w-five last night on tv
Posted: Sun Feb 22, 2009 6:12 am
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Yes, I believe you are right there. It is easy to equate effect by working backwards and saying you can know the cause based on that, like this "Because I seem better after chemo, therefore MS *IS* autoimmune and it worked the way I think it did" Chemo also causes profound system wide changes in the body --just one small example is anemia, which may have a positive effet on MS as anemic mice do not get eae. You can't know without a doubt that "the anemia effect" is not the reason people "seem" better.any of the drugs ms can make it happen on it's own so it seems to be the perfect situation to say or believe what isn't really so.
OK, whatever ails Molson has obviously greatly improved and seemingly reversed, but that is not the norm. In the Tysabri trials one of the patients who died did not turn out to have MS, remember that?Of the 18 patients who have undergone the treatment so far, Molson was the first to show such drastic improvement. The procedure had stalled progress of the disease in many patients, but until Molson, Dr. Freedman had never seen a patient actually get better
So clearly the pathology lab is showing some very negative effects on the brain tissue as a result of the chemo part of the stem cell transplant. Note the writer is not a person who does this treatment but rather a pathologist who looked at brain tissue AFTER such treatment and is documenting the atrophy--which honestly they already knew from MRI was happening in these ASCT patients, but they don't talk about that part.The potential of autologous hematopoietic cell transplantation
has been of considerable interest in recent
years following demonstration that this procedure could
protect against experimental autoimmune encephalitis
in rodents [11]. Pilot studies have revealed that such a
treatment is beneficial in reducing lesion activity and
neurological disability in patients with severe progressive
disease [7, 19], although the procedure is not without
risk.We have recently had the opportunity to evaluate
the brains of four patients who had received
autologous bone marrow transplants in North America
and subsequently died.
Autopsy samples from these patients revealed that in
all cases there was an almost complete absence of inflammatory
markers in the brain, notably of T cells. On
the other hand, there was significant staining for amyloid
precursor protein (APP) inclusions, a marker of
acute axonal damage (Fig. 5). This suggested that even
though inflammation had been abolished, neurodegeneration
was still proceeding in the brains of these patients,
and thus that neurodegeneration was not a direct
consequence, at least in the short-term,of inflammatory
damage to the nervous system.These data are consistent
with the observation from MRI studies that the rate of
brain atrophy is high in patients who have received
hematopoietic stem cell grafts in spite of an apparent
complete cessation of inflammatory lesion activity [10].
A possible explanation for these discordant effects on
inflammation and neurodegeneration would be that
suppression of the normal T cell patrolling of the nervous
system may interrupt correct regulation of microglial
function, allowing microglia to release toxic
substances indiscriminately which can in turn injure
neurons.
Multiple sclerosis is a relatively common and seriously disabling disease of autoimmune pathogenesis, for which there is currently no cure. Available therapies include immunomodulating agents and standard-dose immunosuppressants, which may be helpful but are not curative. Recently, studies in animal models have indicated that control of autoimmune disease can be obtained by high-dose immunosuppression followed by hematopoietic stem cell transplantation (rescue). Autologous transplants for severe and refractory multiple sclerosis were proposed in 1997 and have been performed ever since in selected patients and in the context of phase I/II trials. To date, more than 200 patients have been treated worldwide, and similar results were obtained in different centers: high-dose therapy suppresses inflammation in the brain to a degree superior to any other conventional therapy and seems to delay significantly clinical disease progression. There is, however, a procedure-related mortality risk of 1.5-5%, requiring careful patient selection before transplant. The treatment should be reserved for patients having high chance of response, i.e., young patients with low disability scores but rapidly progressing disease, having inflammatory rather than neurodegenerative changes in the central nervous system. The mechanism of action of transplantation is unclear. The initial concept of immune ablation by high-dose therapy and reconstitution of normal immunity from transplant-derived lymphocyte progenitors has given way to the concept of "resetting" the immune system and of bringing the disease to a lower level of activity. One could also speculate on a tissue repair effect, given the ability of human hematopoietic stem cells to migrate also into the central nervous system. The clinical effect of transplantation remains to be demonstrated in a randomized study. The Autoimmune Disease Working Party of the European Group for Blood and Marrow Transplantation has launched such a trial, comparing transplantation to the currently best available therapy, i.e., mitoxantrone, and in about 5 years we should know whether transplantation offers more than the benefit of a transient immunosuppressive effect.