FancyMyBlood
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I just stumbled on this Norwegian blog that talks about ME/CFS research. Unfortunately, Google Translate is still far away from perfect translations but this is what I got out of it:
- Mella and Fluge are doing an new trial with etanercept (a TNF-inhibitor). They're giving 50mg injections weekly for 52 weeks. 15 non-responders will be recruited out of earlier rituximab studies. After 12 months there will be a follow-up, so the study ends in 2014. Unfortunately it doesn't seem to be placebo-controlled. They hypothesize that the amount of auto-antibodies in the rituximab trial was too high and etanercept may be a alternative treatment. As a second hypothesis they believe that activated T-cells play an important role in symptoms maintenance. Etanercept will 'hit' other facets of autoimmunity, not related to B-cells. At last they hypothesize that some non-responders do fulfill ME/CFS diagnostic criteria but don't have an immunological mediated profile. So a psychological condition with fatigue symptoms.
- The Norwegian health authorities have written an annual report about research projects. Olav Mella was a research director and it states that the rituximab trial supports the hypothesis that ME/CFS is an illness with immune dysregulation, probably caused by auto-immune mechanism(s). The clinical results with a 3-8 month delay seem to indicate a gradually elimination of auto-antibodies. The clinical picture suggests involvement of the nervous system, probably a malfunction is neurotransmission. They then talk about systematically mapping auto-antibodies in sera of patients in their clinical studies and then Google Translate makes it gibberish. It seems to say something about cDNA expression, rat brains, West-immunoblot and immunohistology. Then it get's even more gibberish, which is very unfortunate because it looks like interesting new information (it's about advanced proteomic analysis, 2D electoblabla).
It becomes readable again when they say they have analysis of 50 cytokines in 2011 sera samples of patients pre-treatment. These samples will be used as a basis for the analysis of selected cytokines at a 12 month follow-up after B-cell depletion. They've also started with measuring lymphocytes gene expression after a standarized physical stress test in patient with mild to moderate ME/CFS. They're using RT-PCR - Taqman and the same technique is also used for measure EBV in patients. In collaboration with a Berlin university they measured immunoreactivity against EBV (several and epitopes on the virus), before and after 8 months of rituximab treatment. Both responders and non-responders participated in this. Thanks to the Kavli foundation the search for mechanism and biomarkers will be intensivated in 2012!
There is more on the blog, but it's too much effort to type it all out ATM (reading takes about 5 minutes, typing it out about half an hour!). I hope I translated it alright, if not hopefully a Norwegian patient can correct me and complement the gibberish translations
- Mella and Fluge are doing an new trial with etanercept (a TNF-inhibitor). They're giving 50mg injections weekly for 52 weeks. 15 non-responders will be recruited out of earlier rituximab studies. After 12 months there will be a follow-up, so the study ends in 2014. Unfortunately it doesn't seem to be placebo-controlled. They hypothesize that the amount of auto-antibodies in the rituximab trial was too high and etanercept may be a alternative treatment. As a second hypothesis they believe that activated T-cells play an important role in symptoms maintenance. Etanercept will 'hit' other facets of autoimmunity, not related to B-cells. At last they hypothesize that some non-responders do fulfill ME/CFS diagnostic criteria but don't have an immunological mediated profile. So a psychological condition with fatigue symptoms.
- The Norwegian health authorities have written an annual report about research projects. Olav Mella was a research director and it states that the rituximab trial supports the hypothesis that ME/CFS is an illness with immune dysregulation, probably caused by auto-immune mechanism(s). The clinical results with a 3-8 month delay seem to indicate a gradually elimination of auto-antibodies. The clinical picture suggests involvement of the nervous system, probably a malfunction is neurotransmission. They then talk about systematically mapping auto-antibodies in sera of patients in their clinical studies and then Google Translate makes it gibberish. It seems to say something about cDNA expression, rat brains, West-immunoblot and immunohistology. Then it get's even more gibberish, which is very unfortunate because it looks like interesting new information (it's about advanced proteomic analysis, 2D electoblabla).
It becomes readable again when they say they have analysis of 50 cytokines in 2011 sera samples of patients pre-treatment. These samples will be used as a basis for the analysis of selected cytokines at a 12 month follow-up after B-cell depletion. They've also started with measuring lymphocytes gene expression after a standarized physical stress test in patient with mild to moderate ME/CFS. They're using RT-PCR - Taqman and the same technique is also used for measure EBV in patients. In collaboration with a Berlin university they measured immunoreactivity against EBV (several and epitopes on the virus), before and after 8 months of rituximab treatment. Both responders and non-responders participated in this. Thanks to the Kavli foundation the search for mechanism and biomarkers will be intensivated in 2012!
There is more on the blog, but it's too much effort to type it all out ATM (reading takes about 5 minutes, typing it out about half an hour!). I hope I translated it alright, if not hopefully a Norwegian patient can correct me and complement the gibberish translations