Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-2 (IL-2) production was studied in T lymphocytes and isolated CD4+ T lymphocytes from 12 patients with primary fibromyalgia syndrome and 10 healthy volunteers. The dose and time kinetics of IL-2 production by concanavalin A-stimulated T cells and CD4+ T cells of fibromyalgia patients differed from findings in controls by 1) a need for a higher concentration of mitogen in order to achieve optimal IL-2 secretion, and 2) a delay in the peak time of optimal IL-2 secretion. Unlike normal IL-2 secretion, which was higher after removal of CD8+ T cells, the pattern and degree of IL-2 secretion by cells from fibromyalgia patients were not changed following removal of CD8+ T cells. Addition of calcium ionophore in assays using suboptimal concanavalin A concentrations did not correct the reduction in IL-2 secretion by fibromyalgia patient T cells, but addition of phorbol myristate acetate induced normal secretion of IL-2. These findings suggest that there is a defect in the IL-2 pathway, which is related to protein kinase C activation and does not involve impairment of Ca2+ elevation, in patients with fibromyalgia.
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PMID:Altered interleukin-2 secretion in patients with primary fibromyalgia syndrome. 167 63

Cells of the immune system synthesize prolactin and express mRNA and receptors for that hormone. Interleukin 1, interleukin 6, gamma interferon, tumor necrosis factor, platelet activator factor, and substance P participate in the release of prolactin. This hormone is involved in the pathogenesis of adjuvant arthritis and restores immunocompetence in experimental models. In vitro studies suggest that lymphocytes are an important target tissue for circulating prolactin. Prolactin antibodies inhibit lymphocyte proliferation. Prolactin is comitogenic with concanavalin A and induces interleukin 2 receptors on the surface of lymphocytes. Prolactin stimulates ornithine decarboxylase and activates protein kinase C, which are pivotal enzymes in the differentiation, proliferation, and function of lymphocytes. Cyclosporine A interferes with prolactin binding to its receptors on lymphocytes. Hyperprolactinemia has been found in patients with systemic lupus erythematosus. Fibromyalgia, rheumatoid arthritis, and low back pain patients present a hyperprolactinemic response to thyrotropin-releasing hormone. Experimental autoimmune uveitis, as well as patients with uveitis whether or not associated with spondyloarthropathies, and patients with psoriatic arthritis may respond to bromocriptine treatment. Suppression of circulating prolactin by bromocriptine appears to improve the immunosuppressive effect of cyclosporine A with significantly less toxicity. Prolactin may also be a new marker of rejection in heart-transplant patients. This body of evidence may have an impact in the study of rheumatic disorders, especially connective tissue diseases. A role for prolactin in autoimmune diseases remains to be demonstrated.
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PMID:Prolactin, immunoregulation, and autoimmune diseases. 206 74

To verify whether vagal dysfunction is associated with chronic pain, we evaluated the effects of subdiaphragmatic vagotomy (vgx) on the sensitivity toward noxious stimuli in rats. Vgx rats showed sustained hyperalgesia in the gastrocnemius muscle without tissue damage (no increase in vgx-induced plasma creatine phosphokinase or lactose dehydrogenase levels) accompanied by hypersensitivity to colonic distension. We found a dramatic increase in the levels of metabotropic glutamate receptor 5, protein kinase C (PKC) gamma and phosphorylated-PKCgamma within the spinal cord dorsal horn in vgx rats, which suggests that vgx may evoke sensory nerve plasticity. Morphine produced a dose-dependent increase in the withdrawal threshold in both vgx and sham-operated rats, but the effect of a lower dose in vgx rats was weaker than that in sham-operated rats. Muscle hyperalgesia in vgx rats was also attenuated by gabapentin and amitriptyline, but was not affected by diclofenac, dexamethasone or diazepam. These findings indicate that subdiaphragmatic vagal dysfunction caused chronic muscle hyperalgesia accompanied by visceral pain and both gabapentin and amitriptyline were effective for subdiaphragmatic vagotomy-induced pain, which are partially similar to fibromyalgia syndrome. Furthermore, this chronic muscle pain may result from nociceptive neuroplasticity of the spinal cord dorsal horn.
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PMID:Subdiaphragmatic vagotomy promotes nociceptive sensitivity of deep tissue in rats. 1977 96

The transition from acute to chronic pain states might be the most important challenge in research to improve clinical treatment of debilitating pain. We describe a recently identified mechanism of neuronal plasticity in primary afferent nociceptive nerve fibers (nociceptors) by which an acute inflammatory insult or environmental stressor can trigger long-lasting hypersensitivity of nociceptors to inflammatory cytokines. This phenomenon, "hyperalgesic priming," depends on the epsilon isoform of protein kinase C (PKCepsilon) and a switch in intracellular signaling pathways that mediate cytokine-induced nociceptor hyperexcitability. We discuss the impact of this discovery on our understanding of, and ultimately our ability to treat, a variety of enigmatic and debilitating pain conditions, including those associated with repetitive injury, and generalized pain conditions, such as fibromyalgia.
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PMID:Critical role of nociceptor plasticity in chronic pain. 1978 93