Monday, July 22, 2013

Dr. Michael Knops, Charité, Berlin: chronic immune activation in ME/CFS

HaupttitelCharakterisierung des phänotypischen und funktionellen Immunstatus bei Patienten mit Chronischem Erschöpfungssyndrom
TitelvariantePhenotypical and functional characterisation of immune status in patients with chronic fatigue syndrome
AutorKnops, Michael
Geburtsort: Köln
GutachterProf. Dr. med. C. Scheibenbogen
weitere GutachterPriv.-Doz. Dr. S. Engeli
Priv.-Doz. Dr. med. W. Jabs
Freie Schlagwörterchronic fatigue syndrome; t-cell activation; immune dysregulation; immunoglobuline deficiency; cytokine deviation


Zusammenfassend zeigen die vorliegenden Ergebnisse, dass Patienten mit einem chronischen Erschöpfungssyndrom eine chronische Immunaktivierung und eine Immundeviation zeigen, die eine Einteilung in vier immunologische Subgruppen zulassen. Diese Subgruppen sollten in prospektiven Studien weiter untersucht werden. Zudem wurde festgestellt, dass ein oxidativer und/oder nitrosativer Stress bei CFS-Patienten offenbar eine Rolle spielt, was im Rahmen weiterer Studien genauer untersucht werden sollte. Die neu gewonnenen Erkenntnisse tragen zum Verständnis der Pathogenese von CFS bei und sind Grundlage für die Entwicklung neuer Behandlungskonzepte.

google translated:

 In summary, the present results demonstrate that patients with chronic fatigue syndrome is a chronic immune activation and immune deviation show that allow a classification into four immunological subgroups.

These subgroups should be investigated in prospective studies. It was also noted that an oxidative and / or nitrosative stress in CFS patients appears to play a role, which should be further investigated as part of future studies. The newly gained knowledge contribute to understanding the pathogenesis of CFS and are the basis for the development of new treatment concepts.
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3 comments:

  1. Nice dig Dr SAM. Will share. " the present results demonstrate that patients with chronic fatigue syndrome is a chronic immune activation and immune deviation show that allow a classification into four immunological subgroups. These subgroups should be investigated in prospective studies. It was also noted that an oxidative and / or nitrosative stress in CFS patients appears to play a role, which should be further investigated as part of future studies."

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  2. 1. Any explanation involving "oxidative stress" or "nitrosative stress"("oxidativer und/oder nitrosativer Stress") makes me wary. This type of explanation is fashionable here in Germany for some people, but I would not bet my life on it.

    2. While they are citing these cellular "stresses" very prominently, the Knops/Scheibenbogen group did *not* themselves test anything in that area. They have no own data whatsoever for this nitro/ROS stress. They cite works of other people – people that I find dubious (to put it mildly).

    3. They did not use any healthy controls!!!! They compared the results of their patients against the lab reference ranges!!! Seriously, WTF???? And of course they did not compare it with other diseases. How do these results compare to those from MS patients? Or arthritis? A small group of controls from other diseases would have been interesting. What a wasted chance.

    4. Personally (mildly) interesting is the MCHC value (page 31) on the high side of the reference value that they did find (which coincides with my MCHC values that are consistent somewhere around 35.5 to 36). But this is not a result that is in anyway a slam dunk for "us".

    5. The values that they report are difficult to reconstruct. They should have used plots comparing results for CFS patients with results from healthy controls. By how much are the MCHC values increased in CFS patients? I don't know, as they don't report it. I would not have accepted a study that makes such important things not clear (but then again nobody cares about what I have to say).

    6. The immunology results (CD8, IL2, CD57-/CD8-, CD4, IL5) seem interesting. Whether these results can be reproduced in another group of CFS patients, nobody knows.

    7. The same goes for the IG subgroup deficits.

    8. The correllation between MCHC and the CD*/IL* results seems *very* interesting. But then again, how does this look for healthy controls? Or other diseases?

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