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)

A case of L-tryptophan associated eosinophilia, myalgia, eosinophilic fasciitis, peripheral sensorimotor neuropathy, and multiple white matter lesions on MRI scan is reported. The various effects of eosinophilia on the nervous system are reviewed. The persistence of the neurological complications despite resolution of eosinophilia and steroid therapy is emphasized.
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PMID:Central and peripheral nervous system involvement in the L-tryptophan associated eosinophilia myalgia syndrome. 180 36

We present the case of a 52-year-old woman who developed diffuse induration of the skin and severe edema of the subcutaneous tissue involving the extremities and the trunk, sparing hands, feet and face after 10 years of almost constant oral tryptophan medication. The skin manifestations were similar to those of eosinophilic fasciitis (Shulman syndrome). The patient complained of severe muscle pain and weakness. Laboratory studies revealed an elevated Westergren erythrocyte sedimentation rate and eosinophilia. There were no signs of internal organ involvement and no immunological parameters of progressive systemic scleroderma. Eosinophilia and myalgia resolved in response to intermittent systemic therapy with glucocorticosteroids, whereas the progressive scleroderma and the edema showed only slight improvement after the discontinuation of L-tryptophan.
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PMID:[Eosinophilia-myalgia syndrome and L-tryptophan intake]. 182 70

This report describes three Belgian cases of the eosinophilia-myalgia syndrome associated with the use of L-tryptophan-containing products. Three women, aged 51, 53 and 73 years, were taking L-tryptophan for 2 months to 2 years, at 500, 1500, and 2250 mg d-1, respectively. All developed disabling myalgias, fatigue, and a variable skin rash, in association with marked eosinophilia. In one patient, symptoms and eosinophilia reappeared after rechallenge with L-tryptophan. Discontinuation of the drug resulted in gradual disappearance of the symptoms, signs and laboratory abnormalities in two patients. One patient was treated with corticosteroids because of persisting myalgias. Because of the non-specific clinical manifestations, clinicians from all subspecialties of internal medicine might be confronted with such patients and should be aware of this new entity.
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PMID:L-tryptophan-induced eosinophilia-myalgia syndrome. 182 54

While the pathogenesis of eosinophilia-myalgia syndrome (EMS) remains obscure, the ingestion of L-trypophan (LT) and possibly certain constituents in the LT product might be associated. We investigated the effect of chemically synthesized substances, 1,1'-ethylidene bis[tryptophan] (EBT) and its decomposition product, 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid (MTCA) recently identified in the implicated LT, on the eosinophil differentiation and the induction of IL-1 and IL-6. EBT and MTCA alone did not support colony formation. However, EBT or MTCA in conjunction with IL-2 induced colony-forming activity containing a small number of eosinophils. In addition, these LT constituents induced a significant level of IL-6 but not IL-1 beta in the mononuclear cells from normal volunteers and a patient with hypereosinophilic syndrome. These results suggest that certain constituents of LT product are associated with the pathogenesis of EMS through the induction of colony-stimulating factors and IL-6, hence giving rise to eosinophilia and inflammation.
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PMID:Effect of synthesized constituents in the L-tryptophan product on the differentiation of eosinophils and the induction of IL-6: a possible cause of eosinophilia-myalgia syndrome. 187 26

The following is an outline of one typical case of chronic eosinophilia-myalgia syndrome (EMS). In 1987 a 62-year-old woman began taking L-tryptophan, 1.5 g nightly, due to sleeping difficulty. During the months preceding the appearance of EMS she continued to take L-tryptophan, derived from the biosynthetic production of the Japanese manufacturer "Showa Denko". She has suffered increasingly from severe myalgia and a proximal muscle weakness since July of 1989. In November, 1989 her white blood cell count measured 12.1 X 10(9)/l with 3.6 X 10(9) eosinophil cells/l. The bone marrow exhibited an increased granulopoesis and an extreme increase in the amount of eosinophil cells. The muscle biopsy specimen indicated an inflammation with perivascular distribution. The eosinophil cell count of the blood was quickly normalized via the introduction of prednisone over a short period. In the absence of further immunosuppressive therapy a slow improvement can be seen in the myalgia and in her general condition. Since the beginning of 1990 there has been a slow development of hyperpigmented scleroderma-like skin changes with distal distribution.
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PMID:[Eosinophilia-myalgia syndrome]. 187 21

Five patients with the L-tryptophan-related eosinophilia-myalgia syndrome had a generalized eruption of flesh-colored papules. In all patients, histologic examination revealed a focal accumulation of mucin in the upper mid dermis, associated with increased dermal cellularity. The mucin was composed predominantly of hyaluronic acid, with small amounts of sulfated acid mucopolysaccharides. The cells within the lesion were fibroblasts. The lesions slowly regressed after L-tryptophan was discontinued. Proposed explanations for the L-tryptophan-related eosinophilia-myalgia syndrome have centered on contaminants, chemically related to L-tryptophan, introduced in the manufacturing process. Tryptophan metabolites have been linked with sclerotic cutaneous diseases but have not been previously implicated in cutaneous mucinoses.
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PMID:Papular mucinosis in L-tryptophan-induced eosinophilia-myalgia syndrome. 188 Feb 55

Epidemic eosinophilia-myalgia syndrome (EMS) associated with excess L-tryptophan (Trp) consumption in humans has been declared a major public health problem. The EMS problem has not been observed in pigs, nor has comprehensive pathology associated with EMS in humans been described. Experiments were therefore conducted to evaluate the pathology and effects of excess dietary L-Trp for finishing (79 to 119 kg) pigs and to determine an LD50 of Trp for pigs. In Exp. 1, addition of .1 or 1% Trp to corn-soybean meal diets had no effect on growth performance or leukocyte and relative eosinophil counts or on plasma aspartate transferase, creatine phosphokinase, and lactate dehydrogenase activities. Likewise, untoward pathological effects of Trp feeding were not observed in the animals under study. In Exp. 2, supplementing the basal diet with 0, 2, and 4% Trp caused linear (P less than .05) decreases in weight gain, feed intake, and gain:feed ratio. Mortality could not be produced by acute oral dosing in the LD50 study (Exp. 3), wherein Trp doses between 2.00 and 5.71 g/kg of BW were administered by stomach tube. Vomiting occurred at oral doses greater than 5.71 g/kg of BW. These results suggest that oral ingestion of Trp in pigs is safe and that pigs can tolerate considerable excesses of Trp.
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PMID:Safety of L-tryptophan for pigs. 188 5

The recognition of the eosinophilia-myalgia syndrome associated with L-tryptophan in the United States during 1989 as a disorder resembling the previously described 1981 toxic oil syndrome of Spain has established an increased level of consciousness regarding drug and toxin associated diseases. Both of these disorders were characterized by the development of acute and chronic multisystem features that parallel many idiopathic connective tissue diseases. Common manifestations have included generalized myalgias, fever, transient pulmonary infiltrates, and xerostomia during the early months followed by late stage neuromuscular and cutaneous disease. The most conspicuous laboratory abnormality was a peripheral eosinophilia. One of the most striking clinical findings has been scleroderma-like skin disease manifesting as diffuse fasciitis or hidebound induration. A sensory neuropathy and proximal myopathy in association with skin thickening have established these syndromes as chronic disabling diseases for many of their victims. Mononuclear perimysial and epineurial infiltrates have been distinctive pathological findings. Although the etiology of the eosinophilia-myalgia syndrome and the toxic oil syndrome are unknown, there is epidemiologic evidence to support the presence of contaminants in L-tryptophan and rapeseed oil, respectively, as the causative agents. No therapy has been demonstrated to arrest the evolution of the chronic sequelae in either disorder.
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PMID:The eosinophilia-myalgia syndrome and related disorders. 188 55

Eosinophilia-myalgia syndrome (EMS), a new connective tissue disease was reported and named in 1989 from New Mexico, U.S.A. L-tryptophan has been suspected as the causative agent of EMS. This L-tryptophan was made in Japan, but no definite case of EMS has been reported in Japan. We report 2 patients with EMS. A 72-year-old woman and a 74-year-old woman, who had been treated with oral L-tryptophan 1 g/day for 4 and 5 months by the same doctor simultaneously. The clinical courses of the two cases were similar. A diffuse erythema and swelling appeared on the arms and spread over the whole body. The skin lesions turned into lustrous sclerosis. Eosinophilia was remarkable in the early stage. ANA, DNA anti-body and ENA antibodies were all negative. Neurological examination revealed a mild peripheral neuropathy. No sclerodactylia and no Raynaud's phenomenon in our cases are characteristic findings in EMS. The simultaneous onset of two cases using the same drug at the same time implicates the close relation of L-tryptophan ingestion to EMS.
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PMID:[Two cases of L-tryptophan ingestion induced eosinophilia-myalgia syndrome]. 189 Jul 52

The eosinophilia-myalgia syndrome is a newly described disease associated with ingestion of a contaminant or byproduct of the amino acid L-tryptophan. Patients typically present with intense myalgias, especially of the extremities, and commonly suffer from skin and subcutaneous manifestations (edema and induration of the skin, morphea-like lesions, pruritus). Less frequent findings are cardiorespiratory involvement (cough, dyspnea, pulmonary infiltrates) and neurologic disease (ascending polyneuropathy). Laboratory findings include blood eosinophilia (greater than 10(9) cells per liter), normal to slightly elevated serum aldolase levels, and negative studies for connective tissue diseases (normal erythrocyte sedimentation rate, negative antinuclear antibodies). Tissue damage in eosinophilia-myalgia syndrome is likely related to infiltration by eosinophils with subsequent release of toxic molecules such as major basic protein. Management in severely ill patients includes administration of corticosteroids.
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PMID:Eosinophilia-myalgia syndrome. 189 58


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