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Fibromyalgia, Hepatitis C Infection
and the Cytokine Connection

September 12, 2003

Fibromyalgia and chronic hepatitis C infection share many clinical features including prominent somatic complaints such as musculo-skeletal pain and fatigue. There is a growing body of evidence supporting a link between cytokines and somatic complaints.

This review by researchers in the Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University, discusses alterations of cytokines in fibromyalgia, including increased serum levels of interleukin (IL)-2, IL-2 receptor, IL-8, IL-1 receptor antagonist; increased IL-1 and IL-6 produced by stimulated peripheral blood mononuclear cell in patients with FM for longer than 2 years. Other cytokine alterations discussed include

increased gp130, which is a neutrophil cytokine transducing protein;
increased soluble IL-6 receptor and soluble IL-1 receptor antagonist only in patients with fibromyalgia who are depressed; and
IL-1 beta, IL-6, and TNF-a by reverse transcriptase-polymerase chain reaction in skin biopsies of some patients with fibromyalgia.

In addition, this review describes the mechanism by which alterations in cytokines in fibromyalgia and chronic hepatitis C infection can produce hyperalgesia and other neurally mediated symptoms through the presence of cytokine receptors on glial cells and opiate receptors on lymphocytes and the influence of cytokines on the hypothalamus-pituitary-adrenal axis such as IL-1, IL-6, and TNF-a activating and IL-2 and IFN-a down-regulating the HPA axis, respectively.

The association between chronic hepatitis C infection and fibromyalgia is discussed, including a description of key cytokine changes in chronic hepatitis C infection. Future studies are encouraged to further characterize these immunologic alterations with potential pathophysiologic and therapeutic implications.

ME Thompson and Abarkhuizen. Fibromyalgia, hepatitis C infection, and the cytokine connection. Current Pain and Headache Reports 7(5): 342-347. October 2003.



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