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Plasma cytokine expression in adolescent chronic fatigue syndrome

Discussion in 'Latest ME/CFS Research' started by Denise, Jan 4, 2015.

  1. Denise

    Denise Senior Member

    Plasma cytokine expression in adolescent chronic fatigue syndrome
    • Chronic fatigue syndrome (CFS) might be related to altered cytokine expression.
    • A total of 120 adolescent CFS patients and 68 healthy controls were studied.
    • Individual cytokine levels where similar across the two groups.
    • Cytokine network parameters (ARACNE algorithm) were similar across the two groups.
    • In CFS patients, there were no associations between symptoms and network parameters.
    Chronic fatigue syndrome (CFS) is a prevalent and disabling condition among adolescents. The pathophysiology is poorly understood, but low-grade systemic inflammation has been suggested as an important component. This study compared circulating levels of individual cytokines and parameters of cytokine networks in a large set of adolescent CFS patients and healthy controls, and explored associations between cytokines and symptoms in the CFS group.

    CFS patients (12–18 years old) were recruited nation-wide to a single referral center as part of the NorCAPITAL project (ClinicalTrials ID: NCT01040429). A broad case definition of CFS was applied, requiring three months of unexplained, disabling chronic/relapsing fatigue of new onset, whereas no accompanying symptoms were necessary. Thus, the case definition was broader than the Fukuda-criteria of CFS. Healthy controls having comparable distribution of gender and age were recruited from local schools. Twenty-seven plasma cytokines, including interleukins, chemokines and growth factors were assayed using multiplex technology. The results were subjected to network analyses using the ARACNE algorithm. Symptoms were charted by a questionnaire, and patients were subgrouped according to the Fukuda-criteria.

    A total of 120 CFS patients and 68 healthy controls were included. CFS patients had higher scores for fatigue (p < 0.001) and inflammatory symptoms (p < 0.001) than healthy controls. All cytokine levels and cytokine network parameters were similar, and none of the differences were statistically different across the two groups, also when adjusting for adherence to the Fukuda criteria of CFS. Within the CFS group, there were no associations between aggregate cytokine network parameters and symptom scores.

    Adolescent CFS patients are burdened by symptoms that might suggest low-grade systemic inflammation, but plasma levels of individual cytokines as well as cytokine network measures were not different from healthy controls, and there were no associations between symptoms and cytokine expression in the CFS group. Low-grade systemic inflammation does not appear to be a central part of adolescent CFS pathophysiology.

    • Chronic fatigue syndrome;

    • Adolescent;

    • Inflammation;

    • Cytokine
    Corresponding author at: Dept. of Paediatrics, Akershus University Hospital, N-1478 Lørenskog, Norway. Tel.: +47 91 16 66 81.
    Copyright © 2014 Published by Elsevier Inc .

    In this study Wyller is applying a unique (to him?) definition - broader than Fukuda, more like Oxford with 3 months of fatigue as the only symptom required. :aghhh:
    Valentijn and Simon like this.
  2. deleder2k

    deleder2k Senior Member

    A story about LP and this in todays newspaper VG in Norway.

    This is some of the article;

    @Jonathan Edwards, I guess you agree with Fluge on this? When Wyller is speaking about inflammation, I guess he is referring to CRP? Isn't there a lot of autoimmune diseases with low or no changes in CRP?
    NK17 likes this.
  3. deleder2k

    deleder2k Senior Member

    This is a similar study which came to a different conclusion:

    Cytokine expression provides clues to the pathophysiology of Gulf War illness and myalgic encephalomyelitis.
    NK17 likes this.
  4. Jonathan Edwards

    Jonathan Edwards "Gibberish"

    Lots of autoimmune processes produce no inflammatory signs. I think somebody needs to do a bit of homework from basic medical textbooks. There is only inflammation if the effector mechanism whereby the antibody causes disease also triggers inflammatory mediator relase. There are several mechanisms where this does occur but scores of other mechanisms where it does not. Unfortunately immunology tends not to be a strong point with physicians - even with rheumatologists!
    LaPerla, NK17, aimossy and 6 others like this.

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