Thursday, 22 November 2012

Research: NMO and mitoxantrone reducing relapses is a good thing

Epub: Cabre P et al, Efficacy of mitoxantrone in neuromyelitis optica spectrum: clinical and neuroradiological study. J Neurol Neurosurg Psychiatry. 2012 Nov.


OBJECTIVE: To evaluate the efficacy of mitoxantrone (MTX) on clinical and neuroradiological parameters of patients who had a relapse of neuromyelitis optica spectrum (NMOS) within the 12 previous months.
METHODS: MTX (12 mg/m(2)) combined with methylprednisolone 1 g as three monthly courses followed by three quarterly courses was administered during an observational multicentre open study including 51 consecutive patients (28 NMO, 23 limited forms of NMO) of the French Caribbean and Guyana. The main outcome measure was the reduction of the annualised relapse rate (ARR), and the secondary outcome measures were alteration of disability measured by expanded disability status scale (EDSS) score, the time to onset of the first relapse, and the progression of neuroradiological lesions at 1 year of treatment.
RESULTS: At 1 year of treatment, the ARR dropped from 1.82 to 0.37 (p<0.0001). The mean EDSS score improved by 1.3 points, going from 5.8 at baseline to 4.5 at 1 year (p<0.0001). The number of patients showing gadolinium (Gad)+ spinal cord lesions at baseline, that is, 46.9%, dropped to 10.6% (a 77.4% reduction; p=0.02). The median time to onset of the first relapse was 18 months. IgG-NMO seropositivity was a predictive factor of relapse (p=0.006). A case of acute myeloid leukaemia was observed after a mean time span of 4.8 years.
CONCLUSIONS: In this observational NMO study, MTX decreased dramatically the frequency of relapses, which is directly related to progression of disability or even death in this disorder.

NMO, used to be called Devics MS, is characterised by spinal cord and optic nerve demyelination, although brains are modestly affected also. This is associated with the development of self-reactive antibodies. Mitoxantrone is an anti-cancer drug that kills dividing cells including T cells and so has a prediliction to attack B cells, which have an intrinsic relatively quick turn over rate. This has a dramatic effect on relapse rate and removing relapses is a good thing and removes some of the influences causing disability. We were among st the first to show it inhibits attacks in EAE many years ago and it inhibits relapses in MS. The down side is it has cardiotoxic effects which limits the amount of time you can take the drug and there is also high increased cancer risk. But again tells us that having relapses  is not good this is the case for both NMO and MS.

5 comments:

  1. I am taking Mitoxantrone (together with 5 x 2g Methylprednisolon) for the 2nd year now.

    So far so good. I had lots and hard relapses in 2010 every 6-8 weeks with differnet symptomes some of which are still present. But some symptomes are gone or lets say less dominant as they were 15 months ago.

    I still have Neuromyelitis Optica left (5-7% visus left) and some problems with my hands / fingers.

    Fun fact: my ejection fraction increased from 61 to 67% and no cardiotoxic effects can be seen.

    Any news on Pixantron (Mitoxantron derivate with less cardiotoxic effects)?

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  2. I don;t know about pixantron many prog G does, i guess it would need trials as a new drug

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    Replies
    1. http://en.wikipedia.org/wiki/Pixantrone

      Pixanatrone will probably work in the same way that mitoxantrone does, but who is going to do the studies necessary to get it licensed?

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    2. There are already some studies going on:

      http://www.fondation-charcot.org/view/en/activity/research.html

      But they stopped the studies in Germany because of "administrative issues":

      http://www.charcot-stichting.org/view/nl-en/Publications/2008-2009/nov2008_1.html

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  3. It seems even though interferons dont help nmo and nmo is a different disease to ms - lots of the treatments for nmo are helping ms so something in the two must be similar. I wouldn't be surprised if it turns out there are many subset types of ms like diseases and its how our bodies react to 'whatever' the brings on demyelination /degeneration which is why its so hard to find a cure it is lke looking for a needle in a haystack.
    Do nmo patients have EBV?

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