I Feel Stupid!!!

A board to discuss the Multiple Sclerosis modifying drug Copaxone

I Feel Stupid!!!

Postby Chaz » Mon Sep 15, 2008 10:48 am

I consider myself to be fairly bright, did ok on the SATS, did well in college and so on...

When Brian was diagnosed with MS this year I became the "researcher". I've looked into everything. Investigated all the treatment options, looked into new diets, asked for help in determining good vitamins and other supplements, but I just can't wrap my mind around the treatment studies. I get lost with the numbers and confusing statistics.

I wish there was a completely unbiased, easy-to-read report that laid the facts out plain and simple!!! I feel confident with the decision to go on Copaxone...it SEEMS like the best option for him and he has handled the daily injections well with little to no side-effects, but what is the real story behind this drug? What are the "simpleton" stats?!?! I know that nothing surrounding this disease is a definite, but I'd like to really understand Copaxone. I understand that it mimics myelin and I've seen some reports that say it may slow down progression (or relapse rates) by 30% but I don't know if I even have that right!

I guess what I'm asking is if someone who knows this stuff could lay it out straight for me...or at least point me in the right direction to find it!?!?

MUCH APPRECIATED!

Charlie
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Re: I Feel Stupid!!!

Postby Lyon » Mon Sep 15, 2008 2:27 pm

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Last edited by Lyon on Sun Nov 27, 2011 1:02 pm, edited 1 time in total.
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Postby cheerleader » Mon Sep 15, 2008 7:49 pm

Hey Charlie....
Welcome to the club. Sorry you had to join. You are far from dumb...an MS diagnosis is overwhelming. Even the docs don't understand it, but you are doing all the right things for your husband.

My husband has been on Copaxone for 18 months and is stable, no relapses. He is considered a copaxone "responder." Approximately 1/3 to 1/2 of MS patients stabilize on copaxone. This means the drug is able to modulate their naive t-cells, and keep them from becoming pro-inflammatory. Copaxone is meant to decrease the number of relapses in RRMS. Most responders are early in the disease process and have low EDSS scores. As you know, it's not a cure....but it can slow down the disease process and buy our guys some time.

I knew nothing about this drug when the neuro prescribed it for my husband, but went with her assessment that most men who presented as he did found success with the drug. She referred to it as a "decoy" for his system- that the myelin based protein would provide a decoy for his inflammatory T-cells (destroyer cells sent from the thymus). She also called it a first-line treatment, and said we'd move on to interferons if he did not stabilize. His one year MRI showed no new lesions and none enhancing, so he continues on.

The sad fact is, there are no easy to read reports. The Copaxone site doesn't even address your questions. I've learned to slog thru Pubmed and immunology reports to gain understanding....but it ain't light reading.
Here's some of the reports....
http://www.jimmunol.org/cgi/content/full/170/9/4483
http://lib.bioinfo.pl/pmid:11877472

It takes about 6 months for Copaxone to have a large enough effect on the t-cells to create an anti-inflammatory effect. Alot of folks give up because of site reactions or lack of stabilization. Your neuro will assess the situation in a year or so.

Keep asking questions. Ignorance is not stupidity....and the learning curve on MS is huge. I wish you and Brian all the best-
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: I Feel Stupid!!!

Postby NHE » Mon Sep 15, 2008 8:49 pm

Chaz wrote:I consider myself to be fairly bright, did ok on the SATS, did well in college and so on...

When Brian was diagnosed with MS this year I became the "researcher". I've looked into everything. Investigated all the treatment options, looked into new diets, asked for help in determining good vitamins and other supplements, but I just can't wrap my mind around the treatment studies. I get lost with the numbers and confusing statistics.

I wish there was a completely unbiased, easy-to-read report that laid the facts out plain and simple!!! I feel confident with the decision to go on Copaxone...it SEEMS like the best option for him and he has handled the daily injections well with little to no side-effects, but what is the real story behind this drug? What are the "simpleton" stats?!?! I know that nothing surrounding this disease is a definite, but I'd like to really understand Copaxone. I understand that it mimics myelin and I've seen some reports that say it may slow down progression (or relapse rates) by 30% but I don't know if I even have that right!


I don't know how unbiased this article is, if my memory serves me correctly, R. Arnon was one of the initial developers of copaxone. Anyways, in light of the potential bias, here's an article which discusses copaxone's method of action.

Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications.
Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14593-8.

Glatiramer acetate (GA, Copaxone, Copolymer 1) is an approved drug for the treatment of multiple sclerosis and is highly effective in the suppression of experimental autoimmune encephalomyelitis in various species. The mode of action of GA is by initial strong promiscuous binding to MHC molecules and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the antiinflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express IFN-gamma. Based on this immunomodulatory mode of action, we explored the potential of GA for two other applications: prevention of graft rejection and amelioration of inflammatory bowel diseases. GA was effective in amelioration of graft rejection in two systems by prolongation of skin graft survival and inhibition of functional deterioration of thyroid grafts, across minor and major histocompatibility barriers. In all transplantation systems GA treatment inhibited the detrimental secretion of Th1 inflammatory cytokines and induced beneficial Th2/3 antiinflammatory response. GA was effective also in combination with low-dose immunosuppressive drugs. Inflammatory bowel diseases are characterized by detrimental imbalanced proinflammatory immune reactivity in the gut. GA significantly suppressed the various manifestations of trinitrobenzene sulfonic acid-induced colitis, including mortality, weight loss, and macroscopic and microscopic colonic damage. GA suppressed local lymphocyte proliferations and tumor necrosis factor alpha detrimental secretion but induced transforming growth factor beta, thus confirming the involvement of Th1 to Th2 shift in GA mode of action.


Here's another article...

Glatiramer acetate: mechanisms of action in multiple sclerosis.
Int Rev Neurobiol. 2007;79:537-70.

Glatiramer acetate (GA), formerly known as copolymer 1, is a mixture of synthetic polypeptides composed of four amino acids resembling the myelin basic protein (MSP). GA has been shown to be highly effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). Therefore, it was tested in several clinical studies and so approved for the immunomodulatory treatment of relapsing-type MS. In contrast to other immunomodulatory MS therapies, GA has a distinct mechanism of action: GA demonstrates an initial strong promiscuous binding to major histocompatibility complex molecules and consequent competition with various (myelin) antigens for their presentation to T cells. In addition, antigen-based therapy generating a GA-specific immune response seems to be the prerequisite for GA therapy. GA treatment induces an in vivo change of the frequency, cytokine secretion pattern and the effector function of GA-specific CD4+ and CD8+ T cells, probably by affecting the properties of antigen-presenting cells such as monocytes and dendritic cells. As demonstrated extensively in animal experiments, GA-specific, mostly, T helper 2 cells migrate to the brain and lead to in situ bystander suppression of the inflammatory process in the brain. Furthermore, GA-specific cells in the brain express neurotrophic factors like the brain-derived neurotrophic factor (BDNF) in addition to anti-inflammatory T helper 2-like cytokines. This might help tip the balance in favor of more beneficial influences because there is a complex interplay between detrimental and beneficial factors and mediators in the inflammatory milieu of MS lesions.


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Postby RedSonja » Wed Sep 17, 2008 3:53 am

I can't help, I can only confuse you more!

Everyone has their own version of MS. The drugs don't work the same for everyone. So, when it comes down to it, you have to choose for yourself:

Whether to take medication
Which one to take

If you go for Cop you have to try for 6 months before you know if it is helping. You might have no side-effects at all, or you might have to give up because your body doesn't like it. You won't know till you try. No easy answers, here, I'm afraid.
Bibo ergo sum
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Postby Chaz » Wed Sep 17, 2008 12:38 pm

Thanks everybody!!!

Brian started on Copaxone in February and hasn't had any real issues with it. He was almost instantly OK with the shots and aside from the sting and a little redness has no real complaints...thank god. I've heard horror stories.

I guess what happened recently is that things have slowed down a little (in a good way) but it gave me more time to actually think about some things that I glazed over with at the begining of the year...understanding Copaxone is one of them.

For now things are good so we'll just keep on truckin'...

Thanks again for all the help!
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