Evaluation of the Relationship between Proinflammatory Cytokine Levels and Clinical Findings of Fibromyalgia Syndrome, 2021, Ellergezen et al

Discussion in ''Conditions related to ME/CFS' news and research' started by Andy, Dec 22, 2021.

  1. Andy

    Andy Committee Member

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    Abstract

    Background: Immune system has an important effect on pain-related disorders such as fibromyalgia syndrome (FMS). There is no specific laboratory technique for the diagnosis of FMS, but measuring serum proinflammatory cytokines may help.

    Objective: The purpose of our study was to determine the serum levels of immune mediators and their relationship with FMS symptoms.

    Methods: 25 healthy individuals and 29 FMS patients receiving pregabalin 150 mg/day for a minimum of 3 months were included in this study. FMS patients were diagnosed according to diagnostic criteria of the American College of Rheumatology (ACR 2010). Widespread pain index (WSI), fatigue, waking unrefreshed, cognitive symptoms, somatic symptoms, and Fibromyalgia Impact Questionnaire (FIQ) scores were evaluated in patients with FMS. Serum levels of proinflammatory cytokines (IL-2, IL-6, IL-12, IL-17, IFN-γ, TNF-α) were assessed using enzyme-linked immunosorbent assay (ELISA).

    Results: Proinflammatory cytokine levels were higher in the control group than patients with FMS (P<0.05). A positive correlation was found between age and WSI (P=0.037). In addition, a significant positive relationship was determined between IL-17 level and waking unrefreshed (P=0.049). There was no significant relationship between other cytokines and clinical findings.

    Conclusion: Lower proinflammatory cytokine levels identified in FMS patients may be related to pregabalin treatment, and there may be an impairment in the inflammatory response. On the contrary, IL-17 showed positive correlation with waking unrefreshed.

    At time of posting, PubMed abstract only, https://pubmed.ncbi.nlm.nih.gov/34931619/
     
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  2. rvallee

    rvallee Senior Member (Voting Rights)

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    Looking for inflammatory molecules in a population taking an anti-inflammatory drug seems a bit misguided. One useful conclusion could be made of how pregabalin works, if it does reduce some inflammatory proteins, it's not as if the function of these drugs was well understood, as clearly most "anti-depressants" seem to have immune modulating properties more than anything. Otherwise I fail to see what the point even was when the results would be skewed by design. If at least if was a half-half cohort that could have been useful.

    Odd.
     

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