Tysabri vs CRABS

[Lendi]

What is the differnce in how they work. I'm on tysabri but have been on the CRABS too. I'm just wondering how they differ as far as how they work.

What I mean is; Does tysabri lower the immune system and the CRABS do something else or do they all work about the same but tysabri is stronger.

[0485c10]

The interferons Avonnex,Rebif, Betaseron are "imunmodulators". They work in the immune system. The immune system contains alarm cells called cytokin's that identify virus & foreign tissue that need to be attacked by the immune system. In MS our immune system is mis identifying our myelin as a virus and attacking that incorrectly. The interferon's load a bunch of extra alarm cells, cytokin so the immune system gets too busy attacking these fake alarms to attack the myelin, it had been doing incorrectly.

The immune system becomes 30% too busy attacking these fake alarms to attack the myelin. Interferons don't suppress the immune system, they weaken the immune system by keeping it busy with these fake alarms. Thats were the side affects come from. The immune system attacks with fever, muscle aches ect. The body really think it is fighting a real virus with the interferons but actually they are fakes. the body gets used to them after a while and the side affects stop for most..

Copaxone doesn't work in the immune system, it works in the nervous system. Copaxone works by loading a bunch of dummy myelin cells for the immune system to attack instead of the real thing. It to is 30% effective. There is a 30% chance the immune system will attack these fake myelin cells instead of the real myelin.

Tysabri is an immune suppressant. It a selective immune suppressant. It to works in the immune system. An immune suppresant is a substance that prevents the immune system from doing something. The interferons are immune modulators because it doesn't prevent the immune system from doing something, it just keeps the immune system occupied.

Tysabri, a selective immune suppressant, prevents the white blood cells of the immune system from crossing the blood brain barrier-that's why there is a PML risk.

Tysabri prevents the immune system from getting across the blood brain barrier and into the brain to attack real virus. With out Tysabri preventing the immune system from gettting into the brain, the immune system would fight the virus that cause PML--but since Tysabri selectiively suppresses the immune system from getting into the brain, PML can occur but myelin isn't attack.

THE BIOGEN WEBSITE HAS A VIDEO SHOWING HOW TYSABRI WORKS BY SUPPRESSING THE IMMUNE SYSTEM FROM CROSING THE BBB.

http://www.tysabri.com/tysbProject/t...abri-works.xml

[Alicious]

0485c10, This may be the single most useful post I've read on how the meds work. Thank you!

[twisterred]

0485c10, This may be the single most useful post I've read on how the meds work. Thank you!

Agreed!!

Thank you so much for this explanation.

[LL60]

Would it kill a doctor to sit down and explain things to you in this way!!
Maybe they don't even know?

I'm still waiting for my neuro tell there is a sligh increase with melanoma on Tysabri. 16 months and she hasn't said a thing. I asked my dermatotogist about it, he researched it and said better come in every 6 months. This is after reading something here about it.

I will be paying big bucks next year for health care. It will change our level of living. And yet I still have to depend on lay people and the internet to give me my health information.

Please don't stop. You are all I have. But it does make me mad.

If anyone has not seen that video about how Tysabri works, please watch it. It is very cool. I found it by accident one day and have gone back to watch it many times.

[Redwings]

Would it kill a doctor to sit down and explain things to you in this way!!

Unfortunately, doctors don't have time anymore to explain how medications, and even diseases, work. Their job has been reduced to diagnosing and treating. And if a doctor were to sit down and explain these meds, I hope it would be without the factual errors contained in the preceding explanation.

I'm still waiting for my neuro tell there is a slight increase with melanoma on Tysabri. 16 months and she hasn't said a thing. I asked my dermatotogist about it, he researched it and said better come in every 6 months. This is after reading something here about it.

Regarding melanoma, it would also be helpful for your doctors to read Melanoma in multiple sclerosis treated with natalizumab: causal association or coincidence?; Bergamaschi R, Montomoli C.; Mult Scler. 2009 Dec;15(12):1532-3. The authors' findings were that the incidence of melanoma in Tysabri-treated MS patients was actually lower than in the general population:

"Considering that at the moment the incidence of melanoma is estimable as about 5 per 100,000 multiple sclerosis person-years treated with natalizumab, and that, in the general population, the incidence of melanoma per 100,000 person-years is more than 10, we may speculate that the occurrence of melanoma during natalizumab treatment in multiple sclerosis is purely a coincidence."

Another study looked at the correlation between Tsabri, nevi (moles) and a protein targeted by Tysabri in MS that's also involved in the transformation of nevi into melanoma: Evolution of Nevi During Treatment With Natalizumab: A Prospective Follow-up of Patients Treated With Natalizumab for Multiple Sclerosis.; Castela E et al.; Arch Dermatol. 2010 Sep 20. The researchers found that there was no correlation between Tysabri treatment and changes in the nevi:

"Our results showed the same rate of clinical and dermoscopic changes of nevi during treatment with natalizumab compared with the spontaneous evolution of nevi reported in literature. In accordance with fundamental data, those results suggest that the inhibition of the α(4) integrin does not promote the transformation of melanocytic lesions."

PML has made everyone more careful with Tysabri, but that also includes the possibility that the initial melanoma cases may have been "overinterpreted." That could be why some doctors haven't brought up melanoma. What would be the point of frightening a patient by mentioning cancer if there aren't sufficient data to back up the suspicion? A doctor may discount the "lower-than-general-population" incidence figures and the dermatologic findings and lean toward caution (and there sure isn't anything wrong with that!), but both sides of the issue should be discussed nonetheless.

[0485c10]

Unfortunately, doctors don't have time anymore to explain how medications, and even diseases, work. And if a doctor were to sit down and explain these meds, I hope it would be without the factual errors contained in the preceding explanation.


Regarding melanoma, it would also be helpful for your doctors to read Melanoma in multiple sclerosis treated with natalizumab: causal association or coincidence?; Bergamaschi R, Montomoli C.; Mult Scler. 2009 Dec;15(12):1532-3.

A good source for understanding how these meds work is to read about the immune system not MS & a good easy to read explanation on it is Woman & Autoimmunre Disease by Robert G Lahita, MD, PHD which explains how the immune system causes problem in many auto immune disease and the treatment for them.

I'm not at all surprised by your response Dr. Redwings, it was as I expected. Your threatened.This is the political season where attack adds without support of the attack are aired on the TV frequently, so I'm used to it at this time.

LL60 you need to get your doc's mailing address to Dr. Redwings so he can be compensated for the advanced medical training your doc is getting from Dr. Redwings. This stuff(training ) isn't free!

But he does have a point about doc's not explaining this in a 15 minute appointment.Doc's have "touchy" communications with this stuff because they are accountable for what they say---and this stuff is all in a "grey' area, similar to explaining to a child a grey area. There a nuances in medicine its not a black and white field. There are a lot of "yes it could be that & it might not be that"

Take lack of response to steroids...yes it could be that a person has become progressive and the damage is more neurodegenerative than inflamatory...and yes it could be that a person is just not responsive to steroids regardless of the state of their MS and yes it could be that it was a bad batch of steroids, mixed improperly----and yes it could be something we haven't thought of & do not have sufficient evidence to draw a conclusion yet, and yes it could be...its tough to explain all that detail in a simple nut shell within a 15 minute appointment. And still have time for the rest of their patients.

The nut shells have to be done on internet support boards like this and books like the one I referenced.

Your doc not saying anything about melanoma, when if she said something you could take it to mean melanoma was gonna happen to you after using tysabri for a while---how does she also convey the nuances of the subject within 15 minutes...that it is very unlikely, not proven to have a causal link to tysabri but it has been observed and this is a new med without a lot of data on it yet? People are getting melanoma without using Tysabri so you should be vigilant about Melanomas for that reason, especially if you live in a sun belt. How does she convey all that and be certain you have understood all that she has conveyed within a 15 minute appointment?


The nuances in medicine make it difficult & not a short explanation of why steroids were not effective.

[Alicious]

15 minute appointments? Time to switch docs. None of my specialists sit with me for less than 30, and sometimes it's an hour. I won't accept less in a specialist, and fortunately there are those out there who won't give less than that. If yours won't answer questions well or doesn't have the time, it's time to find a new doc. Not all docs are like this, thank goodness.

[LL60]

OMG, I didn't mean to start anything.

Redwings, my dermo. doc sent me the article and part of another article that he went by. This was last year, so I am sure that what you quoted was sooner, so maybe more actuate. I do live where it is sunny year round and I have had a mild form of skin cancer already, so going every 6 months is a great idea for me anyway. I went 3 years going every 6 months after the skin cancer, then was switched to just yearly. The switch back just makes sense, right?

Everyone keeps talking about what a docter can do in 15 minutes. HA. My neuro has never ever even come close to 15 mintues. When I went on Tysabri she was so upset that she had to go though the whole booklet with me. I have never seen anyone read so fast in my life. It's okay. She is all I have. No other choice.

And besides I have you all. And I do appreciate the support and the information. If you want to put out opposing information, a little gentler please.

The one direct quesion I asked my neuro about Tysabri - what about the rebound effect? She assured me she had never heard of such a thing.

I don't care if she doesn't have "15 minutes" for me. But shouldn't she take some time to keep up on the drugs she is prescribing for me?

[Ikoiko]

The "information" which 0485c10 provided about how these drugs work is VERY WRONG!

[Alicious]

The "information" which 0485c10 provided about how these drugs work is VERY WRONG!

Can you explain how? I'm new to all of this, so having the correct info would be helpful.

[Ikoiko]

LL60, is your neuro an MS specialist? I would be very worried if my neuro had never heard of the rebound effect!!! She is not reading the literature.

[MrsBones]

Can you explain how? I'm new to all of this, so having the correct info would be helpful.

Alicious, the truth is that not even the makers of the drugs know exactly how the drugs work.

If you look at any of the drug sites, you will see statements like the one on Tysabri's site, which happens to be directly below the video 0485c10 linked to. Tysabri's says, and I quote:"The way in which Tysabri works has been studied, but the exact way Tysabri works is not fully known."

NO ONE knows how they work, they make very educated guesses. They can say "thought to" or "believed to" work in a certain way, because they simply don't know for sure that any of them work in a certain way. They can say they work differently from each other because they are different drugs with drastically different active components. They can say what the effects of the drug are, because those effects can be seen.

They can say that all the CRABs are immunomodulators because they can see that the immune system has been modified while on them. They can say Tysabri is an immunosuppressant because they can see that difference.

What they can't say 100% for sure is how or why any of these drugs have any effect on MS. It is all educated guessing.

This is something researchers, doctors and drug makers don't know. The best anyone here can do is repeat what we do know from those researchers or give their own theories.Anything you might read here is just that.

0485c10, Redwings posts are always based on good research and facts. They never get personal. This one is no different. There was no reason for any responses to that post to be personal.

Regardless of intent, in print it just comes across badly and not at all funny. I am sorry if it was meant to be funny and I'm taking it the wrong way, but that kind of thing rarely comes across simply in text.

[Ikoiko]

How the Drugs Work (Briefly)

1. Interferon beta (Avonex, Betaseron, Rebif): It is unknown exactly how interferon beta works, but it is thought to modulate the immune system by enhancing suppressor T-cell activity, reducing proinflamitory cytokine production, down-regulating antigen presentation, and inhibiting lymphocyte trafficking into the central nervous system. <Betaseron.com>

2. Copaxone: Copaxone is a synthetic protein that mimics myelin basic protein (a component of myelin). <NMSS.org> The mechanism of action is not fully known, but copaxone is thought to induce and activate copaxone-specific T-cells <Copaxone.com> and divert them from attacking the central nervous system.

3. 30% Effectiveness: All of the CRABS were about 30% effective in the original clinical studies. That means that relapses and lesions were reduced by 30% IN THE STUDY POPULATION AS A WHOLE, NOT that the drugs are 30% effective in any one patient. They could be 100% effective in one patient, and 0% effective in another patient, with it all averaging out to 30% effectiveness in the group overall. We don't know how to predict who will be successfull on the CRABS, and who will not be. (Although, there has been a recent investigational test to predict who will do well on interferons. This test is not yet available to the general population.)

4. Tysabri: Tysabri reduced relapses in MS patients by 67% during the initial clinical studies. It works by binding to leukocytes (white blood cells) and preventing their transport across the blood-brain barrier of the central nervous system. <Tysabri.com>

[Lendi]

Thank you, thank you, thank you!!! I appreciate the information.

My neuro spends as much time with me as I have questions or need but sometimes he's not the easiest to understand.