Discussion in 'Lyme Disease and Co-Infections' started by msf, Feb 29, 2016.
Would (or does) Rituximab work for such cases?
I KNEW Steere's name would be attached to this.
I was going to ask you about that. I thought he was IDSA, but the abstract talks about Antibiotic-refractory Lyme...
I couldn´t find the whole paper, but this meeting abstract seems to contain their initial findings: http://acrabstracts.org/abstract/ma...me-arthritis-but-not-in-rheumatoid-arthritis/
Steere is The Man, at least when it comes to the IDSA school of thought. He is kinda like the Godfather of Lyme-knees-Lyme-disease. I could write a book about him, but Pam Weintraub beat me to it.lol
He does seem to use antibiotic-refractory arthritis here oddly. I wrote it off as perhaps reflecting the the quirks of arthritis - ie., does normal non-infectous arthritis respond to abx? Is he saying that he is looking at antibiotic resistant Lyme in these knees? If so, why talk about autoimmunity? I don't know.
But my understanding of Steere's position in general when it comes to the Lyme knees saga is that it usually reflects an autoimmune process resultant from an earlier infection that has been resolved.
So....relative to Rituximab, if you believe Steere and company have it right, you roll the dice one way, but if you suspect there is continued Bb presence post-treatment, you roll another?
Maybe he forgot which terminology his ideology prefers.
I was just thinking about what you said about Ritux, and the thought occured to me that, in a patient with seronegative Lyme, would Ritux have much of a negative effect? It can´t get rid of antibodies your body was unable to make in the first place!
I suppose it depends on what you mean by seronegative. I can be seronegative but still be producing antibodies.
Using the CDC's definition, I can be producing Bb antibodies, but if they are not at the right level, it is not deemed sufficient to declare an active infection, and I could be judged seronegative. Hell, I am seronegative by the CDC 2T method if I have a positive ELISA and four WB IgG bands specific to Lyme.
Actually, there are those in the IDSA school - and Steere is one who promoted this early on, I believe - that say a previously infected patient, who has seen Lyme resolved, may produce Bb antibodies for the rest of his life.
I see. So would Ritux have much of a negative effect if your antibody response to the Borrelia was very weak?
I do not know.
Haha, I don´t think anyone does, but I think it is a pertinent question.
I think before considering rituximab one would need some reason to think the antibodies were causing symptoms. What worries me is that the group has reported autoantibodies to about five different antigens over the last few years but there seems little evidence of follow up on any of them. Autoimmune disease do not usually target a whole range of antigens. Nor do hey usually have anything to do with cross reaction to infection. This might be an exception but I would not put a lot of confidence in these results leading to anything repeatable or significant as they stand.
They didn´t show that they were causing symptoms, but they did correlate with clinical findings in this study, so it seems worth following up.
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