it is a secondary mechanism by depleting auto antibodies is the principle behind autoimmune mostly.calms down what is overactive. that is something they will be trying to find out markers wise.
if in phase 3 trials that percentage of success is the same as phase 2 its pretty huge because phase 3 is where results fall down.
Even in autoimmune diseases not everyone responds to the same drugs it would be a massive proof of principle and proof of disease if phase 3 cracks it.
I thought Dr Kolgelnik was doing studies on ritux in usa along with virus modulators and something else is that thru OMI-Merit.?
I would be concerned if people are just going and getting ritux and its not in a controlled study?
If this does pan out another immunosepressant might work for people that didn't respond to ritux but studies need to be done properly?
I don't really know whats going on with the Dr Kolgelnik stuff.
I don't think that all autoimmune things are prescribed prednisone it depends.
It was heartening to see someone write more has come to light sooo looking forward to hearing about that.
Just attended a meeting where Doctor Fluge spoke last week at Stavanger University Hospital. They are moving forward and are preparing their paper for publishing. They where not able to give us all the details of the results of the study they have been conducting as that would make it more difficult to be published in pair reviewed journals, but there were clearly some interesting developements.
On a question from one of the audience members they did however suggest that non experimental treatment using Rituximab could become a reality in 3-4 years. I didn´t get the impression that they were "stuck" because of lack of funding in any way (of course funding is always a challenge but I guess they are able to work within the limits of what they have).
This seems such an important post I wonder if it could have its own thread - I only stumbled across it in here and im sure many others would like to hear this news, especially the statement about rituximab treatments
Rituximab could change everything, at least for those patients who respond to it. Sadly that is not everyone.
It might also change the politics. How can a B cell destroying drug cause remission in a psychosomatic illness? Answer: the placebo effect is not powerful enough to do this, so the psychogenic hypothesis is obsolete for at least a large subset of patients. My gosh, they were wrong again! Add psychogenic CFS to the absurdly long long long long long long long list of failures.
It is as fair to say our immune systems are overactive as underactive. There are imbalances, with some parts given a big oomph, and other parts suppressed. NK cell function is suppressed. It looks like T cells are working too hard. We seem to have a very high turnover of B cells, though this needs a lot more research to be sure. We might have clonal expansion of gamma delta T cells. Some cytokines seem abnormally low or high.
Most immunosuppressants target most of the immune system. They are not specific enough, but might be helpful in really low doses.
Well, I appreciate the specific research now, seeing what happens by targeting just the B cells with rituximab. Because isn't it possible that the insurance cos and govt could try to have us take a broad spectrum immunosuppressant drug such as prednisone is, I think, with all of its harmful side effects, just because it is a lot cheaper?
I agree @alex3619 my illness feels part overactive and part underactive.
I can have both reactions with my heart symptoms "sometimes my heart feels suppressed and hardly beating and at other times it is beating like I have just run a marathon. Just one example.