{"title":"Fibromyalgia Syndrome Review","authors":"M. Spaeth","doi":"10.3109/10582452.2013.855289","DOIUrl":null,"url":null,"abstract":"This investigation studied systemic inflammatory and stress responses, as well as the innate response mediated by monocytes and neutrophils in fibromyalgia syndrome [FMS] patients. Twenty five women diagnosed with primary FMS and 20 agematched healthy women [control group] were enrolled in the study. Circulating ‘‘neuroendocrinestress’’ biomarkers [corticotropin-releasing hormone, adrenocorticotropic hormone, cortisol, NA, eHsp72, serotonin, and insulin-like growth factor-1] were evaluated by enzyme-linked immunosorbent assay. Serum interkeukin [IL]-8 and C-reactive protein concentrations were also determined by enzyme-linked immunosorbent assay, and inflammatory cytokine release by monocytes [IL-1b, tumor necrosis factor a, IL-6, IL-10, IL-18, monocyte chemotactic protein-1 and RANTES] was evaluated by the Luminex BioPlex system. The phagocytic process of neutrophils [chemotaxis, phagocytosis, and microbicide capacity] was also evaluated. The FMS patients showed high circulating levels of IL-8 and C-reactive protein [in 100% of the FMS group], high circulating levels of cortisol, and increased systemic levels of NA and eHsp72. There is also increased release of inflammatory cytokines [IL-1b, tumor necrosis factor a, IL-6, IL-10, IL-18, and monocyte chemotactic protein-1] by monocytes, and enhanced activation of the functional capacity of neutrophils [chemotactic, phagocytic, and fungicidal activities]. The authors conclude that these findings showed an inflammatory state accompanied by an altered stress response in FMS patients, supporting the notion of an inflammatory/stress feedback dysregulation underlying FMS.","PeriodicalId":50121,"journal":{"name":"Journal of Musculoskeletal Pain","volume":"21 1","pages":"371 - 375"},"PeriodicalIF":0.0000,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10582452.2013.855289","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Musculoskeletal Pain","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/10582452.2013.855289","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
This investigation studied systemic inflammatory and stress responses, as well as the innate response mediated by monocytes and neutrophils in fibromyalgia syndrome [FMS] patients. Twenty five women diagnosed with primary FMS and 20 agematched healthy women [control group] were enrolled in the study. Circulating ‘‘neuroendocrinestress’’ biomarkers [corticotropin-releasing hormone, adrenocorticotropic hormone, cortisol, NA, eHsp72, serotonin, and insulin-like growth factor-1] were evaluated by enzyme-linked immunosorbent assay. Serum interkeukin [IL]-8 and C-reactive protein concentrations were also determined by enzyme-linked immunosorbent assay, and inflammatory cytokine release by monocytes [IL-1b, tumor necrosis factor a, IL-6, IL-10, IL-18, monocyte chemotactic protein-1 and RANTES] was evaluated by the Luminex BioPlex system. The phagocytic process of neutrophils [chemotaxis, phagocytosis, and microbicide capacity] was also evaluated. The FMS patients showed high circulating levels of IL-8 and C-reactive protein [in 100% of the FMS group], high circulating levels of cortisol, and increased systemic levels of NA and eHsp72. There is also increased release of inflammatory cytokines [IL-1b, tumor necrosis factor a, IL-6, IL-10, IL-18, and monocyte chemotactic protein-1] by monocytes, and enhanced activation of the functional capacity of neutrophils [chemotactic, phagocytic, and fungicidal activities]. The authors conclude that these findings showed an inflammatory state accompanied by an altered stress response in FMS patients, supporting the notion of an inflammatory/stress feedback dysregulation underlying FMS.