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)

Thyroid function was tested in 13 female patients with primary fibromyalgia syndrome (FS) and 10 healthy age matched controls by intravenous injection of 400 micrograms thyrotropin-releasing hormone (TRH). Basal thyroid hormone levels of both groups were in the normal range. However, patients with primary FS responded with a significantly lower secretion of thyrotropin and thyroid hormones to TRH, within an observation period of 2 h, and reacted with a significantly higher increase of prolactin. Total and free serum calcium and calcitonin levels were significantly lower in patients with primary FS, while both groups exhibited parathyroid hormone levels in the normal range.
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PMID:Thyroid function in patients with fibromyalgia syndrome. 151 69

The cerebrospinal fluid (CSF) levels of calcitonin gene related peptide (CGRP) were 0.94 +/- 0.06 fmol/ml (mean +/- SEM), of substance P, 35.1 +/- 3.2 fmol/ml and of substance P (1-7), 10.8 +/- 1.2 fmol/ml, as measured by radioimmunoassay in 26 female patients with fibromyalgia. No correlation was found between the levels of CGRP and the substance P and substance P (1-7) levels (r = 0.316, p = 0.14). Our results show that the anatomical coexistence of pain related neuropeptides in neurons is not necessarily reflected by the levels of these peptides measured in the CSF. The presence of CGRP in the CSF could be important since it can enhance the nociceptive activity of tachykinins. This may be of importance in the pathogenesis of pain in fibromyalgia.
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PMID:Modulation of pain in fibromyalgia (fibrositis syndrome): cerebrospinal fluid (CSF) investigation of pain related neuropeptides with special reference to calcitonin gene related peptide (CGRP). 248 42

Different changes in neurotransmitters were observed in patients with fibromyalgia. The aim of the study was to confirm the diagnosis fibromyalgia by determination of several of these substances. In 60 patients, who met the ACR classification criteria for fibromyalgia and in 20 sex and age matched controls the following estimations were made: serotonin (EIA), somatomedin C (RIA), calcitonin (RIA), prostaglandin E2 (EIA), oxytocin (RIA), ACTH (RIA), substance P (EIA), TSH (LIA), prolactin (LIA). In comparison to healthy controls, patients with fibromyalgia revealed significantly decreased levels of serotonin, somatomedin C, calcitonin, prostaglandin E2 and a significantly increased level of prolactin. No significant differences were found in the levels of ACTH, substance P and TSH. These results suggest that the diagnosis of fibromyalgia can be confirmed by various biochemical parameters, but further investigations must be carried out to value the diagnostic relevance of these findings.
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PMID:[Biochemical changes in fibromyalgia]. 876 46

The objective of this study was to evaluate the relative efficacy and tolerability of subcutaneously (s.c.) administered salmon calcitonin (sCT) in the treatment of patients with fibromyalgia. Eleven patients who fulfilled the American College of Rheumatology classification criteria for fibromyalgia were studied in a double-blind, crossover trial in which they alternatively received salmon calcitonin (100 IU s.c.) and isotonic saline (1 cc s.c.) for four weeks, with a four weeks wash-out period between the treatments. None of the 11 outcomes measures (seven analog scales, dolorimetry score, and three SIP scores) showed a significant improvement with sCT. The principal side effect observed with sCT was nausea in ten patients and erythema in four patients. These data suggest that sCT given at a dose of 100 IU daily for one month is not effective in the treatment of fibromyalgia.
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PMID:A placebo controlled crossover trial of subcutaneous salmon calcitonin in the treatment of patients with fibromyalgia. 957 36

C-fiber nociceptors not only serve afferent but also local efferent functions. The local efferent functions, such as vasodilatation, axon reflex flare reaction, plasma extravasation, and modulation of neuronal activity, are mediated via a local release of substance P, neurokinin A, and calcitonin gene-related peptide (CGRP) from the peripheral ending. CGRP is the main mediator of the capsaicin-induced flare reaction in the mammalian skin (including humans). In the pig skin the vasodilatation is due to activation of specific heat nociceptors. In the pigeon, antidromic vasodilatation is markedly inhibited by intrinsic galanin. Plasma extravasation in the pig skin blister base or using microdialysis can be evoked by histamine, but not by electrical stimulation or capsaicin. The neurogenic component of the histamine response (64%) appears to be mediated via NK2 receptors and can be modulated by CGRP. There is some evidence that the neuropeptides can also sensitize or stimulate nociceptors. Since in the fibromyalgia syndrome an increased sensitivity of the flare reaction has been observed, the hyperalgesia might be partly due to altered functions of C-fiber nociceptors.
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PMID:Efferent functions of C-fiber nociceptors. 1002 74

Orofacial pain frequently originates from pathologic conditions in the masticatory muscles or temporomandibular joints (TMJs). The mediators and mechanisms that monitor pain and inflammation, centrally or peripherally, are of great interest in the search for new treatment modalities. The neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), and neuropeptide Y (NPY) have all been found at high levels in the synovial fluid of arthritic TMJs in association with spontaneous pain, while serotonin (5-HT) has been found in association with hyperalgesia/allodynia of the TMJ. Interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) have been found in arthritic TMJs, but not in healthy TMJs, in association with hyperalgesia/allodynia of the TMJ as well as spontaneous pain. Anterior open bite, which may be a clinical sign of TMJ destruction, has been found in association with high levels of CGRP, NPY, and IL-1 beta in the synovial fluid of the TMJ. Interleukin-1 beta has also been related to radiographic signs of joint destruction. Prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are both present in the arthritic TMJ, and PGE2 has been shown to be associated with hyperalgesia/allodynia of the TMJ. Very little is known about pain and inflammatory mediators in muscles. However, we know that 5-HT and PGE2 are involved in the development of pain and hyperalgesia/allodynia of the masseter muscle in patients with fibromyalgia, whereas local myalgia (myofascial pain) seems to be modulated by other, as yet unknown mediators. Interaction between the peripheral nervous system (sensory and sympathetic nerves), the immune system, and local cells is probably of great importance for the modulation of pain and inflammation in the TMJ and orofacial musculature.
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PMID:Neuroendocrine, immune, and local responses related to temporomandibular disorders. 1188 48

The impressive pain relief experienced by sufferers of dystonia and spasticity from intramuscular injections of botulinum toxin suggested that patients with other chronic, musculoskeletal pain conditions also may benefit. However, there have been relatively few placebo-controlled studies of botulinum toxin in such non-neurologic conditions as myofascial pain syndrome, chronic neck and low back pain, and fibromyalgia; the results of these studies have not been impressive. One explanation for the lack of positive findings may be the lack of clinically evident muscle spasms (overactivity), despite the presence of muscle tenderness, tightness, or trigger points. Clinical observations of pain relief from injections of botulinum toxin for dystonia and spasticity and its apparent efficacy in treating migraine suggest an anti-nociceptive action independent of its neuromuscular junction-blocking action. Evidence from animal experiments supports this notion, and other data provide plausible physiologic mechanisms in the periphery and central nervous systems. These involve modulation of the activity of the neurotransmitters glutamate, substance P, calcitonin gene-related peptide, enkephalins, and others. However, even if botulinum toxin is firmly established as an analgesic, there is insufficient clinical evidence of its efficacy in treating non-neurologic, chronic, musculoskeletal pain conditions.
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PMID:Botulinum toxin for the treatment of musculoskeletal pain and spasm. 1241 5

Acupuncture has become a widely used treatment modality in various musculoskeletal pain conditions. Acupuncture is also shown to enhance blood flow and recovery in surgical flaps. The mechanisms behind the effect on blood flow were suggested to rely on vasoactive substances, such as calcitonin gene-related peptide, released from nociceptors by the needle stimulation. In a previous study on healthy subjects, one needle stimulation into the anterior tibial muscle was shown to increase both skin and muscle blood flow. The aim of this study was to examine the effect of needle stimulation on local blood flow in the anterior tibial muscle and overlying skin in patients suffering from a widespread chronic pain condition. Fifteen patients with fibromyalgia (FM) participated in the study. Two modes of needling, deep muscle stimulation and subcutaneous needle insertion were performed at the upper anterior aspect of the tibia, i.e., in an area without focal pathology or ongoing pain in these patients. Blood flow changes were assessed non-invasively by photoplethysmography (PPG). The results of the present study were partly similar to those earlier found at a corresponding site in healthy female subjects, i.e., deep muscle stimulation resulted in larger increase in skin blood flow (mean (SE)): 62.4% (13.0) and muscle blood flow: 93.1% (18.6), compared to baseline, than did subcutaneous insertion (mean (SE) skin blood flow increase: 26.4% (6.2); muscle blood flow increase: 46.1% (10.2)). However, in FM patients subcutaneous needle insertion was followed by a significant increase in both skin and muscle blood flow, in contrast to findings in healthy subjects where no significant blood flow increase was found following the subcutaneous needling. The different results of subcutaneous needling between the groups (skin blood flow: p=0.008; muscle blood flow: p=0.027) may be related to a greater sensitivity to pain and other somatosensory input in FM.
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PMID:Peripheral effects of needle stimulation (acupuncture) on skin and muscle blood flow in fibromyalgia. 1498 26

The therapy of pain caused by rheumatic diseases above all must take into consideration the cause of the pain. In rheumatoid arthritis, especially in the early stages, inflammation is the primary cause of the pain. The pain decreases the inflammation subsides following the administration of non-steroidal anti-inflammatory drugs (NSAIDs), or corticosteroids, if necessary. The so-called disease modifying anti-rheumatic drugs do not influence the inflammation or consequently, the pain directly, but rather through mechanisms before the local joint process some of which are not exactly known. In later stages of the progressive joint degeneration the NSAIDs only have a limited effect regarding the inhibition of inflammation. In osteoarthrosis, in which the pain is caused by a secondary inflammation and increasingly by capsular, muscular and tendon involvement, the pain is only treated by NSAIDs in active inflammatory stages; otherwise, the treatment is physical activity and medication. In degenerative and static disorders of the spine the pain is caused predominantly by muscular bracing. Therefore, physical and especially gymnastic therapy play a major role. Whether muscle relaxants have an effect on muscle bracing is doubtful. If there is pressure on the ligaments and, in cases of vertebral dislocation with overstraining of the vertebral joints, therapy with local injections is indicated. The pain in osteoporosis is also predominantly muscular and must be treated accordingly. Above all, high doses of calcium and calcitonin are effective analgesics. Moreover, fluoride also acts as an analgesic once the osteoporosis has stabilized. In most cases fibromyalgia, which is mostly of a psychosomatic nature, cannot be influenced by medical therapy. Instead repeated attempts at treatment help to make the affliction chronic with neurotic fixation. Also, as a rule, myotonolytic and tranquilizing substances are not effective.
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PMID:[The therapy of pain in rheumatic joint-and spine diseases.]. 1841 50

A number of pain conditions, acute as well as chronic, are much more prevalent in women, such as temporomandibular disorder (TMD), irritable bowel syndrome, fibromyalgia, and migraine. The association of female sex steroids with these nociceptive conditions is well known, but the mechanisms of their effects on pain signaling are yet to be deciphered. We reviewed the mechanisms through which female sex steroids might influence the trigeminal nociceptive pathways with a focus on migraine. Sex steroid receptors are located in trigeminal circuits, providing the molecular substrate for direct effects. In addition to classical genomic effects, sex steroids exert rapid nongenomic actions to modulate nociceptive signaling. Although there are only a handful of studies that have directly addressed the effect of sex hormones in animal models of migraine, the putative mechanisms can be extrapolated from observations in animal models of other trigeminal pain disorders, like TMD. Sex hormones may regulate sensitization of trigeminal neurons by modulating expression of nociceptive mediator such as calcitonin gene-related peptide. Its expression is mostly positively regulated by estrogen, although a few studies also report an inverse relationship. Serotonin (5-Hydroxytryptamine [5-HT]) is a neurotransmitter implicated in migraine; its synthesis is enhanced in most parts of brain by estrogen, which increases expression of the rate-limiting enzyme tryptophan hydroxylase and decreases expression of the serotonin re-uptake transporter. Downstream signaling, including extracellular signal-regulated kinase activation, calcium-dependent mechanisms, and cAMP response element-binding activation, are thought to be the major signaling events affected by sex hormones. These findings need to be confirmed in migraine-specific animal models that may also provide clues to additional ion channels, neuropeptides, and intracellular signaling cascades that contribute to the increased prevalence of migraine in women.
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PMID:Mechanisms of pain modulation by sex hormones in migraine. 2163 76


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