Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term fibromyalgia, though often used, is not justified since no fibrosis has been shown on the histological level. The aim of this article is to make a critical analysis of the semiology usually attributed to fibromyalgias, to cite the main related syndromes whose nosology is often unclear (benign myalgic encephalomyelitis, epidemic neuromyasthenia, diffuse idiopathic multifocal pain syndrome, chronic fatigue, AMP desaminase deficiency, etc.), to prefer the purely descriptive term of "persistent, diffuse myalgia with no recognized organic etiology". According to the author's experience, a psychological etiology is detectable in only 25% of the cases. Morphological or functional muscular abnormalities are sometimes found, but their significance is not well known. A real multifactorial vicious circle partly explains the physiopathological complexity.
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PMID:[Does fibromyalgia exist?]. 218 44

A young, previously healthy woman presented with increasing muscle pain, lower limb swelling, fatigue and eosinophilia. She had consumed L-tryptophan tablets (one to two at night) over the preceding five months for management of her insomnia. Her condition slowly deteriorated and she developed generalised oedema and severe lethargy. A white blood cell count was 21.3 x 10(9)/L with 43% eosinophils (Normal range: 4.0-11.0 x 10(9)/L with 1-6% eosinophils. A biopsy specimen of the deep fascia and gastrocnemius muscle demonstrated fasciitis and myositis. The patient failed to recover after cessation of L-tryptophan use but her condition improved rapidly without significant sequelae after systemic treatment with corticosteroids.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 199 19

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

Based on the report of some activity of combination therapy with dacarbazine (DTIC) and interferon alpha-2a (rIFN alpha-2a) in disseminated melanoma, we conducted a phase II study to determine the feasibility and efficacy in a large series of patients. DTIC was administered in 79 patients at the dose of 800 mg/m2 every 3 weeks and rIFN alpha-2a was given daily at the dose of 9 X 10(6) IU for the first 10 weeks and three times a week thereafter. Among the 75 evaluable patients, 25% achieved an objective response, with 8% complete and 17% partial remissions. The regression occurred within a mean time of 1.9 +/- 1.03 months from starting therapy and the mean duration of response was 8.2 +/- 4.2 months. The major side effects were vomiting, anorexia, fever, fatigue, and myalgia. There was one death related to sepsis after myelosuppression. In the other patients bone marrow and liver toxicities were not remarkable. Our data reveal that a combination regimen of rIFN alpha-2a with a cytotoxic agent has some therapeutic activity in the management of advanced malignant melanoma.
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PMID:Phase II study of interferon alpha-2a and dacarbazine in advanced melanoma. 222 Jun 60

Four patients fulfilling the case definition for eosinophilia-myalgia syndrome are described, including one whose disease began in 1986. Each displayed a variety of symptoms: one suffered principally from myalgia and recovered spontaneously on discontinuation of L-tryptophan therapy; one exhibited progressive sclerodermiform skin changes, neuropathy, and myopathy; a third had prominent neuromuscular disease and sclerodermiform skin changes; and the fourth experienced profound weight loss, an axonal polyneuropathy, and perivascular lymphoid infiltrates simulating a lymphoma. Evidence of T-cell activation was present in peripheral blood and affected tissues during the clinically active progressive phase of disease. Among other manifestations pleural effusion, cutaneous vasculitis, joint contractures, and bloody diarrhea were observed. A history of L-tryptophan ingestion should be sought in patients with myalgia, fatigue, or the above outlined symptoms.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Analysis of four patients and implications for differential diagnosis and pathogenesis. 217 45

This study investigated the effects of terminating low dose levels of caffeine (100 mg/day) in 7 normal humans. Substitution of placebo capsules for caffeine capsules occurred under double-blind conditions while subjects rated various dimensions of their mood and behavior. In the first phase of the study, substitution of placebo for 12 consecutive days resulted in an orderly withdrawal syndrome in 4 subjects which peaked on days 1 or 2 and progressively decreased toward prewithdrawal levels over about 1 week. Data from the remaining three subjects provided no evidence of withdrawal. In the second phase of the study, the generality of the withdrawal effect was examined by repeatedly substituting placebo for 100 mg/day of caffeine for 1-day periods separated by an average of 9 days. Despite differences within and across subjects with respect to the presence, nature and magnitude of symptoms, each of the seven subjects demonstrated a statistically significant withdrawal effect. Although the phenomenon of caffeine withdrawal has been described previously, the present report documents that the incidence of caffeine withdrawal is higher (100% of subjects), the daily dose level at which withdrawal occurs is lower (roughly equivalent to the amount of caffeine in a single cup of strong brewed coffee or 3 cans of caffeinated soft drink) and the range of symptoms experienced is broader (including headache, fatigue and other dysphoric mood changes, muscle pain/stiffness, flu-like feelings, nausea/vomiting and craving for caffeine) than heretofore recognized.
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PMID:Low-dose caffeine physical dependence in humans. 226 96

Metabolic fatigue is a characteristic muscle response to intense exercise that has outstripped the rate of ATP replacement. The accumulation of metabolic by-products, namely hydrogen ions and diprotonated phosphate, interferes with actin-myosin interaction, effectively preserving muscle ATP levels by preventing further ATP hydrolysis. Muscle force and metabolite concentrations return to normal in about 5 minutes. Less intense exercise causes a more subtle, non-metabolic fatigue due to a still-undefined disturbance of excitation-contraction coupling, which can last for several hours. In this type of fatigue, greater effort is required to generate submaximal forces. Endurance exercise is mainly limited by the size of muscle glycogen stores and how efficiently they are used. Endurance training permits an athlete to work aerobically at high rates, consuming a mixture of lipid and carbohydrate fuels. When muscle glycogen is used up, exercise can only continue at the relatively low rate supportable by lipid metabolism. Anaerobic exercise is also limited by subjective factors such as dyspnoea and muscle pain, which have objective determinants. Extremely prolonged exercise can lead to general collapse because of dehydration, hyperthermia, or hypoglycaemia. None of these factors explains the phenomenon of asthenia, a subjective sense of exhaustion that produces no objective impairment of physical performance. The metabolic myopathies are experiments of nature that promise to shed new light on the biochemical basis of muscle fatigue. This will require quantitative studies of the kind provided by topical magnetic resonance spectroscopy, correlating physiology and metabolism in vivo.
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PMID:Muscle metabolism during fatigue and work. 226 24

Sixty-three adults with the diagnosis of the postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study of essential fatty acid therapy. The patients had been ill for from one to three years after an apparently viral infection, suffering from severe fatigue, myalgia and a variety of psychiatric symptoms. The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids and either it, or the placebo, was given as 8 x 500 mg capsules per day over a 3-month period. The trial was parallel in design and patients were evaluated at entry, one month and three months. In consultation with the patient the doctors assessed overall condition, fatigue, myalgia, dizziness, poor concentration and depression on a 3-point scale. The essential fatty acid composition of their red cell membrane phospholipids was analysed at the first and last visits. At 1 month, 74% of patients on active treatment and 23% of those on placebo assessed themselves as improved over the baseline, with the improvement being much greater in the former. At 3 months the corresponding figures were 85% and 17% (p less than 0.0001) since the placebo group had reverted towards the baseline state while those in the active group showed continued improvement. The essential fatty acid levels were abnormal at the baseline and corrected by active treatment. There were no adverse events. We conclude that essential fatty acids provide a rational, safe and effective treatment for patients with the post-viral fatigue syndrome.
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PMID:Effect of high doses of essential fatty acids on the postviral fatigue syndrome. 227 Jul 49

The eosinophilia-myalgia syndrome associated with the use of oral preparations of the amino acid L-tryptophan was recognized in late 1989. We describe the clinical and laboratory manifestations, pathological findings and early clinical course of 20 patients with the eosinophilia-myalgia syndrome. Prominent clinical findings included severe myalgias limiting function, fatigue, rashes, edema and weight gain, weight loss, muscle weakness and shortness of breath. Laboratory findings included eosinophilia (often marked), normal erythrocyte sedimentation rate, and elevated aldolase with normal or low creatine kinase values. On biopsy fascial inflammation was always seen consisting of lymphocytes, histiocytes and eosinophils in a perivascular distribution. Invasion of the vascular wall by lymphocytes was seen in 20%. Capillary and arteriolar endothelial cell thickening was found in most cases on electron microscopy and endothelial cell necrosis or mural invasion by lymphocytes was seen in 25% of cases. Two patients improved with no therapy. Ten patients responded to therapy with prednisone alone. Three patients have had progressive disease and one of these died. The relationship of this syndrome to previously described disease entities associated with eosinophilia is discussed.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 227 99

We describe an epidemic of self-limited (6 weeks) thyrotoxicosis which affected 12 index cases, 5 household contacts, and 6 retrospectively identified cases in July, August, and September, 1987 in the town of Winterswijk (28,011 inhabitants), The Netherlands. A small goiter was present in 9 of the 12 index patients, tender upon palpation in only 2. Signs and symptoms of thyrotoxicosis were accompanied by a low grade fever in combination with fatigue, headache, myalgia, and a fine desquamation of the palms and soles. The apparent incubation time between family members was 6 days. Thyroid technetium uptake was decreased in 10 of 11 tested patients. Laboratory findings included elevated sedimentation rates (up to 68 mm/h), increased liver enzymes, lymphopenia in 2 patients, and absence of thyroid autoantibodies. HLA-B35, associated with classical subacute thyroiditis, was found in 1 patient only. An etiological agent was not identified. No evidence was found for thyrotoxicosis factitia. After 10 months, all patients were euthyroid, without a goiter or thyroid autoantibodies. Thus, a new variant of thyroiditis, atypical subacute thyroiditis, was probably the cause of this unusual outbreak. It is unclear at present if this variant of thyroiditis is common in communities and represents a separate disease entity.
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PMID:An outbreak of thyrotoxicosis due to atypical subacute thyroiditis. 229 55


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