Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231528 (myalgia)
 6,565 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peak E substance, a trace impurity in L-tryptophan, has been associated epidemiologically with an outbreak of eosinophilia-myalgia syndrome (EMS) in the USA in 1989. After fractionation and purification of this substance, nuclear magnetic resonance and fast-atom-bombardment mass spectroscopy were used to identify the molecular structures of peak X/X' (formed by the decomposition of peak E substance in a simulated gastric fluid) and peak Y/Y' substances (which are believed to be the intermediates in the transformation of peak E substance to peak X/X' substances). The analyses were also performed on synthesized peak E substance obtained from the reaction of tryptophan with acetaldehyde. The results indicated that the synthesized substance was of high purity and was suitable for use in studies investigating the relationship between peak E substance and EMS onset.
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PMID:Identification of substances formed by decomposition of peak E substance in tryptophan. 154 9

The eosinophilia-myalgia syndrome (EMS) is a recently described systemic disorder distinguished by the development of characteristic muscle spasm, myalgia, neuropathy, and scleroderma-like cutaneous induration. Life-threatening manifestations have included cardiopulmonary and acute ascending neuropathic syndromes. Current evidence indicates that this is a severe illness with the potential for long-term disability. Careful follow-up studies will help to better define new features of this disease, such as the recent awareness of severe neurocognitive abnormalities in some patients. The association of EMS with the ingestion of L-tryptophan may provide important clues toward the understanding of idiopathic fibrosing syndromes, as well as toxin-induced autoimmune phenomena. Rational therapy will be dependent upon a more complete understanding of the pathogenesis of this and related diseases.
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PMID:The eosinophilia-myalgia syndrome: current concepts and future directions. 155 Dec 86

We report a 45-year-old female who had symptomatic gastrointestinal involvement, eosinophils in the cellular infiltrate, and who proved to have L-tryptophan-associated eosinophilia-myalgia syndrome. This case illustrates that gastrointestinal disease can be a major, seemingly primary clinical presentation in this syndrome, and that a drug history, specifically L-tryptophan, needs to be included in the differential diagnosis of "eosinophilic gastroenteritis."
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PMID:Gastrointestinal involvement in L-tryptophan (L-Trp) associated eosinophilia-myalgia syndrome (EMS). 156 9

We describe the histopathologic changes of skin, muscle, vessels, and fascia in 11 patients with eosinophilia myalgia syndrome, a newly described entity that has been linked to the ingestion of L-tryptophan. This syndrome is defined clinically by severe incapacitating myalgias and a peripheral eosinophilia. Arthralgias, edema of the extremities, morbilliform rashes, skin induration, weakness, fatigue, and respiratory weakness may be present as well. The earliest apparent histologic changes were observed at the septa between subcutaneous fat lobules and in the deep dermis or fascia. The septa and fascia were infiltrated with a sparse mixture of lymphocytes and histiocytes. In the deep fascia, in addition to inflammatory cells, there were distinctive, reactive mesenchymal cells that showed features of both histiocytes and fibrocytes. Minimal tissue eosinophilia was seen despite the extent of blood eosinophilia. Dermal thickening and homogenization of collagen bundles occurred with replacement of fat and adnexa (changes indistinguishable from scleroderma or morphea). Vessel walls in the dermis and fascia showed thickening and endothelial swelling, but no overt vasculitis was noted. Skeletal muscle biopsies showed a perimysial, epimysial, and/or fascial inflammatory infiltrate of lymphocytes and distinctive reactive mesenchymal cells with some eosinophils. Minimal myofiber atrophy, regeneration, or necrosis was seen despite the clinical history of severe myalgias in almost all patients. This syndrome should help gain insight into the mechanisms of fibrosis in environmental-induced, scleroderma-like syndromes and in idiopathic, scleroderma-like disorders as well.
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PMID:Pathologic manifestations of the eosinophilia myalgia syndrome: analysis of 11 cases. 156 45

We describe a 53-year-old women with eosinophilia-myalgia syndrome who suddenly developed severe persistent myalgias of her arms, legs, back, and shoulder after a 5-month period of daily L-tryptophan ingestion, associated with fever, progressive stenocardia and left-sided congestive heart failure. Laboratory tests showed a leukocytosis of 11.2/nl with 3.14/nl eosinophils and an elevated erythrocyte sedimentation rate. There was a marked, predominantly proximal sclerosis of her arms, legs and trunk with a brownish discoloration. The skin of her arms and legs appeared dimpled (peau d'orange). Findings of the electrophysiological examinations were consistent with sensory neuropathy and myositis. Remarkable fasciitis and interstitial myositis were present in a biopsy specimen (from skin to muscle) taken from her thigh. However, eosinophilic infiltrates were rare. Angiography revealed an apical obstructive cardiomyopathy. In this paper, we describe the clinical findings, the course over 2 years, as well as the therapeutic management. Furthermore, the most important differential diagnoses are discussed and the literature is reviewed with special attention given to more recent pathogenic insights into this newly recognized multisystem disease.
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PMID:[Eosinophilia-myalgia syndrome with fasciitis and interstitial myositis after L-tryptophan administration]. 157 30

Pulmonary manifestations are not infrequent in the L-tryptophan-induced eosinophilia-myalgia syndrome (EMS). However, previous reports have not described the results of longitudinal pulmonary function, exercise testing, high-resolution computerized tomographic (HRCT) scanning of the chest, or detailed bronchoalveolar lavage (BAL) analysis. We report six patients with EMS who had dyspnea. The diffusing capacity for carbon monoxide was decreased in five patients tested. Exercise testing with arterial blood gas sampling in three patients was consistent with pulmonary vascular or parenchymal disease. Serial exercise testing in two of these patients demonstrated marked improvement temporally associated with corticosteroid treatment. In four patients, HRCT scanning of the chest was abnormal. One of these patients showed no abnormality on routine chest roentgenogram. Two patients undergoing BAL exhibited increased eosinophils in the lavage fluid; a third had elevated lymphocytes. Serial measurements of fibroblast proliferation-stimulating-activity in samples of BAL fluid obtained from serial examinations in two patients exhibited heightened pretreatment activity that returned to the normal range following corticosteroid therapy. In these two patients, increased proportions of T-suppressor/cytolytic (CD8+) cells were observed in the BAL fluid. Despite aggressive immunosuppressive therapy, one of the patients died of respiratory failure. Another remains markedly dyspneic with pulmonary hypertension. Of the remaining four patients, two exhibited resolution of pulmonary symptoms after systemic corticosteroid therapy, and two experienced partial improvement.
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PMID:Pulmonary manifestations of the eosinophilia-myalgia syndrome associated with tryptophan ingestion. 158 84

We reviewed the pulmonary history, dyspnea ratings, and pulmonary function test results in 16 patients with L-tryptophan-induced eosinophilia myalgia syndrome to determine the correlation between reported pulmonary complaints and pulmonary function abnormalities. All patients reported pulmonary symptoms. Dyspnea, seen in 14 of 16 (87 percent) patients, was the most common symptom. The severity of dyspnea was graded by the baseline dyspnea index and the oxygen cost diagram. Pulmonary function testing including maximal static inspiratory and expiratory pressures were measured. The DCO was diminished in 12 of 16 (75 percent) patients. The MSIP was decreased in seven out of ten (70 percent) and the MSEP was decreased in nine out of ten (90 percent) of those patients tested. There was a statistically significant correlation between the severity of dyspnea as graded by the BDI and OCD, and the decrease in DCO. These results and a review of the literature of the pulmonary manifestations of EMS lead us to conclude that patients with EMS have a high prevalence of dyspnea, and it appears to be caused by both lung parenchymal involvement, as well as respiratory muscle weakness.
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PMID:Dyspnea and pulmonary function in the L-tryptophan-associated eosinophilia-myalgia syndrome. 158 85

We report a case of repeated coronary artery spasm with myocardial injury in a 37-year-old woman with the eosinophilia-myalgia syndrome. This patient did not have a medical history of cardiac-related illness or risk factors for coronary artery disease. The presence of eosinophil granule major basic protein in otherwise normal-appearing myocardial tissue, along with normal plasma levels of tryptophan metabolites, suggests that the mechanism of vasospasm in this patient might involve toxic eosinophil proteins or focal myocardial lesions, but not the production of excess tryptophan metabolites.
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PMID:Repeated coronary artery spasm in a young woman with the eosinophilia-myalgia syndrome. 158 64

Eosinophilia-myalgia syndrome (EMS) is a disorder characterized by generalized muscle pain and eosinophilia. The etiology of this syndrome appears to be related to the ingestion of L-tryptophan. Most studies to date describe an associated peripheral neuropathy or combined myopathy and peripheral neuropathy. This report presents 2 EMS patients with myopathy, confirmed by muscle biopsy in 1 case and electrophysiology in both cases. No clinical evidence of neuropathy was found. Both routine and single fiber electromyography failed to demonstrate abnormalities, suggesting neuropathy. Electrodiagnostic abnormalities paralleled the clinical course. After 10 months, both patients continued to have symptoms of muscle cramping and reduced endurance, with mild electromyographic abnormalities, perhaps reflecting changes in their motor unit.
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PMID:Eosinophilia-myalgia syndrome: myopathic electrodiagnostic characteristics. 158 47

A patient suffering from endogenous depression was treated with mianserin and developed agranulocytosis. After recovering from this, and with the depression in remission, the patient was given L-tryptophan. When this medication was removed from the market, due to the newly described eosinophilia-myalgia syndrome, a change was made to oxitriptan, which then caused a serious asymptomatic eosinophilia. No similar cases have yet been reported. Following withdrawal of oxitriptan, the eosinophilia disappeared. Evidence for any other cause of the condition was not found. Causes and physiopathology of drug-induced agranulocytosis and eosinophilia and the circumstances of such complications following use of mianserin and oxitriptan are discussed.
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PMID:[Mianserin agranulocytosis followed by oxitriptan eosinophilia]. 160 92


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