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 series of four patients with pulmonary infiltrates, pleural effusions, hypoxemia, peripheral eosinophilia, and symptoms of dyspnea, fatigue, and weakness is reported. Lung tissue obtained in three patients revealed interstitial pneumonitis, small-to-medium-vessel mixed-cell vasculitis, and alveolar exudate of histiocytes and eosinophils. All patients reported ingestion of L-tryptophan-containing products at a time when an association between L-tryptophan and the eosinophilia-myalgia syndrome was established. This clinical pattern of pulmonary involvement may be part of the continuum of the eosinophilia-myalgia syndrome. The pathophysiology of this syndrome and the relationship with the ingestion of L-tryptophan-containing products have not yet been identified.
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PMID:Acute eosinophilic pulmonary disease associated with the ingestion of L-tryptophan-containing products. 198 92

Pathologic findings in eight patients with the eosinophilia-myalgia syndrome, secondary to L-tryptophan ingestion, are reported. Tissue was obtained by biopsy alone in six patients, by biopsy and autopsy in the seventh patient, and by autopsy alone in the eighth patient. Muscle biopsies in five patients demonstrated an inflammatory infiltrate composed predominantly of lymphocytes, histiocytes, plasma cells, and a few eosinophils. The inflammation involved the perimysial and epimysial connective tissue, the walls of some small blood vessels, the perineurium of small nerve twigs, muscle spindles, and fibrous septae of subcutaneous adipose tissue. In two patients with peripheral neuropathy and one patient without overt neuropathy, denervation atrophy of muscle and perimysial and epimysial fibrosis were present. Sural nerve biopsy tissue taken from two patients displayed prominent axonopathy in one, and minimal changes in the second. Pulmonary changes in the two autopsied patients included endothelial cell damage, endovasculitis and fibromyxoid intimal change im arteries and veins, and interstitial pneumonitis with fibrosis.
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PMID:L-tryptophan and the eosinophilia-myalgia syndrome: pathologic findings in eight patients. 198 73

The recent delineation of a clinical syndrome marked by eosinophilia, myalgia, and scleroderma-like skin changes associated with L-tryptophan use has necessitated the Centers for Disease Control to initiate a health alert. The likely association of L-tryptophan ingestion with a syndrome that mimics eosinophilic fasciitis (Shulman's syndrome) further identifies an environmental agent associated with an inflammatory sclerosing rheumatic disease process. In this report, we present the clinical, morphologic, and enzyme histochemical findings in muscle, skin, and fascia biopsies from 14 cases fulfilling the Center for Disease Control diagnostic criteria for L-tryptophan-associated eosinophilia-myalgia syndrome. The clinical syndrome reveals a high incidence of arthralgia, elbow contracture, and clinical neuropathy. The absence of significant change in creatine kinase or sedimentation rate allows for diagnostic separation from other inflammatory myopathies. Histoenzymatic features in muscle biopsies reveal a preferential epimysial-perimysial noneosinophilic infiltration characterized by acid phosphatase reactive histiocytosis, nonnecrotizing venulitis, perineural inflammation within dermis and perimysium, type II fiber atrophy with superimposed denervation features, and perifascicular alkaline phosphatase reactivity representing early neofibroplasia. The constellation of changes in skin, fascia, and muscle, with the defined clinical syndrome, allows for accurate differentiation from allied syndromes, including eosinophilic polymyositis, scleroderma, idiopathic polymyositis/dermatomyositis, polyarteritis nodosa, and toxic oil syndrome. Accurate differentiation from eosinophilic fasciitis still rests on a history of L-tryptophan ingestion.
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PMID:Neuromuscular manifestations of L-tryptophan-associated eosinophilia-myalgia syndrome: a histomorphologic analysis of 14 patients. 198 74

Recently, the ingestion of tryptophan has been associated with eosinophilia-myalgia syndrome, which is characterized by eosinophilia, myalgias, and several less consistently reported findings. We treated 13 patients who exhibited clinical features of eosinophilic fasciitis who were taking high-dose tryptophan before the onset of clinical symptoms. Twelve patients exhibited eosinophilia, with eosinophil counts ranging from 0.13 to 0.88. The remaining patient was taking oral corticosteroids when her eosinophil count was determined. Eight patients complained of myalgias. Other symptoms included arthralgias, pruritus, cutaneous burning, weakness, fever, rashes, malaise, edema, muscle spasms, and alopecia. 5-Hydroxyindoleacetic acid levels were elevated in four of the eight urine specimens that were tested. Our findings suggest that previously diagnosed cases of eosinophilic fasciitis may represent variants of tryptophan-associated eosinophilia-myalgia syndrome. Derangements in the metabolism of tryptophan may play a role in sclerotic diseases.
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PMID:Eosinophilic fasciitis associated with tryptophan ingestion. A manifestation of eosinophilia-myalgia syndrome. 199 Sep 86

Long-term treatment with high doses of corticosteroids leads to the development of truncal obesity and focal fatty deposition. These deposits characteristically are located on the face, the nuchal and truncal areas, and episternally, as well as in the mediastinum and epicardium. We studied a patient with juxta-articular adiposis dolorosa who had L-tryptophan-associated eosinophilia-myalgia syndrome and was treated with high doses of prednisone. This is the first reported case of adiposis dolorosa occurring as a complication of corticosteroid treatment. Alterations of fat metabolism induced by corticosteroid excess may have played a role in the development of this unusual painful syndrome.
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PMID:Corticosteroid-induced juxta-articular adiposis dolorosa. 199 Sep 89

We have previously shown that Na(+)-coupled transport of glucose and amino acids across the apical membrane of intestinal absorptive cells is accompanied by alterations in cytoskeletal structure and altered sieving of small hydrophilic solutes by tight junctions. Here we report that in response to the essential amino acid L-tryptophan at lumenal concentrations likely to be supraphysiological (1 mM or greater), these responses are so exaggerated as to induce disruption of tight junctions and transepithelial macromolecular leaks. Since these effects of L-tryptophan are energy and Na+ dependent and occur with mucosal but not serosal exposure to L-tryptophan, it appears they are triggered by activation of a Na(+)-nutrient cotransporter in the apical membrane of absorptive cells rather than by the presence of an unidentified trace contaminant. Our findings suggest the possibility that dietary supplementation by L-tryptophan may result in loss of the intestinal epithelial barrier to dietary antigens. We speculate that such a response to supraphysiologic tryptophan may contribute, in part, to the recently recognized curious tryptophan-induced eosinophilia myalgia syndrome.
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PMID:Supraphysiologic L-tryptophan elicits cytoskeletal and macromolecular permeability alterations in hamster small intestinal epithelium in vitro. 199 32

Muscle biopsies of 4 patients with the eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan showed lymphocytic infiltrates with occasional eosinophils largely restricted to interstitial fibrous tissue and perivascular areas. There was inflammation and fibrosis of muscle spindle capsules in 3 patients. In the 2 sickest patients, there was profound muscle atrophy, affecting both muscle fiber types.
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PMID:Eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan: muscle biopsy findings in 4 patients. 199 85

A 62 year old woman taking L-tryptophan developed eosinophilic fasciitis shortly after starting an exercise class. She received prednisone without benefit but improved after azathioprine treatment was started and L-tryptophan was discontinued. As products containing L-tryptophan have recently been implicated in development of the eosinophilia-myalgia syndrome it is suggested that the use of L-tryptophan might have contributed to the development of eosinophilic fasciitis in this patient. Similarities with toxic oil syndrome are noted. Additional studies are warranted to determine the prevalence of L-tryptophan ingestion among patients diagnosed as having eosinophilic fasciitis.
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PMID:Eosinophilic fasciitis associated with L-tryptophan ingestion. 199 70

This report describes two women who presented with severe respiratory failure and diffuse pulmonary infiltrates in the fall of 1989. Both required prolonged assisted ventilation because of severe shunt physiology. Open lung biopsies on admission revealed a small vessel vasculitis as the sole morphologic abnormality in both patients. Both responded to high dose corticosteroids. Neither patient exhibited evidence of systemic vasculitis, and neither had serologic evidence of an immune disorder. Common to both patients was ingestion of L-tryptophan. One patient exhibited several features of the eosinophilia-myalgia syndrome. The other patient did not appear to have the syndrome, but the temporal relationship between the onset of symptoms and initiation of L-tryptophan treatment was striking. The presentation of these patients alters our notions concerning the spectrum of clinical manifestations caused by this agent, and the response to methylprednisolone supports its efficacy in the treatment of this disorder.
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PMID:Acute respiratory failure caused by pulmonary vasculitis after L-tryptophan ingestion. 200 Oct 80

We reviewed 21 cases of eosinophilia-myalgia syndrome to describe the range of clinical findings in these patients. Most patients were women (20 [95%]) and middle-aged (mean, 46 years) and had taken the food supplement L-tryptophan (95%). All cases involved eosinophilia (eosinophil count, greater than or equal to 2.0 x 10(9)/L) and incapacitating myalgias. Fourteen (88%) of the 16 patients tested had mild liver function abnormalities. Aldolase levels were abnormal in all patients tested. Muscle biopsies were done in five patients; four showed eosinophilic perimyositis, and one had interstitial inflammation. No physical finding was pathognomonic or universal, but muscle tenderness, tachycardia, and rash were the most common signs found during physical examinations. Seven patients were treated with prednisone, and six showed improvement in muscle pain and a decrease in eosinophilia. The cause of this disorder is still unknown.
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PMID:Eosinophilia-myalgia syndrome. A clinical case series of 21 patients. New Mexico Eosinophilia-Myalgia Syndrome Study Group. 200 Nov 36


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