Research Article Unique Cytokine Signature in the Plasma of Patients with Fibromyalgia Jamie Sturgill, 1,2 Elizabeth McGee, 2,3 and Victoria Menzies 1,2 1 School of Nursing, Virginia Commonwealth University, Richmond, VA 23298, USA 2 Institute of Women’s Health, Virginia Commonwealth University, Richmond, VA 23298, USA 3 Department of Obstetrics, Gynecology and Reproductive Sciences, University of Vermont, Burlington, VT 05401, USA Correspondence should be addressed to Jamie Sturgill; sturgilljl@vcu.edu Received 19 November 2013; Revised 28 January 2014; Accepted 5 February 2014; Published 11 March 2014 Academic Editor: Jong-Young Kwak Copyright © 2014 Jamie Sturgill et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fibromyalgia (FMS) is a chronic pain syndrome with a complex but poorly understood pathogenesis afecting approximately 10 million adults in the United States. he lack of a clear etiology of FMS has limited the efective diagnosis and treatment of this debilitating condition. he objective of this secondary data analysis was to examine plasma cytokine levels in women with FMS using the Bio-Plex Human Cytokine 17-plex Assay. Post hoc analysis of plasma cytokine levels was performed to evaluate patterns that were not speciied a priori. Upon examination, patients with FMS exhibited a marked reduction in T H 2 cytokines such as IL-4, IL-5, and IL-13. he inding of this pattern of altered cytokine milieu not only supports the role of inlammation in FMS but also may lead to more deinitive diagnostic tools for clinicians treating FMS. he T H 2 suppression provides strong evidence of immune dysregulation in patients with FMS. 1. Introduction Fibromyalgia (FMS) is a chronic pain syndrome in which pathogenesis is complex and cure is not known. It afects approximately 10 million adults in the United States with an estimated 90% of diagnoses being reported in women [1]. he symptom proile of FMS includes pain, fatigue, and distressed mood. Sequelae of FMS include physical and psychological distress, loss of work productivity, reduced quality of life, and increased use of health resources. Annual expenditures for the diagnosis and treatment of FMS are estimated at approximately $20 billion, thus presenting a signiicant bur- den to patients, their families, and society [2, 3]. Although the incidence of FMS is rising, the etiology remains unclear. A major theory is that inlammatory mediators lead to complex neuroendocrine aberrations of the hypothalamic-pituitary- adrenal (HPA) axis [4]. Altered levels of cytokines have been associated with symptoms of pain, fatigue, and distressed mood in multiple conditions including painful peripheral neuropathies, hepatitis C, cardiovascular disease, and cancer [3, 5, 6]. his symptom proile mimics the representative symptoms of FMS. hus, it is theoretically plausible that these nonspeciic inlammatory mediators may also contribute to the symptoms of pain, fatigue, and distressed mood in FMS. To date, results of studies examining the association of cytokine alterations with FMS and its symptoms have been mixed [7–9]. Although researchers have suggested FMS as being an inlammatory state related to a dysregulated immune system or altered stress response, the pathophysio- logical role of cytokines continues to remain unclear [9, 10]. Because there are no diagnostic markers for FMS as well as no identiied etiology for the development of FMS, researchers are still searching for mechanistic signs to identify those who already have or those who are at risk for developing ibromyalgia. T helper lymphocytes are deined by expressing the cell surface molecule known as CD4 and are subdivided further based on the cytokines that they produce. he discovery of the T H 1 and T H 2 paradigm [11] was a pivotal breakthrough in the ield of immunology. his balance and counterbalance of inlammatory mediators were delineated and ultimately led to fundamental additions to the knowledge base of cytokine Hindawi Publishing Corporation Journal of Immunology Research Volume 2014, Article ID 938576, 5 pages http://dx.doi.org/10.1155/2014/938576