It'[s the biggest true treatment trial in the history of ME/CFS – and it could change everything…
The most important treatment trail in the history of ME/CFS has begun. Take a close look at the huge Rituximab trial that could change how ME/CFS is treated and viewed as Fluge and Mella tell us about it, the many substudies embedded in it and why they think ME/CFS may be an autoimmune disorder in the Simmaron Research Foundation sponsored blog:
Thank you so much for reporting on this Cort!
I realise research into M.E. is difficult, esp. as there may end up being different types of M.E., but this research I think is one of the most hopeful, it’s looking at both mechanisms and treatments at the same time!!!
And the fact that they are doing it well (double blind and placebo) is also hopeful, in it’s potential to actually impact sufferers. Also, from day one, this has felt to me like an immune disease (with some neurological elements) so it’s nice to see some solid research focused on immune factors. I wish I could participate 🙁
It seems like a very complete and well-thought out study. There should be no questions about how effective Rituximab is after this study. I imagine that we’ll find a group – hopefully a larger than smaller group – that responds very well.
I’m really excited about the endothelial study! I’ve always kind of intuitively felt that blood vessel dysfunction was key.
I agree, the endothelial stuff is super interesting. Also, how it would/could link a lot of the dysfunctions of M.E. – immune, OI, nervous system.
yes indeed – it could effect all of that…really looking forward to see what they find. I’m bet they have some nice preliminary data to back up this study….Looking forward to their hypothesis paper.
I have one question; how does low bloodvolume fit in this picture? Anybody an idea?
Very exciting research! I recall that Dr. Byron Hyde said years ago that he thought ME is essentially a vascular disease. I wonder if an interview with him would be timely now to see what he makes of this research so far? Thanks for another great article!
Good idea…It would be great to pick his brain right now.
In Dr. Byron Hyde’s definition of ME, he describes it as “A Vascular Pathophysiology” here on page 11:
He has an extensive database of the thousands of ME patients he has diagnosed since the 1980s, which as far as I know have not yet been published or mined for epidemiological purposes. But his own mind would be well worth “picking”!
Very good study. Thank you for your update Cort! ”we are not convinced that ME/CFS is primarily a central nervous system disorder. We believe the sympathetic nervous activation seen in ME/CFS may be (partly) secondary to an underlying (peripheral) pathology.” This is the big guestion more then a decade for me pfff… is it compensation? I Always thought it was. We will see. I bet it is….. 🙂 This is what the abnormal activity of the ANS wil explain.
The comment about worsening on etanercept are very interesting!
A trial on microglial inhibitors could be just as important 🙂
Excellent article Cort, thank you!
The work of Fluge and Mella is both impressive and important. I’ve participated in several clinical studies and know it’s long hard work for all the involved, both patients and medical staff. Unfortunately, Rituximab didn’t help me, but I’m certainly looking forward to their new projects with other drugs.
In the future I hope there will be clear cut indicators of responders and non responders before administering Rituximab. It’s a too heavy drug to get to no avail I believe, the side effects can be nasty. I was lucky in that sense, no major side effects.
I wouldn’t be surprised or even that disappointed if the drug does not end up being recommended for the ME/CFS patient population at large (CCC criteria); i.e that the results are not significant across the large group – but that a nice subset of responders stands out. ..
In general I’ll be that response rates usually go down the bigger the trial gets. It was about 2/3rds. I’ll bet it will drop dramatically… but still show up strong in a nice subset of patients.
I totally agree! And that’s why I wasn’t too disappointed to be a non responder on Rituximab. I have higher hopes in the other drugs they’re looking into.
studies from Lerner in early 2000s indicated ganciclovir could be good for CFS:
He looked at it from a viral perspective. The study from Stanford in 2014 indicates the benefit could be more to do with microglia inhibition than viral inhibition…or maybe both!
Will there be updates during the trial or is it farwell until 2017?
I’ve seen Dr. De Meirleir not being much optmist about Rituximab. Anyone happen to know why there is?
It was something about working for a period of time then causing a relapse. If that’s the case… the study would be just to find why it works for that period?
This is very encouraging and I am very grateful for the work of these dedicated researchers. I just find it hard to believe that an autoimmune disease can start from a viral-like flu epidemic that affects several people in a specific area, but then I just don’t know. There was a comment made about immediate results from killing EBV infected B cells in one patient, but if ME/CFS is caused by a virus in, say, the nervous tissue and not the B cells, that would not be a valid comparison. The delay in symptom relief is seen in autoimmune disorders. Why?
I hope this study can answer some of these mysteries, but I may have to come back as a ghost many years from now and find out.
It’s a good point David…can there really be such a sudden switch (like a light) from healthy to autoimmune disease, via a virus or other trigger?
I haven’t written off autoimmunity but I favour the insult to brain theory. Seems more credible to me, and results are starting to show in research.
ie. highly virulent virus in susceptible individual whacks the system, smacks on microglial activation in brain which gets triggered into a chronic “on”.
Still interested in any views on ganciclovir…..
If my friend’s experience with the autoimmune disease rhuemetoid arthritis is any indicator, I’d say yes, environmental factors can switch on autoimmune disease. He visited a farm, had a major allergic reaction to a crop being grown there, and boom, he had debilitating RA, had to sell his business, and now lives a very limited and painful life.
Ive always said that a sizable cohort of cfs / oi patients are suffering from an autoimmune disorder that through various ways impairs sympathetic vasoconstriction which in turn leads to reduced venous return, stroke volume, compensatory tachycardia and perhaps central parasympathetic withdrawal, reduced cerebral perfusion and consequential reduced cerebral glucose metabolism.
whether the target is alpha 1 adrenoceptors causing faulty venous constriction in micro vessels and the stomach vasculature, cytokine-driven inflammation of the small fibers impairing microvessel blood flow or this model of impaired endothelial parameters presumably leading to increased microvessel filtration, the point is the sympathetic failure to control upright hemodynamics is the primary problem in most oi.
The views of other cfs doctors who have spent twenty years peddling outdated and often unsubstantiated pathophysiological theories are probably fairly irrelevant. Some have made worthy contributions, others have often ignored basic rules of physiology.
The fundamental difference between this research and a lot of past cfs research is that the authors arent trying to peddle it to the cfs patient community but rather concentrating on keeping objective research standards and having it peer reviewed and recognised by the medical establishment.