Friday, 27 June 2014

First line drugs and Genes not much NEDA

Sellebjerg F, Søndergaard HB, Koch-Henriksen N, Sørensen PS, Oturai AB.Prediction of response to interferon therapy in multiple sclerosis. Acta Neurol Scand. 2014 Jun 18. doi: 10.1111/ane.12269. [Epub ahead of print]
OBJECTIVE:Single nucleotide polymorphisms (SNPs) in the genes encoding interferon response factor (IRF)-5, IRF-8 and glypican-5 (GPC5) have been associated with disease activity in multiple sclerosis (MS) patients treated with interferon (IFN)-β. We analysed whether SNPs in the IRF5, IRF8 and GPC5 genes are associated with clinical disease activity in MS patients beginning de novo treatment with IFN-β.
METHODS:The SNPs rs2004640, rs3807306 and rs4728142 in IRF5, rs13333054 and rs17445836 in IRF8 and rs10492503 in GPC5 were genotyped in 575 patients with relapsing-remitting MS followed prospectively after the initiation of their first treatment with IFN-β.
RESULTS:62% of patients experienced relapses during the first 2 years of treatment, and 32% had disability progression during the first 5 years of treatment. Patients with a pretreatment annualized relapse rate >1 had an increased risk of relapse (hazard ratio 1.53, 95% confidence interval 1.24-1.90) and progression (hazard ratio 1.48, 95% confidence interval 1.10-1.99) on treatment and patients with breakthrough relapses in the form of relapses during the first 2 years of treatment had an increased risk of progression during the first 5 years of treatment (hazard ratio 2.04, 95% confidence interval 1.47-2.85).The gene variants in IRF5, IRF8 and GPC5 were not associated with risk of relapse or disease progression.
CONCLUSIONS:Pretreatment relapse rate and clinical disease activity during the first 2 years of treatment may be associated with disease progression in MS patients treated with IFN-β. Genetic analysis of the studied gene variants do not provide additional information.



Predict who will respond and who will not respond to drugs is of interest to neuros treating you, but less of a concern to pharma who just want to sell to every one...which is rather disturbing that they are happy for you to pay for something that may be effectively useless. If you look in genes you maybe be able to work out who responds and who doesn't. This is called pharmacogenomics. Whilst this study they did not really find anything of interest in this respect it does show that 2% of patients experienced relapses during the first 2 years of treatment, and 32% had disability progression during the first 5 years of treatment and relapse history predicts relapse. This is hardly NEDA, is this what you want?

3 comments:

  1. Of course it's not what we want but neuros (including prof G) have been prescribing these injectible / ineffective drugs for some 20 years. I and all those who have the disease want to shut the activity down (inflammation, progression, relapse). Perhaps the question is are the researchers proud of what they have achieved over the last 50 years? (Given that the vast majority of MSers are on these ineffective drugs which were developed in research labs).

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  2. Some of these drugs are not effective enough that is clear, but it is unfair to blame researchers for what has or has not arrived in the therapeutic armoury, likewise neuros are restricted by the tools they have. Most researchers have little influence on what is or is not developed by pharma. When my colleague from QMUL was cloning human beta interferon little did he realize that it would be used in MS many years later. HE would have no clue if it was useful or not.

    but are researchers proud of what they have achieved, I suspect most are....and many researchers do not concern themselves with looking for treatments but disease mechanisms

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  3. This study mirrors my own situation and that is why I discontinued with interferons - its quite hard to convince the neuros though cos they stick to one med forever.

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