Research: beta-interferon & progression

Epub: Greenberg BM et al. Interferon Beta Use and Disability Prevention in Relapsing-Remitting Multiple Sclerosis. Arch Neurol. 2012 Nov 5:1-4. doi: 10.1001/jamaneurol.2013.1017.

CONTEXT:  Interferon beta is widely prescribed to treat MS; however, its relationship with disability progression has yet to be established.

OBJECTIVE: To investigate the association between interferon beta exposure and disability progression in MSers with relapsing-remitting MS.

DESIGN, SETTING, AND PATIENTS:  Retrospective cohort study based on prospectively collected data (1985-2008) from British Columbia, Canada. MSers with relapsing-remitting MS treated with interferon beta (n = 868) were compared with untreated contemporary (n = 829) and historical (n = 959) cohorts. 

MAIN OUTCOME MEASURES:  The main outcome measure was time from interferon beta treatment eligibility (baseline) to a confirmed and sustained score of 6 (requiring a cane to walk 100 m; confirmed at 150 days with no measurable improvement) on the Expanded Disability Status Scale (EDSS) (range, 0-10, with higher scores indicating higher disability). A multivariable Cox regression model with interferon beta treatment included as a time-varying covariate was used to assess the hazard of disease progression associated with interferon beta treatment. Analyses also included propensity score adjustment to address confounding by indication.

RESULTS:  The median active follow-up times (first to last EDSS measurement) were as follows: for the interferon beta-treated cohort, 5.1 years (interquartile range [IQR], 3.0-7.0 years); for the contemporary control cohort, 4.0 years (IQR, 2.1-6.4 years); and for the historical control cohort, 10.8 years (IQR, 6.3-14.7 years). The observed outcome rates for reaching a sustained EDSS score of 6 were 10.8%, 5.3%, and 23.1% in the 3 cohorts, respectively. After adjustment for potential baseline confounders (sex, age, disease duration, and EDSS score), exposure to interferon beta was not associated with a statistically significant difference in the hazard of reaching an EDSS score of 6 when either the contemporary control cohort (hazard ratio, 1.30; 95% CI, 0.92-1.83; P = .14) or the historical control cohort (hazard ratio, 0.77; 95% CI, 0.58-1.02; P = .07) were considered. Further adjustment for comorbidities and socioeconomic status, where possible, did not change interpretations, and propensity score adjustment did not substantially change the results.

CONCLUSION:  Among MSers with relapsing-remitting MS, administration of interferon beta was not associated with a reduction in progression of disability.

“What does this say about IFNbeta? Impossible to assess as the biases in treating someone render this analysis meaningless. The most active MSers will almost certainly be selected for treatment and the more benign cases not. This is like comparing oranges with apples! Deja vu?”

CoI: multiple

16 thoughts on “Research: beta-interferon & progression”

    1. This link is old hat it is Doctors are more dangerous than guns blah, blah blah by the health ranger. This is certainly Deja vu.Please say what the links are when you post them. Is it just advertising and liable? to be removed

    2. Likewise putting the same comment in multiple posts is spamming and will end up being deleted just like has occurred to the this link in which someone has posted in several places on the blog.

  1. I started to read this with a certain amount of trepidation. After that awful study, which resulted in the headline of The Independent 'The MS Drugs don't work and the NHS is paying for them', which anyone with a few braincells and a nice dose of RRMS, knows was rubbish, I was wary.Thanks for Prof G's conclusion. There is NO way to predict disability. Lifestyles, exercise, Vitamin D3 and stress all play a part in this and NOT having relapses is important. If someone was to put together a trial of 200 people on let's say, Rebif44, with the same number of lesions, disease activity, impairment, compared with a the same number of people who have similar symptoms/lesions and watch what happens – no, wait, this can't happen. It would be inhumane and unethical. The most important issue for a person with RRMS is reduction in disease activity. I don't know about progression as I'm just a person with MS and can't see the big picture. I haven't progressed, but who knows if that's down to genes, environmental factors or Rebif. No disease activity is what keeps me going, learning, playing, teaching and singing. Relapses would stop me from doing any of this and I would be a very unhappy and constantly ill MSer. Been there. Don't want to be that ill ever again.

  2. So are you saying the selection process biases the outcome Mouse Dr ?I thought I used the same argument for a drug which showed very promising results not long ago and was dismissed. So if it's like comparing Apples with Oranges would it not require a 'Level Playing Field' to start with if only for comparison purposes when comparing different drugs ?Regards as always.

    1. Dear AndyIt was not me who posted this but Prof G, but selection of people to include in your studies can bias your results. If you pick people with EDSS that does not change then your trial can be doomed.If you look at the historical relapse rate of DMT studies I think they tend to be much higher than they are today.Maybe tell us when you used the argument and we can have another look

  3. Selection bias might be an argument regarding the contemporary untreated group, but can not apply to the historical group, since the latter has all kinds of MS cases.If INFb was worth any of the thousands pounds it costs annually, some benefit should be seen. There are now at least 3 long term studies that prove the rubbishness of INFb. But you keep on dismissing them on statistical grounds. This is pure bias.On the other hand you are very keen on endorsing the single, ridiculous Bayer study about the all cause mortality rate 21 years after INFb treatment initiation, which in final analysis says nothing about MS.

  4. VVFor once I tend to agree with you regarding the effectiveness if Beta Interferon but it's worth bearing in mind that along with the equally (in my opinion) rubbish Copaxone for many years these have been the only available prescribable treatments. This situation has now changed and will continue to change as the new generation of proven effective DMTs come onstream.Now we need to focus on side-effect reduction of DMTs and neuroprotective therapies as adjuncts. Then we can expect to see real progress on disease management and progression.

  5. Since INFb & GA prove themselves worthless, one wonders how they were licenced in the first place: a) Were the trial results prefabricated/exagerrated? b) Were the trial endpoints irrelevant c) both a and b?The answer to this question will reveal the future of the newer DMTs (probably rubbish too).I hope our opinions are parallel lines of a Riemannian space that inevitably intersect.

  6. Not worthless (they do work for some MSers though for the life of me I can't think why) just the only drugs available at the time. The limited efficacy and desperate lack of any alternative probably explains why they were given licences. They wouldn't get one now compared to the new generation of DMTs.The available data so far shows that you're wrong about the new DMTs. I hope that situation continues.I suspect that this may be the only time our opinions ever remotely come close to intersecting given your past history on here 😉

    1. Aubagio under way in the US, whats going to happen in UK?Effacacy level of the glaterons (glaterimer acetate and interferons) but side-effects?

  7. My wife got interferones soon after dx and that experiment lasted about year, and this wasn't good experience. Next morning after injection was quite bad, her legs were spastic and walking not normal. This medicine didn't do any good for her and there was also some abnormality with thrombosyte levels – so after that, she has been without MS medicine.

  8. Yes, they are rubbish, really. I discontinued after 7 months (and regret having taken them, frankly) since my scan without DMTs was the same as the scan with Avonex. That being said, it was really the worsening of my symptoms with Avonex that led to the decision to stop them. I had felt quite good before starting interferons and much better after stopping – the time in the middle was really rather bad & the feeling that something so palpably changes your consciousness (just hours after intake) was alarming. I am glad I stopped and switched to fumarate because it brought my life back & a clear head.

  9. I wish people wouldn't say something is rubbish based on just their personal experience. The drug may have been v bad for you, doesn't mean it's so for everyone.We all know that the first gen drugs are not great, but a small percentage of users reach a disease-free state. Many more become ALMOST relapse-free. Most patients are able to sleep through the flu-like symptoms with the help of paracetomol/brufen.The drugs may or may not do anything for disability in the long run. But improved qol in the short term is no small thing

  10. You will often see publications describing how bad old product are when new products are coming on the market. It makes room for the new ones and weakens biosimilars or generics makers. The Jama study gathers products which have not the same efficacy : so the efficacy of the more efficient ones is lessen by the low efficacy of the other one and we cannot draw any conclusion on each specific treatment from the population analysed in this population.

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