itsjustme wrote:I thought Tysabri worked by being a monoclonal antibody that only attaches to MRTC's rendering them denatured so the T cells won't attack myelin. If that is how it works for MS, then why is Biogen submitting it for Crohn's disease?
TYSABRI ® binds to the alpha4-subunit of alpha4beta1 and alpha4beta7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the alpha4-mediated adhesion of leukocytes to their counter-receptor( s). The receptors for the alpha4 family of integrins include vascular cell adhesion molecule-1 (VCAM-1), which is expressed on activated vascular endothelium, and mucosal addressin cell adhesion molecule-1 (MadCAM-1) present on vascular endothelial cells of the gastrointestinal tract. Disruption of these molecular interactions prevents transmigration of leukocytes across the endothelium into inflamed parenchymal tissue. In vitro, anti-alpha4-integrin antibodies also block alpha4-mediated cell binding to ligands such as osteopontin and an alternatively spliced domain of fibronectin, connecting segment-1 (CS-1). In vivo, TYSABRI ® may further act to inhibit the interaction of a4-expressing leukocytes with their ligand(s) in the extracellular matrix and on parenchymal cells, thereby inhibiting further recruitment and inflammatory activity of activated immune cells.
The specific mechanism(s) by which TYSABRI ® exerts its effects in multiple sclerosis have not been fully defined. In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be secondary to blockade of the molecular interaction of alpha4beta1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Data from an experimental autoimmune encephalitis animal model of multiple sclerosis demonstrate reduction of leukocyte migration into brain parenchyma and reduction of plaque formation detected by magnetic resonance imaging (MRI) following repeated administration of natalizumab. The clinical significance of these animal data is unknown.
1 Crohn's patient that had a previous severely compromised immune system due to being on Azathioprine for 6 years.
This Crohn's patient had stopped all immune system altering drugs at least 8 months before going on Tysabri. He was in relatively good health with the exception of the sometimes uncomfortable Chron's symptoms
msladyinca wrote:Once again, incorrect information was posted:This Crohn's patient had stopped all immune system altering drugs at least 8 months before going on Tysabri. He was in relatively good health with the exception of the sometimes uncomfortable Chron's symptoms
[color=blue][size=14]This patient was extremely ill with not only Crohn's disease, but Malignant Astrocytoma, receiving Remicade, Azathioprine, and then Tysabri with concomitant immunosuppressants at the same time he was receiving Tysabri. Azathrioprine can be incredibly toxic, and can decimate the immune system long after its dosing, leaving the patient susceptible to potentially fatal infection. This information can be found within this own site's research: http://www.thisisms.com/article202.html.
Furthermore, if you research the FDA AERS database, you will find that Remicade was the primary suspect for this patient's death, with Tysabri, Azathioprine and steroids being secondary suspects.
I don't know from where you are getting your information
This patient was doing very well..... fishing and hunting and enjoying his retirement quite nicely. He WAS NOT using any of these other drugs that you have mentioned for a very long time (8 months minimum)
This Crohn's patient's cumulative medical history can be found in many places. For example, from this site's own research, see:
"[he had been] exposed to years of dosing with a cocktail of potentially lethal drugs-- that among other things, can cause delayed immunosuppression, cancer, and even PML itself [suggests Remicade], was participating in a clinical trial with another experimental immunosuppresant. Maybe his case was so bad, he had no other hope, but in such an extreme situation, the fault of his death cannot be placed squarely on Tysabri. That he died is of course tragic, but quite frankly, a serious adverse event is not entirely surprising given his cumulative medical history."
[color=blue][size=14]Anecdotal evidence provided by the family of the patient to only you is not published anywhere in the medical journals that he was "doing very well", and your arguments are with the findings of the FDA, the medical journals, and all published information regarding this patient's cumulative medical history.
You simply have your facts wrong, and anyone else reading your comments can look up the accurate facts as I have indicated them above. Others are more than welcome to make up their own minds when it comes to either your opinion or mine, and reach their own logical conclusions.
Lauren, you can believe what you want to believe from the "accurate facts"
I will Harry, in fact, I feel much more comfortable believing the findings of the FDA, the medical journals, and all published information regarding this patient's cumulative medical history.
My sympathies to the family that lost their loved one. It was a tragedy indeed, but this is the risk that all patients (including myself) must decide for themselves when entering a trial for a new medication. It was his choice to enter the trial, his decision, and one that I will always respect (as should we all).
Have a nice day.
MeadowStream wrote:So let me get this sraight... you are best friends now with the Belgian patient's family even though you live in Canada? After all this time it is a huge coincidence that you suddenly are close to the family, who themselves assessed Remicade as the primary suspect in their 60 year old relative's death from use of immune suppressants. Who could believe this harry? Answer: no one.
MeadowStream wrote:No, I am not coming to Ontario to see your "email." You have some sort of vendetta vs. Biogen and, I think, few want to see you spill your bile toward the company.
Tysabri is now being dosed in over 22,000 patients since being reintroduced in 2006 and there has not been a single case of PML. Meanwhile there have been 100s of myocardial infarctions and arrymthias that have been reported where death was the outcome and a beta interferon was the primary suspect.
How many deaths where Tysabri was the primary suspect? Answer: zero.
Guess what the family of the CD patient apparently reported as primary suspect in cause of death? Answer: not Tysabri. Weird, huh?
Guess what Harry Z doesn't like? Answer: the only efficacious and safe treatment for MS. Weird, huh?
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