The reason for picking people with ANA is that going back over the last twenty years of B cell/plasma cell depletion for autoimmune disease (I did the first formal proof of concept trial in RA in 2001 and the first trial in lupus a bit later) it has become clear that although ANAs directed against protein antigens are likely pathogenic they do not go down much with anti-CD20 and clinical benefit is uncertain. A significant minority of people have such ANA - including healthy people - and I think if ME is autoantibody driven at all it is likely to involve such antibodies in at least a few cases. The story is very complicated.
I am not particularly suggesting that Oystein Fluge changes his current study. But I think if one is going to select cases at all something like ANA is about the only marker of B cell involvement likely to be useful. The same probably applies to Long Covid. I am not impressed by the various reports of other autoantibodies in Long Covidor even any evidence that it involves B cell activation.
Most side effects from rituximab are transient. The only major issue I am aware of, apart from infection, which will occur with any of these agents if Ig levels go down, is sterile pneumonitis with ritux. We identified that very early but the drug company was slow to document it. It may be that sever side effects are less with daratumumab but do we actually know that? I am not sure what you mean by 'heavy' ritux? If daratumumab is going to be better it will have to be 'heavier' in terms of Ig reduction I think.
