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      Machine Learning to Understand the Immune-Inflammatory Pathways in Fibromyalgia

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          Abstract

          Fibromyalgia (FM) is a chronic syndrome characterized by widespread musculoskeletal pain, and physical and emotional symptoms. Although its pathophysiology is largely unknown, immune-inflammatory pathways may be involved. We examined serum interleukin (IL)-6, high sensitivity C-reactive protein (hs-CRP), CXCL-8, and IL-10 in 67 female FM patients and 35 healthy women while adjusting for age, body mass index (BMI), and comorbid disorders. We scored the Fibromyalgia Severity Score, Widespread Pain Index (WPI), Symptom Severity Scale (SSS), Hospital Anxiety (HADS-A), and Depression Scale and the Perceived Stress Scale (PSS-10). Clinical rating scales were significantly higher in FM patients than in controls. After adjusting for covariates, IL-6, IL-10, and CXCL-8 were lower in FM than in HC, whereas hs-CRP did not show any difference. Binary regression analyses showed that the diagnosis FM was associated with lowered IL-10, quality of sleep, aerobic activities, and increased HADS-A and comorbidities. Neural networks showed that WPI was best predicted by quality of sleep, PSS-10, HADS-A, and the cytokines, while SSS was best predicted by PSS-10, HADS-A, and IL-10. Lowered levels of cytokines are associated with FM independently from confounders. Lowered IL-6 and IL-10 signaling may play a role in the pathophysiology of FM.

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          Most cited references52

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          Changes in proinflammatory cytokine activity after menopause.

          There is now a large body of evidence suggesting that the decline in ovarian function with menopause is associated with spontaneous increases in proinflammatory cytokines. The cytokines that have obtained the most attention are IL-1, IL-6, and TNF-alpha. The exact mechanisms by which estrogen interferes with cytokine activity are still incompletely known but may potentially include interactions of the ER with other transcription factors, modulation of nitric oxide activity, antioxidative effects, plasma membrane actions, and changes in immune cell function. Experimental and clinical studies strongly support a link between the increased state of proinflammatory cytokine activity and postmenopausal bone loss. Preliminary evidence suggests that these changes also might be relevant to vascular homeostasis and the development of atherosclerosis. Better knowledge of the mechanisms and the time course of these interactions may open new avenues for the prevention and treatment of some of the most prevalent and important disorders in postmenopausal women.
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            Fibromyalgia.

            Fibromyalgia is a common illness characterized by chronic widespread pain, sleep problems (including unrefreshing sleep), physical exhaustion and cognitive difficulties. The definition, pathogenesis and treatment are controversial, and some even contest the existence of this disorder. In 1990, the American College of Rheumatology (ACR) defined classification criteria that required multiple tender points (areas of tenderness occurring in muscles and muscle-tendon junctions) and chronic widespread pain. In 2010, the ACR preliminary diagnostic criteria excluded tender points, allowed less extensive pain and placed reliance on patient-reported somatic symptoms and cognitive difficulties. Fibromyalgia occurs in all populations worldwide, and symptom prevalence ranges between 2% and 4% in the general population. The prevalence of people who are actually diagnosed with fibromyalgia ('administrative prevalence') is much lower. A model of fibromyalgia pathogenesis has been suggested in which biological and psychosocial variables interact to influence the predisposition, triggering and aggravation of a chronic disease, but the details are unclear. Diagnosis requires the history of a typical cluster of symptoms and the exclusion of a somatic disease that sufficiently explains the symptoms by medical examination. Current evidence-based guidelines emphasize the value of multimodal treatments, which encompass both non-pharmacological and selected pharmacological treatments tailored to individual symptoms, including pain, fatigue, sleep problems and mood problems. For an illustrated summary of this Primer, visit: http://go.nature.com/LIBdDX.
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              Systematic review with meta-analysis: cytokines in fibromyalgia syndrome

              Background To perform a systematic review and meta-analysis on cytokine levels in patients with fibromyalgia syndrome (FMS). Methods Through December 2010 we systematically reviewed the databases PubMed, MEDLINE, and PsycINFO and screened the reference lists of 22 review articles for suitable original articles. Original articles investigating cytokines in patients with FMS were included. Data were extracted by two independent authors. Differences of the cytokine levels of FMS patients and controls were summarized by standardized mean differences (SMD) using a random effects model. Study quality was assessed applying methodological scores: modified Center of Evidence Based Medicine, Newcastle-Ottawa-Scale, and Würzburg Methodological Quality Score. Results Twenty-five articles were included investigating 1255 FMS patients and 800 healthy controls. Data of 13/25 studies entered meta-analysis. The overall methodological quality of studies was low. The results of the majority of studies were not comparable because methods, investigated material, and investigated target cytokines differed. Systematic review of the selected 25 articles revealed that FMS patients had higher serum levels of interleukin (IL)-1 receptor antagonist, IL-6, and IL-8, and higher plasma levels of IL-8. Meta-analysis of eligible studies showed that FMS patients had higher plasma IL-6 levels compared to controls (SMD = -0.34 [-0.64, -0.03] 95% CI; p = 0.03). The majority of investigated cytokines were not different between patients and controls. Conclusions The pathophysiological role of cytokines in FMS is still unclear. Studies of higher quality and with higher numbers of subjects are needed.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                29 August 2019
                September 2019
                : 20
                : 17
                : 4231
                Affiliations
                [1 ]Group of Psychological Research in Fibromyalgia & Chronic Pain (AGORA), Institut de Recerca Sant Joan de Déu, 08950 Esplugues de Llobregat, Spain
                [2 ]Teaching, Research & Innovation Unit, Parc Sanitari Sant Joan de Déu, 08830 St. Boi de Llobregat, Spain
                [3 ]Primary Care Prevention and Health Promotion Research Network, RedIAPP, 28013 Madrid, Spain
                [4 ]Faculty of Psychology, Universitat Autònoma de Barcelona, 08193 Bellaterra (Cerdanyola del Vallès Barcelona, Spain
                [5 ]Department of Rheumatology, Parc Sanitari Sant Joan de Déu, 08830 St. Boi de Llobregat, Spain
                [6 ]Parc Sanitari Sant Joan de Déu, CIBERSAM, 08950 Sant Boi de llobregat, Spain
                [7 ]Department of Psychiatry, Miguel Servet Hospital, Aragon Institute of Health Sciences (I+CS), 50009 Zaragoza, Spain
                [8 ]Department of Psychiatry, Chulalongkorn University, Bangkok 10330, Thailand
                Author notes
                [* ]Correspondence: a.feliu@ 123456pssjd.org (A.F.-S.); ap.aranda@pssjd (A.P.-A.); Michael.Ma@ 123456chula.ac.th (M.M.); jvluciano@ 123456pssjd.org (J.V.L.); Tel.: +93-640-6350 (A.F.-S.)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-5133-9811
                https://orcid.org/0000-0003-3972-1385
                https://orcid.org/0000-0003-2810-7670
                https://orcid.org/0000-0003-3927-8803
                https://orcid.org/0000-0001-5677-1662
                https://orcid.org/0000-0003-0750-1599
                Article
                ijms-20-04231
                10.3390/ijms20174231
                6747258
                31470635
                75079ce5-87a0-4b99-9c47-fdad86f5b989
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 08 August 2019
                : 26 August 2019
                Categories
                Article

                Molecular biology
                fibromyalgia,widespread pain,cytokines,inflammation,neuro-immune
                Molecular biology
                fibromyalgia, widespread pain, cytokines, inflammation, neuro-immune

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