This Is MS Multiple Sclerosis Community: Knowledge & Support

http://www.dispatch.com/content/stories ... s-die.html

1 within 24 hours after taking the oral drug.

I really do hope the same dire warnings in relation to CCSVI that garnered considerable interest, concern, endless blog postings, inflammatory headlines, and general use by every neuro predisposed to dismiss CCSVI out of hand, are brought to bear likewise for another pharmaceutical inspired pipe dream, where a simple little pill is all the rage, so attractive, so alluring, easy replacement for shots, now that 11 DEATHS come to light, NOW it warrants extreme scrutiny?

At least with CCSVI, we can usually trace the cause quite easily, these pills? Just NOW?
O
That, is how the existing system works, we are guinea pigs. At least with CCSVI, we can hedge our bets, make informed decisions, take numerous factors into account before proceeding, or decide not to proceed.

But the pills? Good luck and make sure your affairs are in order, I'll take a novel use of a time tested procedure ANY day over guessing how my particular physiological makeup may react to a new chemical.

Doubt this will get equal airtime though, it's just a drug, there's little controversy nor publicity to be gained by "having a position about oral drugs".

_________________
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap

http://www.medscape.com/viewarticle/751711
There were two deaths (out of 1302 participants) during the clinical studies too.

Sadly, these deaths will be seen as acceptable collateral loss if the final summary of the report can be written in a way that would determine more patients would benefit from the drug than wouldn't.

My view of modern medicine had become terribly jaded since I've been dealing with Emma's MS.

This is how it is done. This was a story published some years ago in the Ecologist magazine (Editor Zac Goldsmith - the supreme environmentalist)
“La maladie imaginaire
If press coverage is anything to go by, Americans started to get Social Anxiety Disorder (SAD) about three years ago. In 1997-98 the condition was referred to about 50 times in the nation's media. But a year later things suddenly got sadder. In 1999 there were more than a billion references to it in the US press.
According to the international Herald Tribune the increase in stories was not spurred by medical developments but was part of a campaign - coordinated by Cahn & Wolfe, a New York Public relations agency. The strategy included pitches to newspapers, radio, TV and testimonials from advocates and doctors claiming that SAD was America's third most common mental disorder with over 10m sufferers; only depression and alcoholism claim more victims. Paxil is the only FDA-approved medication for the treatment of 'Social Anxiety Disorder,' was the caring sharing marketing message. But the plug for the drug was no accident. Cahn & Wolfe was working at the behest of SmithKline Beecham, now known as Glaxo SmithKline. Whilst aggressive campaigns such as this one raise the concern that pharmaceutical companies are seeking new disorders for existing drugs. They also generate an artificial and increasing need for pharmaceutical inventions amongst huge proportions of people who had not until then 'realised' they needed help. What's more, the expensive campaign paid off. In the crowded anti-depressant market, Glaxo SmithKline's 2000 annual report claims that Paxil became the No 1 in the US selective serotonin reuptake inhibitor (SSRI's) market for new retail prescriptions in 2000.”
SAD people, happy Glaxo
The SAD disorder has since been changed to SAD again but this time it stands for Seasonal Affective Disorder!

A Facebook friend of mine found this interesting publication. This drug seems to be a totally CONTRAINDICATION if you are suffering from CCSVI, doesn't it? Arne


FTY720 (Fingolimod) increases vascular tone and blood pressure in spontaneously hypertensive rats via inhibition of sphingosine kinase.

Br J Pharmacol. 2012 Jan 17. doi: 10.1111/j.1476-5381.2012.01865.x. [Epub ahead of print]

Affiliation
Department of Pharmacology & Pharmacotherapy, Academic Medical Center, Amsterdam, the Netherlands.

Abstract
Background and purpose.  FTY720 (Fingolimod) is a recently approved orally administered drug for the treatment of multiple sclerosis. Phase II and III clinical trials have demonstrated that this drug modestly increases blood pressure. We have previously shown that inhibition of sphingosine kinase increases vascular tone and blood pressure in hypertensive, but not normotensive rats. Since FTY720 is reported to have sphingosine kinase inhibitory effects, we investigated whether FTY720 increases vascular tone and blood pressure only in hypertensive rats via this mechanism. Experimental approach.  The contractile and blood pressure modulating effects of FTY720 were studied in vivo and ex vivo (wire myography) in age-matched normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Key results.  Oral administration of FTY720 induced an increase in mean arterial pressure in SHR, whereas a decrease in blood pressure was observed in WKY rats, as measured 24 hours after administration. In analogy to the sphingosine kinase inhibitor dimethylsphingosine (DMS), FTY720 induced major contractions in isolated carotid arteries from SHR, but not in those from WKY. In contrast, the phosphorylated form of FTY720 (FTY720-P) did not induce contractions in isolated carotid arteries from SHR. FTY720-induced contractions (like DMS-induced contractions) proved to be endothelium-dependent and to be mediated by thromboxane A(2) , since these contractions could be inhibited by endothelium denudation, cyclooxygenase and thromboxane synthase inhibitors and by thromboxane receptor antagonism. Conclusions and Implications.  These data demonstrate that FTY720 increases vascular tone and blood pressure only in hypertensive rats, most likely due to its sphingosine kinase inhibitory effect.

© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
http://www.ncbi.nlm.nih.gov/m/pubmed/22251137/

Good find, Arne.

How does an increase in blood pressure affect perfusion? I would think that an increase in blood pressure would worsen the focal points of hypertension caused by combining the pressure in a reflux wave with the pressure in a forthcoming wave, a la Dr. Tucker's equations, but would it improve perfusion at all?

"2.6.3. Serious adverse event/deaths/other significant events
Deaths
A total of 84 deaths were reported in the clinical development program including 12 patients in the MS
and ongoing studies (cut off date: 30 September 2009) and 72 in the renal transplantation completed
studies. Deaths in MS studies are summarised in Table 33.
Table 33 Deaths in all MS studies, completed and ongoing as of 30 September 2009"

Please consult the Gilenya Assessment report located at http://www.ema.europa.eu/docs/en_GB/doc ... 104529.pdf Notice on page 88 section 2.6.3.

Rici

"Anonymous
#28
Yesterday, 03:46 PM
Anonymous

Posts: n/a
Re: MS LEADERSHIP A BUNCH OF LIARS
As an MS patient myself, I find this thread sickening. Bonuses of the sick ? What kind of people are you ?

I DON'T EVEN KNOW HOW THIS DRUG MADE IT TO MARKET......GIVEN THE FOLLOWING INFORMATION.

Please consult the Gilenya Assessment report located at http://www.ema.europa.eu/docs/en_GB/doc ... 104529.pdf Notice on page 88 section 2.6.3. Serious adverse event/deaths/other significant events - Deaths - A total of 84 deaths were reported in the clinical development program

84 deaths in the clinical trial phase ????"

Rici

It really does make you wonder who reads this information and decides that number of lost lives is "acceptable"