Benefit seen with interferon lasts into progressive MS

A board to discuss the Multiple Sclerosis modifying drug Betaseron

Benefit seen with interferon lasts into progressive MS

Postby MSUK » Wed Nov 16, 2011 3:11 am

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Patients with primary progressive multiple sclerosis (PPMS) who took interferon-beta-1b for two years in a randomized trial continued to show improvement relative five years later, Spanish researchers said.

Although the patients received no further interferon treatment after the randomized trial ended, those who had taken the drug during the study had both better scores for functional outcomes and better MRI evaluations at follow-up than those who had been treated with placebo, according to Xavier Montalban, PhD, of Autonomous University of Barcelona, and colleagues.

In addition, the study suggested that interferon-treated patients with better than average benefit during the trial showed less disability progression when they went off the drug, they wrote in the November issue of Archives of Neurology.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1766
MS-UK - http://www.ms-uk.org/
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Re: Benefit seen with interferon lasts into progressive MS

Postby FLJhawk » Fri Feb 15, 2013 8:52 pm

I thought recent studies showed that Betaserone, while reducing lesions, barely impacted the time to disability. I basically stopped taking it for that reason. The bad thing about this disease is you never really now for sure if what you are doing or did or didn't do is making any difference at all.
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Re: Benefit seen with interferon lasts into progressive MS

Postby CaliReader » Sat Feb 16, 2013 7:08 pm

I've been researching this a lot, since I'm still trying to decide whether to inject myself with these drugs.

As FJLhawk pointed out, at least one major study showed interferon does not reduce time to disability.

The reasons I'm still considering this, in spite of my needle phobia, are:

1. Interferon Beta is an antiviral drug, and the viral theory is an alternate theory of MS.
2. Interferon Beta calms systemic inflammation and inflammation is apparently a mechanism of the damage done to our nervous system.
3. There is an ugly mortality study written by Professor Douglas Goodin of the University of California San Francisco, neurologist and professor at the local MS center. I'm not sure how much to trust it, since the professor was paid by Bayer, but he showed that a group people treated with Betaseron in an early trial of the drug were less likely to die of MS related causes than the controls in the same experiment who did not receive interferon treatment. It isn't an easy or cheerful read.

All of this suggests to me that difference in time to disability is not the only important variable in measuring the effect of a drug for MS. Reduction in relapses has its own value. Calming inflammation and reducing oxidative stress is an important task to accomplish by whatever method.

I am not yet personally taking interferon beta. I am considering it. I don't fully understand the statistics around reduction in relapses, so I don't know how much benefit is provided. I also don't trust the conflicts of interest around the big drug companies. I'm not sure how reliable the Goodin study is.

Having said that, here is a very small subset of the research being done around interferon beta and beneficial effects on harmful inflammation, both in MS and in other conditions.


Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage
Pieter M Cobelens, Ivo ACW Tiebosch, Rick M Dijkhuizen, Peter H van der Meide, René Zwartbol, Cobi J Heijnen, Jozef Kesecioglu, Walter M van den Bergh
Crit Care. 2010; 14(4): R157. Published online 2010 August 23. doi: 10.1186/cc9232

Suppression of Inflammation in Ulcerative Colitis by Interferon-β-1a Is Accompanied by Inhibition of IL-13 Production
Peter J. Mannon, Ronald L. Hornung, Zhiqiong Yang, Chuli Yi, Catherine Groden, Julia Friend, Michael Yao, Warren Strober, Ivan J. Fuss
Gut. Author manuscript; available in PMC 2012 August 30.
Published in final edited form as: Gut. 2011 April; 60(4): 449–455. Published online 2010 October 22. doi: 10.1136/gut.2010.226860

Interferon-β treatment in multiple sclerosis attenuates inflammatory gene expression through inducible activity of the phosphatase SHP-1
George P. Christophi, Michael Panos, Chad A. Hudson, Chriso Tsikkou, Cornelia Mihai, Luis J. Mejico, Burk Jubelt, Paul T. Massa
Clin Immunol. Author manuscript; available in PMC 2010 October 1.

PEGylated interferon-β modulates the acute inflammatory response and recovery when combined with forced exercise following cervical spinal contusion injury
Harra R. Sandrow-Feinberg, Victoria Zhukareva, Lauren Santi, Kassi Miller, Jed S. Shumsky, Darren P. Baker, John D. Houle
Exp Neurol. Author manuscript; available in PMC 2011 June 1

J Inflamm Res. 2010; 3: 25–31..
PMCID: PMC3218739
Injectable interferon beta-1b for the treatment of relapsing forms of multiple sclerosis
Slobodan M Jankovic
Abstract
Multiple sclerosis (MS) is chronic inflammatory and demyelinating disease with either a progressive (10%–15%)
or relapsing-remitting (85%–90%) course. The pathological hallmarks of MS are lesions of both white and grey matter
in the central nervous system. The onset of the disease is usually around 30 years of age.
The patients experience an acute focal neurologic dysfunction which is not characteristic,
followed by partial or complete recovery. Acute episodes of neurologic dysfunction with
diverse signs and symptoms will then recur throughout the life of a patient, with periods of
partial or complete remission and clinical stability in between. Currently, there are
several therapeutic options for MS with disease-modifying properties. Immunomodulatory therapy
with interferon beta-1b (IFN-β1b) or -1a, glatiramer and natalizumab shows similar efficacy;
in a resistant or intolerant patient, the most recently approved therapeutic option is mitoxantrone.
IFN-β1b in patients with MS binds to specific receptors on surface of immune cells,
changing the expression of several genes and leading to a decrease in quantity of
cell-associated adhesion molecules, inhibition of major histocompatibility complex
class II expression and reduction in inflammatory cells migration into the central nervous system.
After 2 years of treatment, IFN-β1b reduces the risk of development of clinically
defined MS from 45% (with placebo) to 28% (with IFN-β1b). It also reduces relapses for 34%
(1.31 exacerbations annually with placebo and 0.9 with higher dose of IFN-β1b) and
makes 31% more patients relapse-free. In secondary-progressive disease annual rate of
progression is 3% lower with IFN-β1b. In recommended doses IFN-β1b causes the following
frequent adverse effects: injection site reactions (redness, discoloration,
inflammation, pain, necrosis and non-specific reactions), insomnia, influenza-like syndrome,
asthenia, headache, myalgia, hypoesthesia, nausea, paresthesia, myasthenia, chills and depression.
Efficacy of IFN-β1b in relapsing-remitting MS is higher than that of IFN-β1a, and
similar to the efficacy of glatiramer acetate. These facts promote IFN-β1b as
one of the most important drugs in the spectrum of immunological therapies for this debilitating disease.
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Re: Benefit seen with interferon lasts into progressive MS

Postby CaliReader » Sat Feb 16, 2013 7:17 pm

Here is an even better recent abstract about the role of inflammation in MS.

I don't know whether interferon beta's ability to calm inflammation is enough to make it worthwhile to take the drug. There may be other ways to control inflammation through diet etc.

The scientists seem to agree that inflammation is important in how MS does damage and that interferon beta is one way to slow that process down, at least in RR.

Here is the abstract.

Curr Neuropharmacol. 2011 September; 9(3): 409–416.
doi: 10.2174/157015911796557911
PMCID: PMC3151595
Multiple Sclerosis: Pathogenesis and Treatment
Ingrid Loma* and Rock Heyman
Author information ► Article notes ► Copyright and License information ►
Go to:
Abstract
Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disease of the central nervous system. It affects approximately 400,000 people in the United States and onset is usually during young adulthood. There are four clinical forms of MS, of which relapsing remitting type is the most common. As the etiology of MS is unknown, finding a cure will remain challenging. The main mechanism of injury appears to be inflammation and 8 agents are now FDA approved to help control MS. These agents for relapsing forms of MS target different parts of the immune system, with the end goal of decreasing and avoiding further inflammation. No agents are FDA approved for the primary progressive version of MS. FDA approved agents include four preparations of interferon β (Avonex, Rebif, Betaseron and Extavia), glatiramer acetate (Copaxone), mitoxantrone (Novantrone), natalizumab (Tysabri) and fingolimod (Gilenya). There are several drug undergoing phase II and III trials. The heterogeneity of the MS disease process, individual patient response, and medication toxicities continue to challenge the treating physician.
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