Hepatitis C and Fibromyalgia

First, Happy Nurses Day! To all my nursing colleagues out there, thanks for your tireless efforts on behalf of patients everywhere. Nursing is a demanding profession; heavy in the hard sciences and skillful in the art of working with human beings. You have my full respect and admiration!

One of my fellow Nurse Practitioners attended a conference about Fibromyalgia, one of those diseases that are very difficult to diagnose and understand. Lately, I've been having a lot more joint and muscle pain and I just thought it was because I've been more active. When you have HCV, it takes your muscles much longer to recover from strenuous activity, so I chalked it up to doing more. Then I spoke with Erin and I thought twice about the fibromyalgia connection. I've been reading up on it and it does make sense, pathophysiologically. Here is an excerpt from an article I found in Medline (from PubMed), for your reading pleasure:

Fibromyalgia, hepatitis C infection, and the cytokine connection.

Thompson ME, Barkhuizen A.

Source

Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University, 3181 Sam Jackson Park Road OP-09, Portland, OR 97239, USA. thompsmo@ohsu.edu

Abstract

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