marcstck wrote:This abstract looked at a population of 23 patients who underwent high-dose cyclophosphamide treatment, and concludes that the treatment was very effective in treating RRMS, but ineffective in treating SPMS and PPMS patients. This pretty much confirms what most of us have been hearing about the treatment...
I've gone through this paper again and again and, as with every other HDC study, I've come to the conclusion that the researchers are insane or playing coy in their assumptions that the treatment lacks effectiveness in SPMS and PPMS.
Where they universally get on the wrong track is the assumption that the treatment itself is in ANY WAY responsible for any of the "improvements" seen in RRMS. The best any researcher should expect of an MS treatment and the most generous primary endpoint should involve signs of stopping the disease mechanism. ANY improvement ONLY involves the treatment allowing the body to heal itself.
What has always SEEMED to be ineffectiveness of treatments in the SPMS and PPMS phases is the reduced obviousness of the effects of the healing process in those phases. It's widely accepted and should be obvious that in SPMS and PPMS the symptoms are less owed to inflammation and more owed to myelin and axon damage and therefore stopping the disease process in SPMS and PPMS isn't going to provide such profound results. None the less, stopping the disease process in any phase is still EQUALLY SUCCESSFUL regardless of whether or not profound results are noticed.
I've yet to see a HDC study in which the follow up period showed a sizable percentage of SPMS or PPMS disease progression after treatment, and THAT is what spells success or failure.
I see very little evidence to suggest that immune dysfunction plays much of a role in the SPMS/PPMS disease process. What gets lost amidst all the research is that the autoimmune response is more a symptom of MS then the cause of MS. In my opinion, a combination of exposures to pathogens and/or toxins in combination with a genetic predisposition sets the MS disease engine in motion, which in turn leads to an autoimmune response.
My belief is that retroviral DNA embedded within the genome of susceptible patients is activated by these pathogens/toxins, and the immune system is responding to this activated viral DNA resident in the patient's own cells.
I know firsthand that immunosuppression, at least in my case, has done nothing to impede the progress of my "atypical" PPMS. I've been on Tysabri, Rituxan, CellCept, and methotrexate, as well as going through a course of plasmapheresis, none of which has made the slightest dent in my disease progression. If the immune system was playing a significant part in the damage of my nervous system, certainly some result would have been seen through this myriad of treatments. I do suffer from other autoimmune syndromes (Hashimoto's, psoriasis), so there is an autoimmune process at work here, but there is also some unknown process going on that is compromising my nervous system.
Certainly, the autoimmune response plays a large role in the disease process of RRMS patients. Cutting off that response, whether by revimmune or ASCT, could very well set the immune system back to a point before it was activated by the presence of "smoldering" infection, toxins, and a genetic subtype.
My suspicion is that if "cured" revimmune or ASCT patients were to be exposed to the same combination of pathogens and/or toxins that they were earlier in life, they could very well see a return of the disease, perhaps many years after undergoing treatment.
I'm also of the opinion that PPMS is an entirely different disease altogether. The only resemblance my disease profile has to that of an RRMS patient is that we both suffer from "creeping paralysis". My test results and the insidious nature of my disease bare very little resemblance to those of my RRMS cousins...