Beta Interferon on 7 year progression

Treatment with interferon beta delays the onset of secondary progressive MS. #MSBlog #MSResearch

“This uncontrolled observational study confirms an increasing number of real-life data sets that treatment with DMTs, in this case IFN-beta, delays the time to the onset of SPMS. The only outlier is the data set from the University of British Columbia, which has been heavily criticised. All the leading MS statisticians I have spoken to about in relation this study have issues with the methodology.”

“Unfortunately, the therapeutic nihilists and denialists out there won’t accept real-life data and will only accept data from randomised controlled trials. The problem with the later is that the time to onset of SPMS or EDSS 4.0 the a relatively widely accepted surrogate for the onset of SPMS takes a long time and it would be unethical to do 5 or 7 years study to show this. What do you think?”.

Drulovic et al. Interferon-beta and disability progression in relapsing-remitting multiple sclerosis. Clin Neurol Neurosurg. 2013;115 Suppl 1:S65-9.

OBJECTIVE: To assess the impact of interferon (IFN)-beta treatment on the progression of unremitting disability in IFN-beta treated and untreated relapsing-remitting (RR) MSers using prospective cohort study.

METHODS: A cohort of 419 RRMS (236 IFN-beta-treated and 183 untreated) MSers was followed for up to 7 years. Cox proportional hazards regression models adjusted for the number of relapses in the last year before first visit was used to assess the differences between the two groups for the three end points: secondary progression (SP), and sustained Expanded Disability Status Scale (EDSS) score 4 and 6. Time from disease onset was used as survival time variable.

RESULTS: The IFN-beta-treated group showed a highly significant reduction (hazard ratio [HR], 0.34, 95% confidence interval [CI] 0.19-0.61, p<0.001) in the risk of SP when compared with untreated MSers. There were significant differences in favor of the IFN-beta-treated group for the end point EDSS score of 4 (HR=0.45, 95%CI 0.28-0.73, p=0.001) and EDSS score of 6 (HR=0.34, 95%CI 0.16-0.75, p=0.007).

CONCLUSION: This observational study further supports the notion that IFN-beta could have potential beneficial effect on disease progression in RRMS.

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.


  • The disease algorithm that you have posted in past blogs has shown two distinct MS pathologies: inflammatory mediated by adaptive immune response and innate immunity or slow burn mediated by microglia. It seems logical that in order for interferon beta to be effective in slowing disease progression there must be a connection between these two processes. If progressive disease is no longer under the influence of anti-inflammatories then we are treating only half the disease. MS researchers need the equivalent of a grand unifying theorem to put the debate about the effectiveness of immunomodulatories to rest.

  • Okay, so I'm a CIS'er, 2 years after my first (mild) relapse. My neurologist in Spain (it seems that the NHS is not alone when deciding to wait until your second relapse before starting any treatment) decided to wait until my second flare-up episode. Then I contacted Dr. Helen Tremlett (who led the study you are criticizing from British Columbia University that claimed that Interferons had no efficacy against the natural course of MS), and she told me that my MSologist was acting wisely. That study was class I scientific evidence, and this study posted here is not. Who should we believe?

  • Why was the Helen Tremlet study class I evidence? This was on obsevational study, not a placebo controlled randomized trial.

    The problem is you cannot have long term controlled trials because it is unethical. Get it? But one thing is clear, those that go untreated have more brain atrophy than those that are on DMD's.

    Is Beta Interferon the best drug to prevent atrophy? Probably not, but it seems there is evidence that it is better than nothing.

  • Please explain a little more about what these results mean for the individual patients.
    Would all of them have been worse off without the beta-interferon?

    • I think it is impossible to predict how an individual person is going to do on any given therapy. The point is that you have to look at the accumulated evidence of longterm results, the vast majority of which points to the first line DMD's are effective for many over the long term.

      In my case, knowing that Copaxone has seemed to halt disease progression in people on the long term follow up studies as well as talking to people who have been stable for decades gives me an incentive to stay with the therapy (it ssems to be working for me though I've only been on it for a year).

      The problem with MSers is that they focus on the outliers such as the Zomboni's and Tremlett's and conclude that they are right even though the evidence is against them. It is unfortunate that these types of studies are published before they are fully vetted, but it ultimately comes down to the MSer to decide what to beleive in and it seems too many are easily manipulated into making wrong decisions.

By Prof G



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