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)

Abnormal metabolism of tryptophan is one of the possible aetiological factors in the L-tryptophan-induced eosinophilia-myalgia syndrome (EMS). We studied the plasma levels of tryptophan and serotonin and the urinary excretion of kynurenine and 5-hydroxyindoleacetic acid after oral intake of L-tryptophan in 1 subject with EMS and 2 healthy subjects. The test was repeated with concomitant administration of pyridoxine. In the patient there were elevated levels of plasma tryptophan during the loading and increased elimination of kynurenine in the urine both during and after the L-tryptophan test. During pyridoxine administration tryptophan levels and kynurenine elimination were much reduced, and kynurenine elimination was similar to that of controls. This study (i) confirms that an abnormal metabolism of L-tryptophan occurs in EMS patients and (ii) shows that this can be corrected by pyridoxine.
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PMID:L-tryptophan-induced eosinophilia-myalgia syndrome. II. Partial correction of abnormal tryptophan metabolism by pyridoxine. 172 62

The iatrogenic L-tryptophan-induced eosinophilia-myalgia syndrome, often considered to be a "new" disease, has proven to be a remarkable mimic of the classic sclerosing rheumatologic disorders. Although subacute cutaneous lupus erythematosus remains a clinically defined entity, supportive histologic and immunopathologic findings have recently been proposed. Rheumatoid neutrophilic dermatitis needs to be added to our usual differential diagnosis of a neutrophilic dermatosis without leukocytoclastic vasculitis. The antiphospholipid syndrome is associated with noninflammatory vascular thrombosis and often has recognizable cutaneous findings. Finally, ANCA are a valuable adjunct in the systemic evaluation of patients with vasculitis syndromes and suggest a common pathogenesis for several of the systemic vasculitides.
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PMID:Collagen vascular disease. 173 Jan 64

The eosinophilia-myalgia syndrome (EMS) is a unique entity associated with products that contain L-tryptophan (L-trp). Studies of the underlying etiopathogenic processes are underway. EMS is a distinct syndrome, but shares features with eosinophilic fasciitis and other variants of systemic sclerosis. A wide spectrum of clinical manifestations has been described, but there is no consensus regarding treatment. We report the clinical and laboratory features of 12 patients. All were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and analgesics with transient or minimal effect. Two received D-penicillamine (DP) and colchicine, with minimal improvement; one had no response to azathioprine (AZA). Eleven received corticosteroids and had improvement of general symptoms, arthralgias, arthritis, myalgias, skin changes, eosinophilia, and leukocytosis. Nevertheless, all but the latter two findings recurred when corticosteroids were tapered. Seven patients who were unresponsive to the former treatments received low-dose pulse oral methotrexate. Six exhibited continued improvement after a mean follow-up of 4.5 months, with good drug tolerance. Corticosteroids were tapered and, in some instances, discontinued without relapse or complications. One patient improved but later died of aspiration pneumonia. We conclude that methotrexate (MTX) is a therapeutic alternative for patients with severe or refractory EMS.
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PMID:Treatment of the eosinophilia-myalgia syndrome. 174 39

By November 17, 1989, the MMWR published the 154 first reports of a syndrome consisting of myalgia and eosinophilia (EMS), occurring with the consumption of L-tryptophan containing products (L-TrpCp) and which might represent a new clinical entity. To standardize reporting over the country, the CDC of Atlanta developed the following case definition: 1) a peripheral blood total eosinophil count of more than 1 x 10(9) cells per liter 2) generalized myalgia sufficiently severe to affect a patient's ability to pursue daily activities 3) the exclusion of infections or neoplastic conditions. The FDA then, announced its intention to seek a nationwide recall of all tryptophan containing products, followed by other european countries (UK, Germany, France). In France, a first decree (January 4th 1990) completed by a decree on May 11th confirms this decision for one year. This measure did not concern the medicinal products or some dietary supplements for newborn or young children. Since December 11th, 1989, 24 cases have been reported to the Regional Adverse Drug Reaction Monitoring Centres in France. These cases share the same features as the cases notified previously in the USA: overrepresentation of females, no relationship with the time and the daily intake, clinical similarities to the Shulman syndrome, and unknown prognosis. Now, more than one year after the onset of this illness, it seems that discontinuation of the ingestion of L-TrpCp can resolve or improve the symptoms in most cases, but sometimes the syndrome can persist. The causal relationship between the ingestion of L-TrpCp and this syndrome has been established. Whatever the mechanism for the development of EMS among tryptophan users remains unclear, as well as the role of eosinophilia and the factors for fibroblast proliferation. The epidemic emergence of this syndrome in July 89 raises the possibility of the contamination of tryptophan during the manufacturing process. To confirm this hypothesis, the same unusual peak in HPLC analysis was found both in case-associated L-Trp lots and in implicated-japanese manufacturer L-Trp lots in USA. But this would not explain the previous EMS reports before this contamination. Other hypotheses consist an inabnormality of tryptophan metabolism and/or an autoimmune process.
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PMID:["Eosinophilia-myalgia" syndrome due to L-tryptophan containing products. Cooperative evaluation of French Regional Centers of Pharmacovigilance. Analysis of 24 cases]. 175 78

Tryptophan, an essential amino acid commercially available as a dietary supplement, has been implicated in the development of a new and potentially fatal clinical entity: eosinophilia-myalgia syndrome (EMS). EMS reached epidemic proportions in the US in late 1989 and early 1990, with 1536 cases and 27 deaths reported as of August 1990. Features of the syndrome include intense, debilitating myalgias and marked peripheral eosinophilia. Vasculitis, neuropathy, and pulmonary involvement also may be observed but are not pathognomonic. Death typically ensues from ascending polyneuropathy with resulting paralysis and respiratory arrest. Treatment involves discontinuation of tryptophan ingestion. Administration of prednisone may not always alleviate or reverse the symptoms. Recovery is generally slow. The etiology of EMS has been traced to a contaminant in the bulk manufacturing process of tryptophan by a single Japanese company. Efforts are currently underway to confirm the structure of the contaminant by laboratory synthesis and to define its biologic and toxic effects using an animal model for EMS.
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PMID:Tryptophan toxicity: a pharmacoepidemiologic review of eosinophilia-myalgia syndrome. 176 43

Two female patients who fulfilled the criteria for L-tryptophan-induced eosinophilia-myalgia syndrome (EMS) had, together with morphea-like and fasciitis-like sclerotic changes of the skin, lesions that clinically mimicked pseudoxanthoma elasticum (PXE). Histology was compatible with the diagnosis; electron microscopy did not reveal calcium deposits. PXE-like changes may represent an additional feature of the pleomorphic L-tryptophan-induced EMS.
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PMID:L-tryptophan-induced eosinophilia-myalgia syndrome. I. Report of two cases with pseudoxanthoma-elasticum-like skin changes. 176 22

The Center for Disease Control has received numerous reports of an eosinophilia-myalgia syndrome related to products containing L-tryptophan. The case is reported of eosinophilia-myalgia syndrome and polyneuropathy associated with myeloperoxidase specific antineutrophil cytoplasmic antibody.
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PMID:Detection of antineutrophil cytoplasmic antibody in a patient with L-tryptophan induced eosinophilia-myalgia syndrome. 177 99

Animal models have proven very useful in furthering insight into a number of muscle diseases. Studies of ethanol-fed rats are being used to understand the pathogenetic mechanisms underlying acute and chronic myopathy induced by ethanol. Several animal species, including mice, dogs, and cats, develop X-linked muscular dystrophies, which have genetic defects identical to those of Duchenne muscular dystrophy. As in the human disease, these animals lack dystrophin. They are being used to investigate the mechanisms by which lack of dystrophin results in weakness and to examine myoblast transfer as a treatment modality. A model of eosinophilia-myalgia syndrome has recently been induced in Lewis rats by the feeding of L-tryptophan samples that were implicated in the clinical syndrome in humans, making possible studies of the pathogenesis of this interesting new entity. A dermatomyositis-like syndrome occurs spontaneously in dogs, and polymyositis-like illnesses can be induced in mice by immunization with muscle or following infection with selected viruses, especially enteroviruses. Study of the latter is helping us understand mechanisms in the etiology and pathogenesis of inflammatory myositis and virus-induced autoimmunity.
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PMID:Animal models of myopathy. 177 47

The scientific excitement that follows the recognition of a new disease has been reflected in the numerous publications describing the clinical, histopathologic, and pathogenetic aspects of the eosinophilia-myalgia syndrome (EMS) during the period covered by this review. The clinical picture that has emerged during the past 2 years indicates that EMS is a multisystemic disease with prominent cutaneous, hematologic, and visceral manifestations that frequently evolves into a chronic course and can occasionally be fatal. Considerable progress has been made toward understanding the etiology and pathogenesis of EMS. The demonstration of an association with the ingestion of L-tryptophan-containing products originating from a single source has led to the identification and characterization of a putative etiologic agent present as a contaminant in these preparations. Although the accumulation of eosinophils, lymphocytes, macrophages, and fibroblasts in the affected tissues suggests that these cells play important roles in the pathogenesis of EMS, the precise mechanisms of their involvement have not been established. Several studies have demonstrated the activation of eosinophils and the deposition of eosinophil-derived toxic proteins in affected tissues. Fibroblast activation and increased expression of genes coding for various connective tissue macromolecules have been demonstrated employing in situ hybridizations with complementary DNAs. Furthermore, interleukin-5 and transforming growth factor-beta have been implicated as potential mediators in the pathogenesis of EMS. The explosive epidemic of EMS has emphasized the importance of chemical and environmental factors in the development of systemic disorders characterized by chronic inflammation and fibrosis. It is expected that further study of the pathogenesis of EMS will provide valuable information regarding the mechanisms responsible for these obscure disorders.
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PMID:The eosinophilia-myalgia syndrome and eosinophilic fasciitis. 177 54

A case is presented of interstitial pneumonitis and pulmonary vasculitis ascribed to the ingestion of an L-tryptophan preparation. An unintended rechallenge supported the causal relationship. There was neither myalgia nor peripheral eosinophilia. Bronchoalveolar lavage fluid contained 12% eosinophils but few were present in the surgical lung biopsy specimen. Lung infiltrates receded after withdrawal of the drug and treatment with steroids. Dyspnoea and pulmonary hypertension persisted. Cyclophosphamide had no effect. Sclerodermiform skin lesions appeared as a late sequel. Chromatographic analysis of the L-tryptophan revealed no suspect impurities.
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PMID:Interstitial pneumonitis and pulmonary vasculitis in a patient taking an L-tryptophan preparation. 178 80


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