I don't remember any details from that article.
I have read and highlighted the article twice and I still find it confusing!
That antibodies didn't drop in nonresponders could just mean that B cells were not being killed. It tells us that elimination of some antibody makes the difference between response and nonresponse, but not what antibody it is.
I guess I had assumed that B cells were killed (and went down to zero like mine) by the Rituximab in all subjects in the study, but maybe this was an incorrect assumption on my part? I do agree that they could only report on the autoantibodies that they measured and that the responders could in fact have other autoantibodies go down that were not measured.
I am in this group b/c I have an autoantibody that attacks the calcium channel and anti GAD65 (and probably others that just have not been measured) so it is hard to say which autoantibodies being reduced are causing my improvements. I have also done IVIG prior to, and in addition to, the Rituximab so it is hard to determine causality in my case.
@Gingergrrl I feel a bit like I have a new face. I'm not sure I like it.
I'm not sure if I like it either!
Maybe it is a face that has to grow on you LOL.
You could have been monitoring any antibodies in the responders, and you would have seen a drop. The fact that they were monitoring those specific antibodies doesn't make them clinically significant.
That makes sense but I still find it interesting that these specific autoantibodies dropped in the responders (vs. the non responders).
It is certainly confusing.
I feel relieved that it is confusing to you, b/c then I don't feel so bad that it is confusing to me!
If these autoantibodies cause symptoms then you would expect more of them in ME than normal.
I think that very few ME patients (and people with autoimmune disease/autoantibodies in general) have been tested for these specific autoantibodies so the sample size would be very small.
It is very hard to give a precise explanation why but from looking at the data I did not feel confident that it made a convincing case for these antibodies having a direct role in symptoms. So I think measuring them at present is not going to provide any useful information about whether to be treated or not.
My gut instinct is that I disagree, based on reading that article and on conversations with my doctor, and I feel that these autoantibodies do play a role but I lack the background to be able to back this up with anything significant
.