as an induction therapy, the main differences between ocrelizumab and rituximab will be tolerability.
Thankyou, I will print this off and show to my neurologist.
MouseDoctor, we have been using chimeric antibodies for decades and all is well. Rituximab is not expensive compared to other drugs for MS and yes, the cheap generic copies are just round the corner. I hope they will provide an affordable alternative for lots of MS patients worldwide.
I share your sentiment but am worried the reality is different. Will there be global use? The cost of rituximab is still outside the ability to pay in some places.With regard chimerics, we have been using polyclonal antibodys eg anti thymocyte globulin, I am not sure what your point. Sure rituximab can be used. Infliximab is chimeric used arthris. The facts are that rituximab elicits binding antibodies in about 15-25% of people and a number of tisthose make neutralizing antibodies which higher than ocrelizumab, but miles less than alermtuzumab. Does that make rituximab worse that ocrelizumab not necessarily.Can Roche show their product is better than rituximab, they will have their work cut out. But if and once ocrelizumab is licensed will that be the signal to use rituximab? Can you convince your colleges to turn their back on pharma?If you can, what's your secret? Collective disobedience or being in charge of budgets. Sweden largely uses rituximab.Compared to MS drugs most things are not expensive and happy you are using rituximab (many pepole are using this in SwedenWill you swop to the generics when available or show band loyalty?What would you do if Roche removed rituximab from the market but at over $7 billion a year why would they do that.Why not generic cladribine (has the cancer fear stuck?) if you arguing on a cost basis? It can be aboutsix-ten times cheaper than rituximab and you loose costs accociated with infusions.Can we improve how rituximab is used to make it safer and reduce the numebr of infusions..I think you can.
We now give one rituximab infusion twice a year in RA (after initial 2 infusions to start with.)As for the costs... I would like a new Tesla and I could buy it, but I don't ... because the price(high) does not reflect the additional benefit(small) of driving and insuring a new car. I guess the same will be true with ocrelizumab.
Is twice a year too much?
For most RA patients 1 rituximab infusion every 6 months seems to be enough.But I guess the hospital will buy cheap rituximab biosimilar drug as soon as it becomes available.
When used topically (!) a new Alzheimer's drug that targets tau regrows teeth by boosting stem cell production (!!)http://www.nature.com/articles/srep39654
Ramiel Nagel a dental health educator writes about how teeth can remineralize and repair naturally by modifying your diet. I've not read much about it but it sounds interesting. So I wonder about diet and myelin repair in MS, if it helps in some way.
What is the rumble in the jungle?
The rumble in the jungle refers to the next 'burning debate' at the ECTRIMS-ACTRIMS meeting in Paris later this year. Please the following post:http://multiple-sclerosis-research.blogspot.com/2017/01/researchspeak-who-trumps-who-t-cell-or.htmlThe idea is to get the big beasts of the MS world to debate whether MS is a T or B cell mediated disease. If you are young, you may not recall the 'rumble in the jungle'; it is probably the most historic boxing matches in history. The following is the opening paragraph from Wikipedia: The Rumble in the Jungle was a historic boxing event in Kinshasa, Zaire (now Democratic Republic of the Congo) on October 30, 1974 (at 4:00 am). Held at the 20th of May Stadium (now the Stade Tata Raphaël), it pitted the undefeated world heavyweight champion George Foreman against challenger Muhammad Ali, a former heavyweight champion. The attendance was 60,000. Ali won by knockout, putting Foreman down just before the end of the eighth round. It has been called "arguably the greatest sporting event of the 20th century".Debating is almost a sport in the UK and the analogy with boxing is not a bad one. We have already sent-out debater and referee invitations for the rumble. Let's hope we can get two MS big beasts to fight each other and an impartial match referee to take them to task on their claims.
Looks like we have found some heavy weights.
My question is probably naïve but do certain kinds of music help improve walking ability in some pwMS? I ask this as I have seen a video of a person with Parkinson's disease and their gait improves quite a bit when they listen to music they can find the rhythm with. I know Parkinson's and MS are different.
Previous research has noted that music can improve gait in several pathological conditions, including Parkinson's disease, Huntington's disease and stroke(Nombela 2013). Perhaps pwMS could try listening to music when doing the Timed 25 Foot Walking Test at home and see if there are improvements.
On the latest episode of QI the host Sandi Toksvig said that you can prevent muscle loss in an arm encased in plaster by visualising moving those muscles. I couldn't find much online on the subject but there were some articles reporting 'evidence' of trial participants improving muscular and cognitive strength over time by imagining carrying out tasks.What do you think about this?
I'm very curious to understand the gender variations involving MS. Would Galanin gene polymorphism have any role in the differences in manifestation or development of MS for each sex, where the polymorphism of the galanin gene, varying inversely for women and men, could give more concrete clues to predict who would develop the disease, and in what way, if more "soft" or more aggressive? Https://www.ncbi.nlm.nih.gov/pubmed/27870457
Was made aware of this through a newsletter from DMSG just now and thought to post it here in case others are interested - a study looking at safety of Gadolinium MRI during pregnancy (according to this study, it's NOT safe in pregnancy to use gadolinium): https://www.ncbi.nlm.nih.gov/pubmed/27599330
Synesthesia is found in 4.4% of the population, as a lower estimate, which is equivalent to 1 in 23 people. But a little research seems to indicate synesthesia may be higher in pwMS than the general population. What do you think? Interesting stuff. So I asked myself what colour is middle C on the piano? I say yellow. Synesthesia is a neurological phenomenon in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second sensory or cognitive pathway.
Not as rare as you think: http://teachneuro.blogspot.co.uk/2012/01/synesthesia-not-as-rare-as-you-think.html
Just seen this UK story - http://www.bbc.co.uk/news/health-38669588What does this mean for those of us already on pricey DMTs ?Thanks
I know there was a post on compassion in care recently by Prof G. I feel it's important to discuss self-compassion for pwMS. I see it time and time again that some pwMS give themselves a hard time for having MS, me included. I have been on a self-compassion course and it has helped.
Re: "Self-compassion"I have just done a post on this topic.http://multiple-sclerosis-research.blogspot.com/2017/01/clinicspeak-thinkhand-self-compassion.html
When having a treatment such as HSCT is there a specific blood test WBC, leucocytes or lymphocyte level etc that should be reached which could indicate if the treatment is likely to be effective or not.
lol i would gladly stand to be corrected on this issue (seriously): but if only. no study has looked at this issue. can we extrapulate from what we know of other treatments? - if so, please share.the only thing i'm aware of is repeated LPs to monitor ocbs...........if you ever get an answer to this (after asking another 19 times), please do let me know :)
Can we extrapolate from other treatments...maybe, you have to decide what you think is important, once editors say yes...we will share.In some cases oligoclonal bands persist after HSCT indicating that the CNS compartment has not be touched enough, but may depend on the regime. I am sure if Matt Perry is reading, he can provide so appropriate references on this aspect. I don't have time to dig.
Can someone please explain or discuss the Ottawa MS trial where they appear to have reversed MS? I have a feeling that this treatment may not be suitable for my husband-PPMS- but really would like it if you discussed the latest findings. I trust your judgement and don't want to look elsewhere for information that may be incorrect
I presume you mean the HSCT trial published. We posted on this previously and in fact got the people from Ottawa to do it.http://multiple-sclerosis-research.blogspot.com/2016/06/guestspeak-prof-mark-freedman-on-their.htmlThis is what you call an immunoablation approach so you use harsh immunosuppressive agents to destroy your current immune system. You collect bone marrow dervived stem cells before you destroy the immune system. They also used cyclophosphamide which makes your hair fall out but gets into the brain in the hope that it kills off the immune activity within the brain. You make the stem cells come into the blood and collect them and once you kill off the immune system with drugs you return the blood stem cells (which make new blood cells not brain cells) and they create a new immune system.You willl need to have new vaccinations as your old immune system is gone. Whilst you have no immune system you are at severe risk from infection and this can potentially kill you in the ottoawa study one person died. But the risk rate appears to be about 0.5-1% depending on the centre.Your neurtrophils provide the first bit of protection and it takes about 3 weeks for enough cells to return so you can then fight infection.However to offset the risks, the results look like there is a good effect in terms of stopping relapsing disease. It does not reverse disease and so do not expect the deficits to reverse. If you saw the BBC programme where the chap starts in a wheelchair and ends up walking, I am told that he had relapsed and was in a wheel chair because he had not recovered from the relapse...with time he probably would be walking even without the need of the HSCT. It was a pretty poor programme. You may get better because this may allow the natural repair process and also it gets rid of your disease. This approach is best suited for people with relapsing MS, although some people with progressive MS benefit because they have active disease. It does not nessesarily stop progression. There is also a risk that the treatment does not work.You should be able to discuss this with your neurologist. Another approach is non abalative HSCT where the immunosuppression is not as harsh and this re-boots rather than replaces the immune system. This also appears to give good results in terms of blocking relapsing disease activity. However it has not been put head to head with some of the more active MS drugs and in some cases the treatments also use continued use of immune depletion for a few years after the stem cell transfer. This may be a bit of a fudge becuase the two years of rituximab which some people get may essentially be doing what two years of alemtuzumab without a transplant is doing based on the Cambridge ten year data.Used the search term HSCT and you will find more information and talk to your MS nurse or neurologist. There is a London HSCT group and trials are being discussedHope this helps
The main centres in the UK would be Sheffield and London, but many places do this as it is one of the routine treatments of Cancer, so you could always ask your MS nurse/neurologist to see if you could talk to the heamatologists who do the proceedure.P.S. I am not a physicians so please confirm any details with you neurologist
Thanks MouseDoctor, this was very informative. I was just wondering... do the HSCT treatment come with the same risk of secondary autoimmune diseases as alemtuzumab? And if not, why is alemtuzumab different?
Do HSCT come with risk of seconndary Autoimmunities.In short.... yes this has been reported. Obviously if alemtuzumab has been used in the treatment regime this is a risk, but was reported in the studies by Burt et al. 2015. However the risk was lower than with alemtuzumab.Why is alemtuzumab different? A number of reasons. We have a submitted manuscript where we give a, plausible explanation, and a solution. It is in hands of reviwers how quickly we spill the beans.
lol thanks for the update on this, have been wondering for ages.
Very interesting piece indeed; http://www.sciencedirect.com/science/article/pii/S2211034817300093. Well done.
Should we rebrand MS as a dementia by ProfG maybe he will do a post on this, although I am sure the contents have been rehearsed on the blog.
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Wonder if you are next door neighbours with Dre, who claims to hail from Bradford? ProfG may want to answer but is busy.1. The 10 year cambridge data show NEDA of 2 cycles in about 50% add another cycle and add about another 35% (Tuohy et al. 2015) so for 2 years of drug 85% are disease (based on NEDA-3. No relapses, MRI lesions or progression) free for 5-7years. Is that the C word? Time will tell. However when it works people seem to be happy. The phase III NEDA rates are not as impressive as phase II results.The NEDA rates are even more impressive with HSCT.2. Maybe what happens to the people who get HSCT?3. To gain optimum effect you need to start early as possible, but it is clear that some aspects do not respond quickly to DMT that affect relapses put out the flames but one a fuse is set off within a nerve circuit it burns. This is seen with HSCT.4.Ask people taking natalizumab, but it is clear that it can be a very effective treatment.5. You should ask people who read the blog...there are some ideas given by people when the blog was closed last year.6. It was not really negative in the subgroup progressing, but in brief the trial was too short and there was a big plaecbo effect, so people did not progress as expected. The trial did not focus on the (rapid) progressors. However people are not going to go back and repeat such studies.7.The Charcot project is ongoing. The trial with raltegrovir did not proove positive. It could be it is a bad idea or it could be that raltegrovir was not the correct drug, as raltegrovir is an intograse inhibitor, HERV have already intograted.8. We have, look at the original posts in 2009 and those today. We recieve no funding or support, so we have worked within the limitations of Google Bloogger9. You are lucky you have a response to 1-8. As the tone of the question is unpleasant. The best protection against being preyed upon by unscruplious people is knowlege. What are your answers'...but maybe if they are trumpish we dont wish to debate.
I don't understand your selection criteria as to which comments you put in a lot of effort to answer MD!
The Yorkshire TrumpsterFriday, January 27, 2017 5:22:00 pm1. Prof G do you claim alemtuzumab to be curative in MS? Prof G claims a lot of things under the banner of the concept of theories. As he keeps droning on, no theory is proven until it is shown to be a fact. Most MS theories (or dogmas if you prefer to call them that) are, at this stage, not proven. Apparently, no one but pharma are interested in funding MS trials and apparently the forces of supply and demand don’t motivate pharma to perform trials which would answer real questions. In more uplifting news, apparently the wonderful dude from the Tisch Centre woke up one day and found someone was willing to fund a large portion of his MS trial (FB told me so, so don’t hold me to it…)2. Could something cure MS even though no-one knows why MS happens?Yes, theoretically. Whether we would recognise that it’s a cure at the relevant time without knowing why MS happens is a different question you haven’t asked….3. Why do some patients who go onto alemtuzumab continue to progress? I could put forward 3 answers to this (as a non scientist)… but I suspect this is one of those questions that are asked to prove a point. Anyhow, whether therapies effective at suppressing new lesion creation and (perhaps) CNS inflammation are effective at delaying or preventing progressive MS if given early enough (and what is early enough) is an experiment in making…. If only we could show how much disability is caused by focal inflammation and how much by the undefined neurodegenerative progression… if could tell this in any given individual with MS, I would prolly sleep much better at night. Why do some patients choose to stay on natalizumab despite being at risk of developing PML? Because their neuros recommend it? Because they’ve felt better after taking tysabri and are unwilling to give it up? Because they are more scared of MS than the relatively uncommon PML? I don’t know, I can’t speak for all of them, but if the answer is all of the above plus some more: what’s your point?Why do people choose to read your blog? Because I’ve looked at all the blogs and while I don’t agree with a lot of stuff that’s said on this one, the authors try, they seem to care and while they are certainly right as often as they are wrong (perhaps – I’ve done no trials to test this theory of mine): until we know what causes ms and how to stop it, it’s as good as I’m going to get. Why was the CUPID trial negative? Dunno. I can’t be bothered to even look up which drug the Cupid progject relates to and I don’t keep them on top of my head. If you have a point to make, make it.Why did the Charcot Project fail? Dunno. I can’t be bothered to even look up which drug the Charcot progject relates to and I don’t keep them on top of my head. If you have a point to make, make it. Why haven't you updated the format of your blog? Dunno. Why is the earth round?Why are desperate MSers so gullible?Gee, I have no clue. Do gullible people not deserve the best the world is able to offer?Ps. I don’t have MS. Does that mean I’m not gullible?
And why are you, trolls, so boring?Living complaining will not solve anything, unless you're a frustrated researcher who always tries to undermine, disrupt the work of others, right?!
because we can!
"frustrated researcher"...isn't that redundant?
Could you comment on this letter on alemtuzumab:http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(16)30382-9/abstractIn different MS forums people often describe "worsening" of their MS symptoms in the first months after alemtuzumab that in many cases gets better with time and no other interventions. Is this real or is it a myth? I cannot see anybody formally describing it in the descriptions of the drug (formularies etc).
This referes to one of the secondary B cell autoimmunities, however worsening of symptoms can occur as a consequence of the cytokine storm that happens when alemtuzumab starts killing cells. It seems to reactivate old lesions.
From a patient point of view I can not say this is the cause.Short lasting bouts of MS activity continued for 3-4 months after the infusions both times, I doubt alemtuzumab continues to circulate for so long. And if you look at others experiences published through out the interwebz, this is very common. My guess this has something to do with combination of steroid withdrawal, immune reconstitution, viruses, etc.
High dose vit B1 (Thiamine) for fatigue in MS. A paper in 2013 reported high dose B1 improved MS fatigue. Other studies report thiamine helps fatigue after stroke and IBD. Thiamine is affordable.BMJ Case Rep. 2013 Jul 16;2013. pii: bcr2013009144. doi: 10.1136/bcr-2013-009144. High dose thiamine improves fatigue in multiple sclerosis.Would be good if thiamine for MS fatigue can be researched further.
I've been on Tecfidera for a couple of years and have noticed I seem to be moving my lower face and tongue quite a bit as though I have a dry mouth most of the day or could it be Tardive Dyskinesia. Or MS progression. I have noticed this over the last month and wonder is Tardive Dyskinesia a side effect of Tecfidera? I do not take any other medication. Only ibuprofen a few times a month and vitamin D and B complex. thanks
I was wandering about Vitamin D supplementation during pregancy where the mother doesn't have MS but father has RRMS...There is a family history of MS on both sides to a small degree (the mothers father has RRMS and fathers grandmother had MS). So both Family lines have some history of MS which I imagine makes risks to offspring more pronounced than the normal population.The routine UK advice is 400IU for pregnant women (which seems small, the father takes 5,000IU daily and monitors bloods at around 175 nmol). Most of the posts on this subject I have found on the blog are catered for pregnant women with MS.Should the mother consider supplementing more than 400IU per day in these circumstances, and maybe also monitoring blood levels?Not sure if this is the correct place to ask, please let me know if you prefer an email etc...Many Thanks
maybe slightly unclear above!The Pregnant couple: Mother doesn't have MS (but has family history) - Father of the baby has RRMS (and also family history)Family history: the pregnant mothers father has RRMS and the father of the babies grandmother had MS...
Alemtuzumab causes prolonged lymphopenia ( or even low total white count) and there are general rules for avoiding f. ex. Listeria infection post-alemtuzumab. When can a person with MS return to work after alemtuzumab treatment (assuming all is well otherwise?). Are the any rules about how high the white count/granulocyte count/lymphocyte count should be before it's OK to live without constant Antibac rubbing and worrying about Listeria lurking in the cheeses/salad/cold cuts?
Recurrent urinary tract infections in MS, are there cases these are the same strain bacteria in the bladder? Could the bacteria be living in the walls of the bladder. I used to have several UTI's a few years, not for a while though. I don't have a record of what strain of bacteria they were. It would be good to keep a personal record of the strain.
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