I think this is a sensible approach to managing ms. The takeaway you get from Team G is that everyone has to be on "highly effective" therapies. The author's noted above that Tysabri has no consistent effect on brain atrophy so Team G has to remove this from their classification of a highly effective treatment.It's good to hear other people in the MS community describe what seems to be a logical approach to treating this disease. As for Team G one has to wonder where their motives are coming from.
No I'm an MS patient. I would really like to hear some valid arguments about what is wrong with the approach outlined in the article instead of meaningless responses such as you want everyone on highly effective therapies.Also, how can you recommend with a clear conscious the use of Tysabri when it has no effect on brain atrophy? Your mantra is "time is brain" so if the evidence goes aginst one of your most promoted drugs and you continue to recommend it there seems to be alternative motives. Please explain.
The only problem is the results of that study were not evaluated in a blinded, controlled analysis which is most likely why the authors from the study above concluded that there is no evidence it has any effect on BVL.Out of one side of Team G's mouth there is an expectation for gold standard evidence but when the data does not fit their promotional drugs they talk on the other side of their mouths. Real professional.
What about the placebo-controlled phase 3 trial, which found reduced atrophy in the second year? http://www.ncbi.nlm.nih.gov/pubmed/17452584And what about the phase 3 comparison study with interferon, which found the same thing?http://www.ncbi.nlm.nih.gov/pubmed/20236661I suppose that you could believe that pseudoatrophy in the first year is not a real phenomenon (and is just an excuse for not finding an effect on atrophy in the first year). But this seems to be fairly consistent across trials of natalizumab and across trials of other drugs as well.
Note the exact phrasing in the article linked to in the first comment: "No early and consistent effect on BVL." This is, strictly speaking, true. Natalizumab has no effect on brain volume early, i.e. in the first year. But all of the controlled and non-controlled studies that I am aware of show that it does have an effect after the first year.
When you take tysabri your brain shrinks because you get rid of the inflammation/swelling so if you compare to placebo there is not evidence of stopping atrophy, however if you rebaseline after the effect of inflammation has been removed then I suspect the rate of change is slower.
I think that the jury is still out whether or not it prevents BVL, but looking at the MOA of this drug it may prevent cells from getting into the brain that could be protective:http://m.nro.sagepub.com/content/early/2014/01/06/1073858413516799.abstractBecause of this it is no surprise to me that it does not seem to prevent BVL. No one at this point can know what effect Tysabri will have in the longterm but personally I would not want to be on this drug long-term.
Can you kindly comment or write a post on this publication?http://www.sciencedirect.com/science/article/pii/S2211034815001066someone posted the link yesterday on this blog.thank you
I think this is a sensible approach to managing ms. The takeaway you get from Team G is that everyone has to be on "highly effective" therapies. The author's noted above that Tysabri has no consistent effect on brain atrophy so Team G has to remove this from their classification of a highly effective treatment.It's good to hear other people in the MS community describe what seems to be a logical approach to treating this disease. As for Team G one has to wonder where their motives are coming from.
Well if the motive is wishing to get the most effective therapies to as many pwMS as possible, then guilty as charged.
You're not NICE's "brain expert" by any chance?
No I'm an MS patient. I would really like to hear some valid arguments about what is wrong with the approach outlined in the article instead of meaningless responses such as you want everyone on highly effective therapies.Also, how can you recommend with a clear conscious the use of Tysabri when it has no effect on brain atrophy? Your mantra is "time is brain" so if the evidence goes aginst one of your most promoted drugs and you continue to recommend it there seems to be alternative motives. Please explain.
http://www.ncbi.nlm.nih.gov/pubmed/22570359
http://multiplesclerosisnewstoday.com/2015/07/13/new-ms-study-shows-tysabri-improves-cognitive-impairment/
http://www.ncbi.nlm.nih.gov/pubmed/21707826
The only problem is the results of that study were not evaluated in a blinded, controlled analysis which is most likely why the authors from the study above concluded that there is no evidence it has any effect on BVL.Out of one side of Team G's mouth there is an expectation for gold standard evidence but when the data does not fit their promotional drugs they talk on the other side of their mouths. Real professional.
This is the evidence to hand at the moment I'm sure there will be more in the future.
http://www.ncbi.nlm.nih.gov/pubmed/23763388
What about the placebo-controlled phase 3 trial, which found reduced atrophy in the second year? http://www.ncbi.nlm.nih.gov/pubmed/17452584And what about the phase 3 comparison study with interferon, which found the same thing?http://www.ncbi.nlm.nih.gov/pubmed/20236661I suppose that you could believe that pseudoatrophy in the first year is not a real phenomenon (and is just an excuse for not finding an effect on atrophy in the first year). But this seems to be fairly consistent across trials of natalizumab and across trials of other drugs as well.
Note the exact phrasing in the article linked to in the first comment: "No early and consistent effect on BVL." This is, strictly speaking, true. Natalizumab has no effect on brain volume early, i.e. in the first year. But all of the controlled and non-controlled studies that I am aware of show that it does have an effect after the first year.
When you take tysabri your brain shrinks because you get rid of the inflammation/swelling so if you compare to placebo there is not evidence of stopping atrophy, however if you rebaseline after the effect of inflammation has been removed then I suspect the rate of change is slower.
I think that the jury is still out whether or not it prevents BVL, but looking at the MOA of this drug it may prevent cells from getting into the brain that could be protective:http://m.nro.sagepub.com/content/early/2014/01/06/1073858413516799.abstractBecause of this it is no surprise to me that it does not seem to prevent BVL. No one at this point can know what effect Tysabri will have in the longterm but personally I would not want to be on this drug long-term.
Ugh is this a ccsvi conference. we really are the enemy…..depressing