Hi adreno and nanonug, this is close to my current working hypothesis. If Rituximab works, if it can be validated to be completely restorative in even a minority of patients, and temporarily restorative in the majority of patients, then the symptomology is B cell mediated. These B cells pump out an array of cytokines and probably some self targeted antibodies. If patients recover as we have been led to believe by the phase 2 clinical trial, then it follows that neurological issues must be restored following treatment of the immune system. Even if the issue is B cell carried infection (e.g. herpes viruses) this reasoning still follows.
The only quandery about this is what is stopping the one third of non-responders from improving? Is it a dosage/protocol issue as some suggest? Is it due to comorbid conditions or other complications? Are these people suffering from a different condition with similar symptoms? Do these patients have serious spine or brain lesions that are resistant to healing? Or is there some other reason?
This doesn't mean we shouldn't treat the hormone deficiences though, only that we should not expect too much from such treatment. It most probably will not be curative.
Bye, Alex
Alex, I think rituximab is not the only road to Rome. Treating the viral infections, that lead to the autoimmune reaction, and dampening the excessive immune response (inflammation) might be another way to go. It's the road I'm taking, as I still find rituximab too risky at the moment.
Again, curcumin looks very promising in treating autoimmune, inflammatory, and fatigue conditions. It's a very powerful inhibitor of NF-kB. I think you'll find the following interesting:
Downregulation of B lymphocyte stimulator expression by curcumin in B lymphocyte via suppressing nuclear translocation of NF-?B.
Huang G, et al.
Eur J Pharmacol. 2011 Jan 10;650(1):451-7. Epub 2010 Oct 13.
Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Third Military Medical University, Chongqing 400038, China.
Abstract
Overexpression of B lymphocyte stimulator (BLyS) is closely involved in the pathogenesis and progression of some autoimmune diseases. Curcumin, a pharmacologically safe agent, has been shown to possess potent anti-inflammatory properties. However, it is not clear whether curcumin affects the expression of BLyS. In this study, we report that curcumin inhibits the expression of BLyS and that a DNA-binding site for the transcriptional factor NF-?B in the BLyS promoter region is required for this regulation. Moreover, we find that curcumin reduces the DNA-binding activity of NF-?B to the BLyS promoter region and suppresses nuclear translocation of p65, suggesting that curcumin may suppress BLyS expression via negatively interfering with NF-?B signaling. These results suggest that curcumin may serve as a novel therapeutic agent in the treatment of autoimmune diseases by targeting BLyS.
PMID 20950605