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)

31Phosphorous nuclear magnetic resonance (31P NMR) spectroscopy of painful calf muscle was performed in 12 patients with fibromyalgia (FS) and 7 healthy subjects during rest, aerobic and anaerobic exercising conditions, and postexercise recovery. Ratios of inorganic phosphate and creatinine phosphate (Pi/PCr) and pH were calculated from the collected 31P NMR spectra. Resting values of Pi/PCr were normal in the patients. Patients delivered only 49% of the muscle power of the controls (p = 0.005). Patients and controls had similar rates of Pi/PCr and pH changes during work and recovery. The controls were able to change their Pi/PCr and pH more than the patients, due to the greater workload reached. However, statistical significance was reached only for the anaerobic static exercise (p = 0.003). It was concluded that patients with FS have a reduced voluntary capacity for work, but normal biochemical response to work and recovery.
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PMID:31P magnetic resonance spectroscopy of skeletal muscle in patients with fibromyalgia. 817 65

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

31P Magnetic Resonance-Spectroscopy was performed at the site of tender points in the trapezius muscle of patients with primary fibromyalgia syndrome. Earlier, in vitro studies have reported changes in the high energy phosphate-metabolism in biopsies taken from tender points of fibromyalgia patients. The observed alterations could not be confirmed with in vivo Magnetic Resonance-Spectroscopy.
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PMID:In vivo 31P magnetic resonance spectroscopy (MRS) of tender points in patients with primary fibromyalgia syndrome. 194 70

Virtually all the reports on muscle biopsy in chronic muscle pain conditions, except those of primary fibromyalgia syndrome (PFS) published recently, have inadequate methodologic information, particularly on definition of cases, and lack controlled materials, so that no firm conclusions may be made. A limited number of controlled studies of muscle biopsy in PFS suggest that results are negative by usual light microscopic, histochemical, and electron microscope examinations. The findings of abnormal rubber band-like structures and interconnecting network of reticular or elastic fibers in muscle fibers of certain PFS patients in a single study need to be confirmed by other centers by careful controlled and blinded observations. The findings that high-energy phosphate levels in tender PFS muscles are significantly reduced appear valid and important, and need to be independently confirmed by well-designed controlled and blinded studies. Finally, biopsy reports of unspecified or unclarified muscle pain syndromes should not be assumed to be those related to PFS, and such invalid references must be avoided.
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PMID:Muscle biopsy findings in primary fibromyalgia and other forms of nonarticular rheumatism. 264 73

31phosphorus nuclear magnetic resonance (31P NMR) spectroscopy of painful calf muscle was performed in 12 patients with fibromyalgia and 7 healthy subjects during rest, aerobic and anaerobic exercising conditions, and postexercise recovery. Ratios of inorganic phosphate and creatine phosphate (Pi/PCr) and pH were calculated from the collected 31P NMR spectra. Resting values of Pi/PCr were normal in the patients. Patients only tolerated 49% of the workload tolerated by the controls (P = 0.005). Patients and controls had similar rates of Pi/PCr and pH changes during work and recovery. The controls were able to change their Pi/PCr and pH more than the patients, due to the greater workload reached. However, statistical significance was only reached for the anaerobic static exercise (P = 0.003). It was concluded that fibromyalgia patients have a reduced voluntary capacity for work, but with a biochemical response to work and recovery similar to healthy subjects.
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PMID:[Magnetic resonance spectroscopy in fibromyalgia. A study of phosphate-31 spectra from skeletal muscles during rest and after exercise]. 783 99

This article describes the use of combining spectral electromyographic signal techniques with phosphorus magnetic resonance (31P-NMR) spectroscopy for the purpose of studying muscle disorders. The quantification of muscle fatigue by electromyographic spectral variables such as the median frequency is summarized. Its development as a laboratory and clinical tool is presented, with an emphasis toward its potential as an assessment procedure. Similarly, the use of 31P-NMR spectroscopy for noninvasive measurement of phosphate metabolites and intracellular pH during fatigue are described. The limitations of this procedure are presented and compared with surface electromyographic techniques. Suggestions are made for combining these techniques for the purpose of monitoring muscle metabolic and electrophysiologic changes in situ during fatiguing exercises. A recent study in which these techniques were combined to evaluate the underlying mechanisms of fatigue in patients with fibromyalgia is described.
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PMID:Combined use of surface electromyography and 31P-NMR spectroscopy for the study of muscle disorders. 824 97

Physical inactivity accelerates bone loss. Since patients with fibromyalgia are relatively physically inactive, bone mass and markers of bone metabolism were determined in 12 premenopausal women with fibromyalgia and in healthy age matched female control subjects. No differences were found in lumbar bone mineral density, femoral neck bone mineral density, serum levels of alkaline phosphatase, osteocalcin, ionized calcium and phosphate. The urinary excretion of both hydroxyproline and calcium relative to urinary creatinine excretion was significantly higher in patients with fibromyalgia, p = 0.01. This was linked to lower urinary creatinine excretion (p = 0.02) probably reflecting lower physical activity in the patients with fibromyalgia. We conclude that bone mass and turnover are generally not affected in premenopausal women with fibromyalgia.
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PMID:Bone mass and turnover in fibromyalgia. 833 12

Muscle tissue oxygen tension was measured by a polarographic oxygen fine-needle probe, and inorganic phosphate and creatine phosphate spectra were recorded using magnetic resonance spectroscopy in patients with chronic low back pain and in patients with fibromyalgia. Results were compared with healthy controls. The tissue oxygen tension was markedly higher in those with tense muscles than in normal subjects. Magnetic resonance spectra for inorganic phosphate were higher in patients demonstrating muscle contraction, and intracellular pH was shifted in the alkaline direction in cases with increased muscle tension. Results show that hypoxia is not the result of increased muscle tension, as was thought previously, but results from oversupply of oxygen demanded by the muscle, leading to increased capillary perfusion and rising oxygen tension.
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PMID:Tissue oxygen measurement and 31P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia. 903 15

Fibromyalgia, a chronic condition of widespread pain, stiffness, and fatigue, has proven unresponsive to drugs, the use of which is based on the 'serotonin-deficiency hypothesis'. An alternative hypothesis-failed transcription regulation by thyroid hormone-can explain the serotonin deficiency and other objective findings and symptoms of euthyroid fibromyalgia. Virtually every feature of fibromyalgia corresponds to signs or symptoms associated with failed transcription regulation by thyroid hormone. In hypothyroid fibromyalgia, failed transcription regulation would result from thyroid-hormone deficiency. In euthyroid fibromyalgia, failed transcription regulation may result from low-affinity thyroid hormone receptors coded by a mutated c-erbA beta 1 gene, yielding partial peripheral resistance to thyroid hormone. The hypothesis of this paper is that, in euthyroid fibromyalgia, a mutant c-erbA beta 1 gene (or alternately, the c-erbA alpha 1 gene) results in low-affinity thyroid-hormone receptors that prevent normal thyroid hormone regulation of transcription. As in hypothyroidism, this would cause a shift toward alpha-adrenergic dominance and increases in both cyclic adenosine 3'-5'-phosphate phosphodiesterase and inhibitory Gi proteins. The result would be tissue-specific hypothyroid-like symptoms despite normal circulating thyroid-hormone levels.
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PMID:Mutations in the c-erbA beta 1 gene: do they underlie euthyroid fibromyalgia? 907 94

Fibroblast growth factor 23 (FGF23), a recently discovered phosphaturic substance playing a key role in genetic and oncogenic phosphate diabetes, is involved in the physiological regulation of phosphate metabolism. Moderate idiopathic phosphate diabetes (IPD) leading to male osteoporosis and diffuse pain resembling fibromyalgia has been described. The aim of our study was to define the role of FGF23 in the mechanism of IPD. The study concerned 29 patients with IPD, mean age 53 +/- 11 years, of whom 72% were men. Fifteen subjects without bone disease and with normal serum phosphate and calcium levels were used as controls. Phosphate diabetes was confirmed by phosphate reabsorption level <85% and phosphate reabsorption threshold (TmPO4/GFR) <0.83. Known causes of phosphate diabetes were excluded. Fasting level of FGF23, serum phosphate, 1-25(OH)2D3, and parathyroid hormone were measured in patients and compared with FGF23 and serum phosphate in healthy controls. Spinal and hip bone mineral density (BMD) were measured by osteodensitometry. Sixteen of 29 patients had diffuse pain, 10 had osteoporosis according to the World Health Organization criteria, and 11 had osteopenia. Serum phosphate was significantly lower in patients than in controls, but FGF23 levels did not differ. Compared to patients with normal bone status, patients with osteopenia and osteoporosis had significantly decreased FGF23 levels, whereas serum phosphate was identical in the two groups. In all patients, serum phosphate and FGF23 were positively correlated and FGF23 and 1-25(OH)2D3 were negatively correlated. FGF23 seems not be a cause of IPD, and the FGF23/phosphate/1-25(OH)2D3 axis appeared to be functional.
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PMID:Normal FGF23 levels in adult idiopathic phosphate diabetes. 1914 64


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