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)

To test the hypothesis that plasma tryptophan and/or its transport ratio is decreased in primary fibromyalgia (PF), we measured plasma tryptophan and its transport ratio in 29 patients with PF and 30 healthy controls without significant pain, in a blinded manner. Twenty-one other amino acids were also similarly analyzed among these study subjects. Transport ratio of tryptophan was found to be significantly (p less than 0.01) decreased in PF compared with the control group (0.09 +/- 0.02 vs 0.10 +/- 0.02). Plasma tryptophan level was lower in PF (45 +/- 10 nmol/ml) than in healthy controls (51 +/- 15 nmol/ml), showing a trend towards significance (p less than 0.09). Additionally, plasma histidine and serine levels were found to be significantly (p less than 0.01) lower in patients with PF than in controls. Our results suggest that a decreased brain serotonin level, as possibly reflected by a decreased transport ratio of plasma tryptophan, may play a pathophysiologic role in PF.
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PMID:Plasma tryptophan and other amino acids in primary fibromyalgia: a controlled study. 155 7

Free plasma tryptophan levels in patients with fibrositis syndrome were measured by Moldofsky and Warsh with the view that the pathogenesis of fibrositis syndrome might involve a functional deficiency of serotonin. The hypothesis was supported by the finding of an inverse relationship between tryptophan concentration and the severity of musculoskeletal pain. Our study examined the total serum amino acid pool in fibrositis syndrome. Twenty patients with primary fibrositis syndrome and matched normal controls were evaluated clinically. After denaturation of macromolecules, serum amino acids were quantitated by automated analysis. Patients with fibrositis syndrome exhibited significantly lower levels of total serum tryptophan (p = 0.002), as well as 6 other amino acids: alanine (p less than 0.0005), histidine (p = 0.001), lysine (p = 0.02), proline (p = 0.039), serine (p = 0.028), and threonine (p = 0.013). These findings support the serotonin deficiency hypothesis for fibrositis syndrome pathogenesis but also imply a more generalized defect in amino acid homeostasis among affected individuals.
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PMID:Serum amino acids in fibrositis/fibromyalgia syndrome. 260 10

Chronic fatigue syndrome (CFS) is a disorder that causes general fatigue and chronic widespread pain. A 28-year-old male visited an outpatient department due to general fatigue and pain involving the entire body. He did not suffer from fibromyalgia, but he was diagnosed with CFS. At the initial visit, he complained of lack of concentration, memory decline, frequent urination, insomnia and occasional difficulty of emotional control, as well as general fatigue and pain involving the entire body. Four tablets of Neurotropin per day alone were administered. General fatigue and pain were gradually alleviated one week later. His sleep condition, concentration power, and memory also improved two weeks later. Medication was discontinued from 11 weeks based on the patient's judgment as he felt little general fatigue and pain involving the entire body. Treatment was completed 3 months later. The symptoms disappeared and did not recur five months after the discontinuation of Neurotropin. He was looking for a job without fatigue and pain 8 months later (5 months after the cessation of treatment). The functional mechanisms of Neurotropin in CFS are unknown.
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PMID:Efficacy of neurotropin in chronic fatigue syndrome: a case report. 1659 51

Alfred Nobel never spoke publicly about his problems of ill health, but a detailed, subjective record has recently been published in the form of 216 letters written to his mistress during an 18-year period. His descriptions of constant pain, debilitating migraine, and "paralyzing" fatigue permit a hypothesis that he might have had a long struggle with fibromyalgia. This does not preclude his having suffered other illnesses as well. He thought he had heart disease, which his physicians denied until his final years, when he was diagnosed with angina pectoris. He died of a cerebral hemorrhage in 1896 at the age of 63. His letters describe a 30-year search for diagnosis from the best physicians in Europe. He was ridiculed by many people as a hypochondriac, and he never received a diagnosis for "the pain that will not go away." This may well have contributed to the bitterness and depression of his final years. Increasing worldwide interest and research in this elusive syndrome will hopefully prevent a repetition of the Nobel story of a century ago.
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PMID:Alfred nobel. 1907 79