they had two doctors trying to see thousands of very ill patients from worldwide plus issues going on behind the scenes (like all organizations face)
It's possible to give basic info without much effort, just by comments made during interviews, presentations and conferences. You don't have to have to do a study to give a rough estimate of what percentage of your ME/CFS patients rituximab is curing / putting into full remission during an interview.
Maybe the OMI want to keep their rituximab treatment quiet, because Fluge and Mella have recommended that ME/CFS patients should not be given rituximab out of clinical trials at this stage, so perhaps they feel it is a controversial, touchy subject. There is no mention of rituximab anywhere on their website.
Anyway, the fact that Dr Chia says his patients are not getting good results from rituximab ties in with the same lackluster response to rituximab we have seen on these forums (one good response, one or two mediocre responses, out of the 14 patients who posted their results on this forum).
I did not mean that they preferentially selected patients with certain autoantibodies to the exclusion of others.
When you said that "
I suspect that many American patients are trying Ritux without solid evidence that they have autoantibodies," I thought you were suggesting a theory that US patients might be getting poorer results than the Norwegians because the US patients were not ensuring they had autoantibodies before getting treated.
I was referring to the article in which it stated that the responders had the autoantibodies and showed a decrease in autoantibodies after Rituximab. I don't have the link right now but I have the printed copy and it's called "Antibodies to B adrenergic and muscarinic cholinergic receptors in patients with chronic fatigue syndrome"
The link to that paper is
here, and a PR thread discussing it is
here. It's not easy to understand the implications of this paper; however, as far as I can see:
Although ME/CFS patients responding to rituximab showed a reduction in certain elevated autoantibodies they may have had prior to treatment, and the non-responders showed no such decline in the same elevated autoantibodies, I don't think that translates into a requirement to have these particular autoantibodies beforehand in order for rituximab to work for ME/CFS.
In other words, even if you did not have prior elevated autoantibodies, you can still be a rituximab responder (but if you did have prior elevated autoantibodies, then the study observed that these would fall in responders, but not in non-responders).
Only 29.5% of ME/CFS patients had some autoantibodies significantly elevated compared to controls; but 60% of the patients treated with rituximab experienced either a partial or complete remission. So that shows you don't need these autoantibodies to be a responder.
Think of it like this: it could be that ME/CFS is caused by a completely different autoantibody (call it autoantibody X) to the ones measured in this study. We can hypothesize that it's when rituximab reduces the production of autoantibody X that ME/CFS is ameliorated or cured. But since we don't know that X is, we can only measure the effects of rituximab on other known autoantibodies. And we find, perhaps not surprisingly, that in the rituximab responders, these known autoantibodies are reduced; but that finding may just indicate that rituximab is working to reduce autoantibodies in general — reducing autoantibodies of all types, including autoantibody X.
As far as I could see (but I am a bit tired today), there was no indication in the study that ME/CFS patients with prior elevated autoantibodies were more likely to respond to rituximab.