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