Friday, 23 October 2015

Meta Analysis of the Week time is it Shat ing

Yang C, Hao Z, Zhang L, Zeng L, Wen JSodium channel blockers for neuroprotection in multiple sclerosis. Cochrane Database Syst Rev. 2015 Oct 21;10:CD010422. [Epub ahead of print] BACKGROUND:

Multiple sclerosis (MS) is an autoimmune, inflammatory, demyelinating disease of the central nervous system (CNS), which can occur in many parts of the CNS and result in a wide range of symptoms including sensory impairment, fatigue, walking or balance problems, visual impairment, vertigo and cognitive disabilities. At present, the most commonly used MS treatments are immunomodulating agents, but they have little effect on the disability. Experimental studies show that sodium (Na+) accumulation leads to intracellular calcium (Ca2+) release, and the increased calcium levels can activate nitric oxide synthase and harmful proteases and lipases. These factors contribute to axonal injury in people with MS. If partial blockade of voltage-gated sodium channels could result in neuroprotection, this would be of benefit for preventing disability progression in these people. Neuroprotection is emerging as a potentially important strategy for preventing disability progression in people with MS.
To assess the efficacy and safety of sodium channel blockers for neuroprotection in people with MS to prevent the occurrence of disability and alleviate the burden of the disease.
MAIN RESULTS: Only one study evaluating lamotrigine in secondary progressive MS was eligible. One hundred and twenty people were included, 61 randomly assigned to lamotrigine treatment and 59 to placebo treatment. The average age of participants in the two groups was 51.9 years and 50.1 years, respectively. The proportion of male participants was 27.5%. The period of follow-up was 2 years. No data were found on disability progression and people who experienced relapses. No significant differences were found for serious adverse events between the two groups. Treatment with lamotrigine was associated with more rashes (20% vs 5%, P value 0.03) and transient, dose-related deterioration of mobility (66% vs 34%, P value 0.001) than placebo. Furthermore, no significant difference between the two groups was found in the magnetic resonance imaging (MRI) measurements of cerebral atrophy, Expanded Disability Status Score changes, Multiple Sclerosis Functional Composite score changes. This study was judged to be at high risk of bias. This review will be updated when the three ongoing studies we identified are completed.
AUTHORS' CONCLUSIONS: The quality of evidence was judged to be very low due to the low number of available studies and included participants. There is a lack of evidence to address the review question on the efficacy of sodium channel blockers for people with MS. Assessment of the three ongoing trials might change this conclusion. Further high-quality large scale studies are needed.

If more people were doing posts, I may be tempted to do EAE cure of the week.  No! I hear you say. Mr.Angry would be having more pointless rants 

But it is the treatment of the future. Or we take it apart a pile of pants and I get a kicking from our peers.

However it looks like we do meta-analysis of the week....No I hear me say....Mr Angry is happy to say EAE research is rubbish but maybe time to look at the meta anlaysis by our neuros. 

EAE studies are hard work and cost loads to do...Meta analysis cost little and is paper fodder for Neuros. 

However as Keith Lemon would say..."Sha ting"...I would say "Shat Out".

Prof G says don't believe every thing you read. 

I agree If you do data analysis like a robot, you get results that come from the bot:-).

Do sodium channels blockers save nerves. You do a search and find one paper and you analyse it and conclude that it shows it does not work.....

However, you understand what this is doing and out see that the outcomes are not fit for purpose because it is based on atrophy by MRI. 

This shrinks more than the placebo because it is anti-inflammatory and gets rid of water...but you really do a search and you find that 50% in the trial were not taking their drug and then you realise that it is not worth doing the analysis 

Then you read that in the people taking the drug there was less neurofilaments in their blood so they were losing less nerves and hey the drug works... So your meta analysis is worthless. 

You do abit of focused reading and it means you do a trial in optic neuritis and it works to save nerves.... then who needs meta analysis? 


  1. just like the cladribine meta-analysis- pure fodder!

    1. Not really.......because this is the type of data that will be used to try and convince the regulators that they made a mistake and that cladribine should not have been rejected by the FDA./EMA

      Merck Serono has a copy, which is independent of them, which they will add to their portfolia as the go back to the EMA with movectro.

      Likewise it can be used for other purposes

      Hugs & Kisses XXXXX

    2. but the conclusions aren't definite, stats not rigorous.
      loveyoueventhoughyourworkisn'tperfect xxxx

    3. Well, as the Dude would say, "Well, that's just your opinion, man."

    4. How can conclusions be definite...they can't be

      P.S. Dan Altmann is one of the best MS statisticians in the World
      Loveyoumorethoughyouarefullof Hugs & Kisses XXXX

      Would Merck Serono be trying to resurrect Movectro if they really thought it causes cancer. Our analysis questions this and the other three trials published at AAN 2014 showed this not to be the case.

      Presumably they also have the real-life data from follow up of people in Russia and Australia.

      Maybe you are a rep trying to make sure that the mud sticks.

    5. can you put up some links of previous meta-analyses altmann has published?
      lovethatyoudon'tunderstandstatistics xxxx

    6. Even better, why not contact Dan Altmann directly with your concerns?


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