Wow, so many conflicting agendas and viewpoints on this thread, that have in many places steered this conversation way off path.
As I stated in my previous post, the crux of the BMJ article (which was basically an analysis piece, not a study itself) has to do with the financial implications of the CRAB drugs not meeting projected expectations, and the impact that this failure had on the NHS.
The endpoint the NHS was looking at was disease progression; none of the official US CRAB drug trials used progression as an endpoint, instead using relapse rate and the number of enhancing lesions as seen on an MRI. Because the drugs did impact those two endpoints to a statistically significant factor, they were approved for use in the treatment of multiple sclerosis. There was an overall suspicion that reducing relapse rates and enhancing lesions would impact disease progression, but this was a hope rather than a fact.
There has been increasing evidence that these drugs do not impact disease progression, at least to the amount initially desired. Copaxone actually does come closest to appear to have some significant impact, and some studies have also shown that the drug may have immuno protective properties.
Contrary to an assertion made earlier in this thread, relapse rates are far more readily quantified then disease progression. A relapse is an identifiable event, in which a patient suffers a fairly quick onset of dramatically increased symptoms, which eventually remit to a place somewhere near the patient's initial baseline condition. Progression, on the other hand, is extremely hard to quantify, because it can take quite some time for progression to become apparent by objective means. I've had many neuro visits when I'd known that my disease has progressed, but the progression I felt failed to be evidenced in my neurologic workup.
Copaxone was in fact tested on PPMS patients when it was first introduced. Those tests were initially deemed a failure, based more on the fact that the disease progressed so slowly that there was very little difference between the control and treated group. Later parsing of the data did suggest that copaxone might have some impact on a subset of the PPMS population (men who displayed some signs of inflammation). The same was true for thy Rituxan PPMS trials, which were initially deemed a failure, but upon later review the results turned out to be equivocal for a subset of patients.
The reason why progression was not chosen as an endpoint for the FDA trials of the CRAB drugs was precisely because it is so hard to track.
After more than a decade on the market, there's little doubt that the CRAB drugs do impact relapse rate and enhancing lesions for some MS sufferers, based both on study results, the experience of clinicians, and patient reports. For many patients, the reduction in relapse rate is a huge improvement in quality of life, even if the drugs don't ultimately alter the progression of their disease. The relief from crippling relapses certainly makes the life of successfully treated patients more bearable.
How all this relates to CCSVI is beyond me. The fact that the CRAB drugs do have some effect on the disease in no way disproves the CCSVI theory, and in fact only strengthens it. CCSVI postulates that disrupted hemodynamics in the CNS lead to inflammation in the brain and spinal cord, due to a variety of factors. Drugs that modulate or suppress the immune system would be expected to have some effect given this model.
The attempt to discredit the CRAB drugs to somehow validate CCSVI reminds me of those who try to poke holes in the theory of evolution to somehow prove creationist ideology. If Darwin's original theory does have some identifiable flaws, all that is proven is that our understanding of evolution is imperfect, it in no way relates whatsoever to claims that the earth is only 5000 years old, that men coexisted with dinosaurs in the not so distant past, and that all life on the planet follows the blueprint of an omnipotent deity. Likewise, discrediting the CRAB drugs does nothing to prove or disprove CCSVI. In fact, proving that drugs that impact the immune system have no impact at all on MS would shed some doubt on CCSVI, which is an elegant explanation as to how and why the immune system attacks the CNS tissues.
It's vitally important to take a sober, rational, and impartial look at the constant stream of newly minted MS research information and discoveries. Approaching them with bias, and bending them to fit a set of preconceived notions does nothing to further the cause that one is biased towards.
We must present CCSVI as a rational, fact-based theory that will hopefully soon be backed up by concrete independent research data. We must guard against painting ourselves (the proponents of CCSVI) as a lunatic fringe prone more to hyperbole and hysteria than to rational discourse.
Please note, I'm not calling anyone here a lunatic, I'm just saying that thoughtful analysis trumps knee-jerk reaction more times than not...
Just a quick word on the Cochrane review materials. These are all retrospective studies, which look at research results from completed trials. Cochrane does no trials of their own. While retrospective studies do have value, they can be prone to subjectivity, especially in the choice of which studies are included in the retrospective review. My own experience in looking at Cochrane results has often found their conclusions sometimes questionable. Since I'm not a physician or research scientist, that opinion and two bucks will get me on the subway...
As for the unholy alliance between drug companies, governments, and the medical establishment, I posted an essay on Wheelchair Kamikaze entitled "The Medical Industrial Complex: Sick People Required". Readers seemed to find it interesting, and if you care to have a look, here's the link:
http://www.wheelchairkamikaze.com/2010/ ... eople.html