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Abstract: Cytokines Play an Aetiopathogenetic Role in Fibromyalgia: A Hypothesis and Pilot Study

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By D. J. Wallace, M. Linker-Israeli, D. Hallegua, S. Silverman, D. Silver and M. H. Weisman • www.ProHealth.com • December 21, 2001



Author Affiliations: Department of Medicine/Division of Rheumatology, Cedars–Sinai Medical Center/UCLA School of Medicine, Los Angeles, CA, USA


Objective. To measure soluble factors having a possible role in fibromyalgia (FM) and compare the profiles of patients with recent onset of the syndrome with patients with chronic FM.

Methods. The production of cytokines, cytokine-related molecules, and a CXC chemokine, interleukin (IL)-8, was examined. Fifty-six patients with FM (23 with <2 yr and 33 with >2 yr of symptoms) were compared with age- and sex-matched healthy controls. Cytokines and cytokine-related molecules were measured in sera and in supernatants of peripheral blood mononuclear cells (PBMC) that were incubated with and without lectins and phorbol myristate acetate (PMA).

Results. No differences between FMS and controls were found by measuring IL-1ß, IL-2, IL-10, serum IL-2 receptor (sIL-2R), interferon (IFN- ), and tumor necrosis factor (TNF- ). Levels of IL-1R antibody (IL-1Ra) and IL-8 were significantly higher in sera, and IL-1Ra and IL-6 were significantly higher in stimulated and unstimulated FM PBMC compared with controls. Serum IL-6 levels were comparable to those in controls, but were elevated in supernatants of in vitro-activated PBMC derived from patients with >2 yr of symptoms. In the presence of PMA, there were additional increases in IL-1Ra, IL-8 and IL-6 over control values.

Conclusions. In patients with FM we found increases over time in serum levels and/or PBMC-stimulated activity of soluble factors whose release is stimulated by substance P. Because IL-8 promotes sympathetic pain and IL-6 induces hyperalgesia, fatigue and depression, it is hypothesized that they may play a role in modulating FM symptoms.

Correspondence to: D. J. Wallace, 8737 Beverly Blvd Suite 203, Los Angeles, CA 90048, USA











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