Prof G,I've seen the extension study publications for the Alemtuzumab trials. Is there any data on NEDA statistics longer term? All I've seen is 39% were NEDA at 2 years in the CARE-MS trials.
What has been released about the Ocrevus side effect profile? Has there been an official paper published? How does it compare to alemtuzemab?
Nothing released just like nothing released on the very positive effects. Alle have heard are the meeting reports and one suspects the side effect profile will be no worse than many other agents
Any information on this??
This is the latest abstract to be presented at ECTRIMS 2016. The topic has been blogged about before, please put alemtuzumab into the search box.Alemtuzumab provides durable improvements in clinical outcomes in treatment-naive patients with active relapsing-remitting multiple sclerosis over 6 years in the absence of continuous treatment (CARE-MS I)A.J. Coles1, A.N. Boyko2, J.A. Cohen3, J. De Sèze4, E.J. Fox5, E. Havrdova6, H.-P. Hartung7, J.S. Inshasi8, P. McCombe9, K.W. Selmaj10, P. Vermersch11, B. Van Wijmeersch12, D.H. Margolin13, K. Thangavelu13, C.E. Rodriguez13, X. Montalban14, on behalf of the CARE-MS I Investigators 1University of Cambridge School of Medicine, Cambridge, United Kingdom, 2Pirogov Russian National Research University & Demyelinating Diseases Center, Usupov Hospital, Moscow, Russian Federation, 3Cleveland Clinic, Cleveland, OH, United States, 4University of Strasbourg, Strasbourg, France, 5Central Texas Neurology Consultants, Round Rock, TX, United States, 6First Medical Faculty, Charles University in Prague, Prague, Czech Republic, 7Heinrich-Heine University, Duesseldorf, Germany, 8Rashid Hospital and Dubai Medical College, Dubai, United Arab Emirates, 9University of Queensland, Brisbane, QLD, Australia, 10Medical University of Łódź, Łódź, Poland, 11University of Lille Nord de France, Lille, France, 12University of Hasselt, Hasselt, Belgium, 13Sanofi Genzyme, Cambridge, MA, United States, 14MS Center of Catalonia, Barcelona, Spain Background: In the phase 3 CARE-MS I clinical trial (NCT00530348), alemtuzumab significantly reduced annualised relapse rate (ARR), MRI disease activity, and brain volume loss versus subcutaneous interferon beta-1a over 2 years in patients with active relapsing-remitting multiple sclerosis (RRMS) who were treatment-naive at baseline (BL). An extension study (NCT00930553) has shown durable efficacy through 5 years in the absence of continuous treatment.Goal: To evaluate 6-year clinical efficacy and safety of alemtuzumab in patients who were treatment-naive at BL.Methods: In CARE-MS I, patients received 2 courses of alemtuzumab 12 mg (Month 0: 5 days; Month 12: 3 days). At the end of Year 2, patients who completed the study could enter the extension, with as-needed alemtuzumab for relapse or MRI activity. Another disease-modifying therapy could be provided per investigator discretion. Assessments: ARR, proportion of patients free from 6-month confirmed disability worsening (CDW; ≥1-point Expanded Disability Status Scale [EDSS] increase [≥1.5-point if BL EDSS=0]), with 6-month confirmed disability improvement (CDI; ≥1-point EDSS decrease [BL score ≥2.0]), no evidence of disease activity (NEDA), and adverse events (AEs).Results: Through 6 years, 325/349 (93%) patients who enrolled in the extension remained on study. ARR remained low through the extension (0.12 at Year 6). Through 6 years, 77% of patients were free from 6-month CDW and 34% achieved 6-month CDI. Proportions of patients with stable or improved EDSS remained high through the extension (81% at Year 6); the majority of patients achieved NEDA annually in the extension (57% at Year 6). These efficacy results were achieved with most patients (63%) receiving no additional treatment after their initial 2 courses of alemtuzumab. The overall rate of AEs decreased over time. The rate of thyroid AEs peaked at Year 3 and subsequently declined. Infusion-associated reactions decreased with additional treatment courses. The serious AE rate was low, including the rate of serious infections, which declined throughout the extension.Conclusion: Clinical efficacy of alemtuzumab was maintained for 6 years in patients who were treatment-naive, despite most receiving no additional treatment since the initial 2 courses of alemtuzumab. Based on these findings, alemtuzumab may provide a unique treatment approach with durable efficacy in the absence of continuous treatment for RRMS patients.
Thank you. I have read everything on Barts MS and from other sources regarding Alemtuzumab. The search function is very helpful.I'm looking for NEDA statistics specifically. I'm not interested in the other statistics that don't look at all available measures of disease activity. So 57% NEDA at year 6... is this 57% of all participants who originally enrolled? Or are they rebaselining every year, which I understand takes into account time for the treatment to take effect, but it also excludes those whose disease progressed.Given that 39% were NEDA at 2 years, where on earth does 57% at 6 years come from. A more specific explanation around NEDA for the Alemtuzumab extension results would be very much appreciated.
Lies, damn lies and statistics! Correct me if I’m wrong, but seems there are some classic pharma weasel words in this.First of all, at first glance you could be forgiven for thinking this is saying that 57% of patients were NEDA across the 6 years; A conclusion which would be categorically incorrect!Of the original CARE-MS1 cohort:- 94% of those with ‘highly active disease’, treatment naïve, enrolled in the extension study- 39% were NEDA across years 1-2 (61% were not).- 58% were NEDA in Year 3 (42% were not)- 58% were NEDA in Year 4 (42% were not)- 61% were NEDA in Year 5 (39% were not)Here comes the rub (conveniently left out of this misleading abstract); The key phrasing here is "achieved NEDA *annually*."In other words, these are not cumulative NEDA rates. Rather, they are looking at isolated one year intervals. So a patient could relapse in year 1, 2, 3, and 4 – but if they’re stable for one year in year 5, they go into the year 5 NEDA results.The bit any patient should be interested in is the following (cumulative NEDA sustained across the extension period):“34% had NEDA sustained over years 3-5”.- Or, in other words, a 2:1 majority (66%) either relapsed, progressed, or had MRI activity within the first 3 years of the extension study“49% had no evidence of disease activity” [in years 3-5]. Again, a majority (51%) did…Now, yes, you could say “But look, the NEDA rate is getting progressively better over the years (58%, 58%, 61%), but then you see 7% of the extension study participants dropped out. Which may account for that (we don't know, as the abstract doesn't clarify their status at the point of dropping out).You could also pick fault with this being open label, having the results include 6% of patients who were treated with a secondary DMT during the trial period, or with the fact that the definition of EDSS progression has been extended from 1 to 1.5 in those with baseline EDSS 0 (presumably to further boost the results?). Results still not to be sniffed at; But seems like the reporting of this is deliberately misleading, to over-egg the benefits.A different summary of the same study: http://www.neurology.org/content/86/16_Supplement/S51.003Great news? Or an irresponsible (mis)reporting of the facts? Discuss…M
Thank you!! Pity no one from Team G could provide this information, or even better dedicate an entire post to it. There's still a lot of interest in Lemtrada. So thank you for answering the original question, much appreciated.34% at year 5 were NEDA (not 'in' year 5, but of the original cohort of patients). 39% at 2 years to 34% at 5 years demonstrates to me a reasonably durable effect for those that did attain it?What is concerning is that the statistics are even being represented in this way. Why mislead the public by presenting results in a way that on first glance look impressive? Grateful for people like yourself who can dissect and simplify the information. V ;)
I was deleted in response to this post Anon12.50, but you are correct that reporting on Alemtuzumab information leaves something to be desired. The recent posts on the occurrence each year of people getting thyroiditis after alemtuzumab is another case about 5% year 1 10% year 2, 20% year 3, 10% year 4, 10% year in fact totalling 59% yet they report only 40% of people got thyroiditis so some people have thyroid disease over two years. So it is not clear when it is occurringSo even when reporting side effects it is not clear.There are many other things that they have have not been reporting or reporting in unusual ways, whilst you have Anon 1:17 you dont need us to comment But we cannot Conflict of interests are given
Are you saying you cannot comment because of conflict of interest? I find that a bit stunning. Perhaps I misunderstand.
Yes, you don't misunderstand, but I don't want to explain at the moment sorry. All will be revealed
What happened to the ARTEMIS trial?
No funding for HSCT trials yet
The ARTEMIS trial is not a HSCT trial.The ARTEMIS trial. It is the Charcot 2 trial.The Charcot Project is currently developing a clinical trial protocol to test a specific anti-viral therapy that is active against EBV, a herpes virus that is strongly associated with MS.
My mistake, as far as I know it is not funded yet also, but thats the Gs not me.
If there is a link between EBV and MS could Spironolactone SPR be modified as a treatment? As its and effective EBV inhibitor.
Spironolactone blocks Epstein–Barr virus production by inhibiting EBV SM protein function, Dinesh Verma et al., Proceedings of the National Academy of Sciences (PNAS), www.pnas.org/cgi/doi/10.1073/pnas.1523686113, 14 March 2016.
"It's remarkable that a drug we have used safely in the clinic for over 50 years is also an effective EBV inhibitor. It goes to show how basic research can reveal things we would never have found otherwise."Dr. Swaminathan, who is chief of infectious diseases at University of Utah Health Care and professor of internal medicinehttp://www.medicalnewstoday.com/articles/307852.php
I was reading in my uni library today a book on communicating with patients. I was wondering if there are many papers on doctors communicating with MS patients or suspected MS patients? I can't seem to find many. I think this could be quite an interesting area of study especially as consultation times can be short. The importance of showing empathy and picking up cues etc.
It seems that there was miscalculations in the study who presented the possible gene primary progressive MS and more aggressive forms... It seems they are unable to replicate the the results of the study. https://www.statnews.com/2016/09/09/multiple-sclerosis-gene-attack/
Are there any studies/trials requiring pwRRMS who are not taking a DMT?
yes search Canbex to see if you fit the billCoI I'm conflicted
I searched but I didn't find, I don't know if I did the right search, but what would be the blocking drugs integrin related to Neutrophils? This study speaks of an unexpected setting of connection between neutrophils and the integrin adhesion molecule ICAM, wich for I understand that the causes neutrophils pass through the walls of blood vessels. It appears that some people actually looking at the role of neutrophils in diseases such as MS (it reminds me of some publications made by MD and some comments MD2) and neutrophils are the immune cells of the immune system front line. And they are recruited mainly when it is before an infection. Why then would neutrophils aggregate, accumulate and cause an inflammatory response? http://www.nature.com/articles/ncomms12658
I'm filling in the MS Brain Health your experiences of MS services around the country questionnaire, I have MS. It's a great idea to do this to give feedback. However, I find the format for answering is not that helpful. Question 2 - Out of the five areas three are poor, two are ok, but I can't give this as my answer.
More about the Gut and MS at ECTRIMS 2016?"Researchers found Th17 cells, an immune cell type believed to be involved in MS mechanisms in the intestines of MS patients but not in their blood. Also, Th22 cells were found only in the gut. MS patients also had more activated Th17 cells and less anti-inflammatory cells known as regulatory T-cells (Tregs) in their intestinal mucosa, compared to control individuals".https://multiplesclerosisnewstoday.com/2016/09/15/ectrims2016-immune-cells-linked-autoimmunity-found-in-ms-patientshttp://www.neurology.org/content/86/16_Supplement/P3.007
Could bright light help male MSers?Low testosterone is associated with disability in men with multiple sclerosis(Bove 2014).Bright light 'increases sexual satisfaction in men'. Scientists from the University of Siena in Italy found that using a light box, similar to those used to treat some forms of depression, increased testosterone levels.http://www.bbc.co.uk/news/health-37383689
Could using a light box slow down or reduce disability in male MSers by increasing testosterone levels?
In the news today Consultants' private work: The gloves are offWill this movement lead to better care by NHS neurology consultants? From the consultants that do both NHS and private consultations. The ones that delegate much work to junior doctors. http://www.bbc.co.uk/news/health-37379464
Before you start Digging ProfG and DrK don't do private work so save yourself the time
This was not a dig at Prof G and Dr K, I'm sorry I didn't highlight that. I can tell they both care about their patients very much. It is the other neurology consultants (not specifically MS neurology consultants)I have some concerns about. If improvements can be made in MS care and neurology care in general that must be a good thing?
I am wondering how common Beau's lines are in the fingernails or toenails of MSers? They can be caused by an illness in the body. Beau's lines are horizontal ridges, going across the nail, and should not be confused with vertical ridges going from the bottom (cuticle) of the nail out to the fingertip. I seem to get them in connection with a relapse.
Have any study, research pointing to the use of Tribulus Terrestris in people with MS, both men and women, is harmful?It has some herbalists who spend Tribulus to reduce fatigue. But from what I saw it seems to increase the natural production of Testosterone, so it would be something to to men but perhaps harmful to women, or non?Quickly I googled and found nothing about ....
I have been reading about ruxolitinib has been found to restore hair growth in 75% of patients with alopecia areata (an autoimmune disease), the second most common form of hair loss.I wondered if this drug could induce remyelination in MS? Working on a similar pathway like biotin?
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