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)

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

In the second part of their article on the emerging field of neuroimmunology, the authors present an overview of the role of neuroimmune mechanisms in defence against infectious diseases and in immune disorders. During acute febrile illness, immune-derived cytokines initiate an acute phase response, which is characterized by fever, inactivity, fatigue, anorexia and catabolism. Profound neuroendocrine and metabolic changes take place: acute phase proteins are produced in the liver, bone marrow function and the metabolic activity of leukocytes are greatly increased, and specific immune reactivity is suppressed. Defects in regulatory processes, which are fundamental to immune disorders and inflammatory diseases, may lie in the immune system, the neuro endocrine system or both. Defects in the hypothalamus-pituitary-adrenal axis have been observed in autoimmune and rheumatic diseases, chronic inflammatory disease, chronic fatigue syndrome and fibromyalgia. Prolactin levels are often elevated in patients with systemic lupus erythematosus and other autoimmune diseases, whereas the bioactivity of prolactin is decreased in patients with rheumatoid arthritis. Levels of sex hormones and thyroid hormone are decreased during severe inflammatory disease. Defective neural regulation of inflammation likely plays a pathogenic role in allergy and asthma, in the symmetrical form of rheumatoid arthritis and in gastrointestinal inflammatory disease. A better understanding of neuroimmunoregulation holds the promise of new approaches to the treatment of immune and inflammatory diseases with the use of hormones, neurotransmitters, neuropeptides and drugs that modulate these newly recognized immune regulators.
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PMID:Neuroimmune mechanisms in health and disease: 2. Disease. 887 36

Somatic symptom disorder is excessive anxiety towards persistent symptoms that do not have an identifiable physical origin. Fibromyalgia is a stress-related illness. The overwhelming majority of fibromyalgia patients seeking medical care are women. Most fibromyalgia sufferers fulfil the somatic symptom disorder diagnostic criteria. The objectives of this article are the following: 1) to examine fibromyalgia and somatic symptom disorder analogy. 2) to discuss stress-evoked neuropathic pain sexual dimorphism, and 3) to propose a neuropathic pathogenesis that may explain how stressed women could develop fibromyalgia. Recent research demonstrates a clear link between fibromyalgia and small fibre neuropathy. Dorsal root ganglia contain the small nerve fibre nuclei. In rodents, physical, chemical, or environmental stressors lead to dorsal root ganglia phenotypic changes and to hyperalgesia. This phenomenon is much more frequent in females. Prolactin, oestrogens, and progesterone alter dorsal root ganglia physiology, establishing abnormal connections between the stress response system and pain pathways. Rather than a mental somatic symptom disorder, fibromyalgia patients may have a stress-induced neuropathic pain syndrome. Sexually dimorphic dorsal root ganglia physiology may explain why it is women who more often develop fibromyalgia. Understanding fibromyalgia as a real stress-evoked neuropathic pain syndrome may lead to more compassionate patient care and may open new avenues for gender-related neuropathic pain investigation.
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PMID:Fibromyalgia in women: somatisation or stress-evoked, sex-dimorphic neuropathic pain? 3294 Feb 5