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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

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

In an overview of the problem of occupational muscle pain the evidence indicates that injury is more common the greater the load and the worse the posture in which the work is performed. The commonest are backstrains or ligament or joint damage due to overuse. Fatigue is associated with alterations in energy metabolites in muscle while pain is often due to microscopical damage to the cellular architecture. The progress of pathological changes in muscle following occupational injury may be similar to those seen in primary fibromyalgia (fibrositis) because of a final common pathway involving calcium-induced secondary damage. Occupational muscle pain frequently occurs in the muscles supporting the upper limb girdle and head in workers engaged in repetitively performing skilled manipulations or activities requiring high or sustained mental concentration. It is suggested that both occupational myalgia of this kind may be due to an imbalance in the use of muscles for postural activity (holding or supporting fine movements) compared to phasic use in dynamic work. While there are undoubtedly muscular indications of damage these may be secondary to alterations in (unconscious) central motor control mechanisms.
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PMID:Hypotheses of peripheral and central mechanisms underlying occupational muscle pain and injury. 328 51

It is suggested that chronic fatigue syndrome/fibromyalgia is caused by virus injury to the calcium channels leading to larger quantities than usual of calcium ions entering the striated muscle cells. Should this be true, then treatment with a calcium antagonist (CA) may possibly be of value.
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PMID:The etiology and possible treatment of chronic fatigue syndrome/fibromyalgia. 796 20

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

Calcium ions have a key role in the physiology of muscular contraction: changes in calcium ion concentration may be involved in the pathogenesis of fibromyalgia. Although, since the plasmatic level of calcium in fibromyalgia patients is always in the normal range, it seemed interesting to evaluate the intracellular calcium concentration. The study was carried out on two groups of subjects: 70 affected by fibromyalgia and 40 healthy controls. The results obtained show that in fibromyalgia patients the intracellular calcium concentration is significantly reduced in comparison to that of healthy controls: the reduced intracellular calcium concentration seems to be a peculiar characteristic of fibromyalgia patients and may be potentially responsible for muscular hypertonus. The effective role of this anomaly in the physiopathology of fibromyalgia and the potential role of drugs active on the calcium homeostasis are still to be confirmed.
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PMID:Role of intracellular calcium ions in the physiopathology of fibromyalgia syndrome. 1144 22

Building on the work of the late John Myers, MD, the author has used an intravenous vitamin-and-mineral formula for the treatment of a wide range of clinical conditions. The modified "Myers' cocktail," which consists of magnesium, calcium, B vitamins, and vitamin C, has been found to be effective against acute asthma attacks, migraines, fatigue (including chronic fatigue syndrome), fibromyalgia, acute muscle spasm, upper respiratory tract infections, chronic sinusitis, seasonal allergic rhinitis, cardiovascular disease, and other disorders. This paper presents a rationale for the therapeutic use of intravenous nutrients, reviews the relevant published clinical research, describes the author's clinical experiences, and discusses potential side effects and precautions.
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PMID:Intravenous nutrient therapy: the "Myers' cocktail". 1241 Jun 23

Characterized by chronic widespread joint and muscle pain, fibromyalgia is a syndrome of unknown etiology. The American College of Rheumatology's classification criteria for fibromyalgia include diffuse soft tissue pain of at least 3 months' duration and pain on palpation in at least 11 of 18 paired tender points. Symptoms are often exacerbated by exertion, stress, lack of sleep, and weather changes. Fibromyalgia is primarily a diagnosis of exclusion, established only after other causes of joint or muscle pain are ruled out. The initial workup for patients who present with widespread musculoskeletal pain should include a complete blood count, erythrocyte sedimentation rate, liver function tests, hepatitis C antibody, calcium, and thyrotropin. The musculoskeletal system, the neuroendocrine system, and the central nervous system, particularly the limbic system, appear to play major roles in the pathogenesis of fibromyalgia. The goal in treating fibromyalgia is to decrease pain and to increase function without promoting polypharmacy. Brief interdisciplinary programs have been shown to improve subjective pain. Fibromyalgia is a complex syndrome associated with significant impairment on quality of life and function and substantial financial costs. Once the diagnosis is made, providers should aim to increase patients' function and minimize pain. This can be accomplished through nonpharmacological ahd pharmacological interventions. With proper management, the rate of disability appears to be significantly reduced.
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PMID:A review of fibromyalgia. 1562 68

Gamma-hydroxybutyrate (GHB) is mainly known because of its popularity as a drug of abuse among young individuals. However this substance increases slow-wave deep sleep and the secretion of growth hormone and besides its role in anaesthesia, it is used in several therapeutic indications including alcohol withdrawal, control of daytime sleep attacks and cataplexy in narcoleptic patients and is proposed for the treatment of fibromyalgia. GHB is also an endogenous substance present in several organs, including brain where it is synthesized from GABA in cells containing glutamic acid decarboxylase, the marker of GABAergic neurons. GHB is accumulated by the vesicular inhibitory aminoacid transporter (VIAAT) and released by depolarization via a Ca2+ dependent-mechanism. A family of GHB receptors exists in brain which possesses hyperpolarizing properties through Ca2+ and K+ channels. These receptors--one of them has been recently cloned from rat brain hippocampus--are thought to regulate GABAergic activities via a subtle balance between sensitized/desensitized states. Massive absorption of GHB desensitize GHB receptors and this modification, together with a direct stimulation of GABAB receptors by GHB, induce a perturbation in GABA, dopamine and opiate releases in several region of the brain. This adaptation phenomenon is probably responsible for the therapeutic and recreative effects of exogenous GHB.
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PMID:[A mechanism for gamma-hydroxybutyrate (GHB) as a drug and a substance of abuse]. 1574 3

Wind-up is described traditionally as a frequency dependent increase in the excitability of spinal cord neurons, evoked by electrical stimulation of afferent C-fibers. Different kinds of wind-up have been reported, but wind-up of Abeta fibers in hyperalgesic states has gained little attention. In this paper, we present a cybernetic view on Abeta fiber wind-up and consider the involved molecular mechanisms as feedback and feedforward processes. Furthermore, our previous hypothesis, the sprouting phenomenon, is included in this view. Considering the proposed model, wind-up in hyperalgesic states might leave out in three different ways: (1) blocking the NMDA receptors by increasing extracellular Mg2+, 2) blocking the receptors and channels that contribute to Ca2+ inward current, and 3) blocking the Abeta fibers by local anesthetics. It seems that wind-up may be inhibited more effectively by using these three blocking mechanisms simultaneously, because in this case, the feedback process (main controller), the feedforward process (trigger), and Abeta stimulation (trigger) would be inhibited concurrently. Wind up may aggravate the pain in clinical hyperalgesic situations such as post-surgical states, some neuropathic pains, fibromyalgia syndrome, and post-herpetic neuralgia. Surely, clinical studies are needed to validate the effectiveness of our abovementioned suggestions in relieving such clinical pains.
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PMID:A cybernetic view on wind-up. 1656 45


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