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)

The clinical constellation of leukocytosis, thrombocytosis, and low or absent stainable neutrophil alkaline phosphatase (NAP) is considered characteristic of chronic myelogenous leukemia (CML). CML with eosinophilic differentiation (eosinophilic leukemia) is well described, and leukemia and other clonal hematologic malignancies are associated with the syndrome of eosinophilic fasciitis. We describe leukocytosis, thrombocytosis, eosinophilia, mild basophilia, and absent stainable NAP, initially suggesting the diagnosis of CML in a patient with the eosinophilia myalgia syndrome associated with L-tryptophan use, a condition resembling eosinophilic fasciitis. Cytogenetic and molecular genetic studies failed to demonstrate a clonal proliferation of eosinophils.
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PMID:Absent neutrophil alkaline phosphatase in the eosinophilia myalgia syndrome associated with L-tryptophan use. 201 75

Induration of the skin develops in a majority of patients with the eosinophilia-myalgia syndrome associated with L-tryptophan, and bears striking clinical and histopathological resemblance to eosinophilic fasciitis (EF). These similarities have led to the suggestion that eosinophilia-myalgia syndrome and EF are the same disease. To study the relationship of eosinophilia-myalgia syndrome and EF, we ascertained the prevalence of L-tryptophan use in a cohort of patients with EF, and compared their clinical and laboratory findings to those of patients with eosinophilia-myalgia syndrome associated cutaneous involvement. None of 11 patients who were diagnosed as having EF between 1970 and 1989 used L-tryptophan containing preparations prior to the onset of their illness. Marked clinical and laboratory test differences were observed between patients with EF and eosinophilia-myalgia syndrome. Patients with eosinophilia-myalgia syndrome had a more acute onset, more severe symptoms, higher frequency of rash and of pulmonary, cardiac, gastrointestinal, neurologic, myopathic and thyroid involvement compared to patients with EF. Corticosteroid therapy resulted in improvement of cutaneous involvement in 88% of patients with EF but it was only partially successful in patients with eosinophilia-myalgia syndrome. Hospitalization and fatalities occurred only among patients with eosinophilia-myalgia syndrome. These observations demonstrate that eosinophilia-myalgia syndrome is a more severe disease with multisystemic involvement that can be clinically distinguished from EF. In contrast to eosinophilia-myalgia syndrome, EF is not associated with L-tryptophan ingestion.
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PMID:Eosinophilic fasciitis is clinically distinguishable from the eosinophilia-myalgia syndrome and is not associated with L-tryptophan use. 202 21

The eosinophilia-myalgia syndrome was first reported from New Mexico, USA, in 1989. Since then, there have been further reports from the USA, Canada and Europe. Patients with the eosinophilia-myalgia syndrome present with myalgias, morbilliform and urticarial rash, oedema, sclerodermiform lesions, fever, pneumonia, fatigue and peripheral eosinophilia (greater than 1,000/mm3). The ultimate cause is postulated to be a contamination produced by Bacterium amyloliquefaciens during the production of L-tryptophan by genetic engineering techniques. HPLC analysis revealed that the causative agent was a condensation product of 1 mole acetaldehyde and 2 moles tryptophan. Clinical and laboratory findings of the eosinophilia-myalgia syndrome, Shulman syndrome and toxic-oil syndrome are discussed.
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PMID:[Eosinophilia-myalgia syndrome]. 205 61

Since 1989 there has been an increasing number of reports on the association of L-tryptophan (LT) and eosinophilia-myalgia syndrome (EMS). It has now become evident that the clinical picture of EMS can vary. We report two further cases reflecting the clinical spectrum of the disease. The first patient had been taking LT for 8 years before the onset of myalgia. Subsequently, this patient developed an illness clinically and histologically resembling eosinophilic fasciitis. The second patient had been taking LT for 8 months before the onset of symptoms, which included myalgia, severe oedema of the lower extremities and induration of the skin involving arms, lower legs and abdomen. Discontinuation of LT and administration of oral steroids resulted in little improvement of the skin changes in the first patient. However, in the second patient skin involvement improved rapidly, whereas the neurological disorders have become more prominent.
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PMID:[Eosinophilia-myalgia syndrome after L-tryptophan intake]. 205 64

A recently developed animal model for the L-tryptophan-associated eosinophilia myalgia syndrome was used to examine the small intestine and colon, because there is clinical involvement at these sites in patients. Increased perivascular inflammatory infiltrates rich in degranulating mast cells, eosinophils, and monocytes were seen in the lamina propria of experimental animals when compared with controls. L-Tryptophan-associated disease also shares many clinical features with idiopathic scleroderma/eosinophilic fasciitis, in which there is gastrointestinal involvement as well. These features are similar to those found in the recently described animal model. The apparent morphologic and clinical similarities between these entities suggest that the animal model is suitable for further studying the pathogenesis of the gastrointestinal involvement in all these diseases.
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PMID:Environmental pathology. Mast cell and eosinophil infiltration in intestinal mucosa of Lewis rats treated with L-tryptophan implicated in human eosinophilia myalgia syndrome. 206 62

Myopathies are not an unusual complication of drug therapy. The major symptoms in drug-induced myopathies are proximal muscle weakness, increased muscle enzyme levels, electromyographic changes and histological lesions. Some drug-induced myopathies are associated with neuropathy. Drug-induced myopathies can be classified according to the presence or absence of muscular pain and associated neuropathy. Among painless myopathies, we can distinguish myopathies without neuropathy (corticosteroids), myopathies with neuropathy (colchicine, chloroquine and hydroxychloroquine) and myasthenic syndromes (D-penicillamine, antibiotics, beta-blockers). Among painful myopathies, the classification is similar: painful myopathies may or may not be associated with neuropathies. Painful myopathies include polymyositis (D-penicillamine, cimetidine, zidovudine) and other myopathies without polymyositis (clofibrate, statines, cyclosporin). Among the painful neuromyopathies, eosinophilia-myalgia syndrome is a recently described disorder associated with the use of L-tryptophan. Combinations of drugs (for example, a fibrate and a statine or cyclosporin and colchicine) can induce severe myopathies. If such drugs are used together a vigorous surveillance to detect any sign of myopathy is warranted. Instead of classifying drug-induced myopathies according to clinical features, a histological classification can be proposed. Many drugs can induce vacuolar myopathy (colchicine, chloroquine, amiodarone, cyclosporin, drugs causing hypokalaemia and lipid-lowering agents), some others cause a mitochondrial myopathy (zidovudine) or a necrotizing myopathy as seen with vincristine. Overall, several criteria for reporting drug-induced myopathy can be recommended: lack of pre-existent muscular symptoms, a free period between the beginning of the treatment and the appearance of symptoms, lack of another cause accounting for the myopathy, and complete or incomplete resolution after withdrawal of the treatment. Rechallenge of the treatment is not advisable because of the risk of a serious relapse. The exact mechanisms by which drugs cause myopathies are unknown. Some cases may be due to metabolic changes, whereas others may be immune mediated. Nevertheless, the aspect these conditions have in common is the regression of the myopathy with the discontinuation of the drug.
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PMID:Drug-induced myopathies. 207 Apr 26

To identify chemical contaminant(s) associated with eosinophilia-myalgia syndrome (EMS), case and control lots of tryptophan were analyzed by HPLC with both UV and FL detection. Numerous contaminant peaks appeared on the chromatograms and some of them were identified as 5-hydroxytryptophan, indol aldehyde, indol, etc; from the retention time of authentic compounds. Among these, three peaks were significantly associated with case lots. One corresponds to di-tryptophan aminal of aldehyde (peak E). Others are unknown contaminants, UV-5 (FL-7) and UV-28 (FL-36). The structural elucidation and toxicological implication of UV-5 (FL-7) are currently in progress.
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PMID:Characterization of contaminants in EMS-associated L-tryptophan samples by high-performance liquid chromatography. 207 Apr 71

We present a case of the eosinophilia-myalgia syndrome in a patient taking large doses of L-tryptophan for sedation. He developed the now-classic findings of myalgias, skin changes, and marked eosinophilia. This syndrome was first recognized in late 1989, and epidemiologic studies have demonstrated an association of the clinical syndrome with ingestion of L-tryptophan. The mechanism of toxicity remains unknown. Casual use of L-tryptophan has been diminished by its rapid removal from the nutrition counter of health food stores.
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PMID:L-tryptophan use and the eosinophilia-myalgia syndrome. 208 50

Eosinophilia, brawny induration, and tenderness of the skin and deeper tissues, and eosinophilic and lymphocytic infiltration of skin, deep fascia, and muscle characterize the acute eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan. Many patients have a florid inflammatory myopathy. We evaluated 10 patients with this syndrome in whom peripheral neuropathy was a prominent or the only presenting feature. Two of these patients with severe neuromuscular disease required mechanical ventilation, and 1 died. Clinical severity appeared to be positively associated with the total dose of L-tryptophan ingested. Although the inflammation is generally thought to be more severe in skin, fascia, and muscle, inflammation, especially in the epineurium of sural nerve, was sometimes striking and often accompanied by vasculopathy and angioneogenesis. These cases draw attention to a new preventable syndrome with peripheral nerve involvement, emphasize the value of tissue biopsy for its diagnosis, and raise issues related to pathogenesis.
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PMID:Peripheral neuropathy in the eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. 202 3

In 1989, the Centers for Disease Control recognized the existence of an epidemic illness characterized by myalgia and eosinophilia in individuals taking preparations containing L-tryptophan. We evaluated 3 patients with eosinophilia-myalgia syndrome who presented with subacute progressive neuropathies. The neuropathies were predominantly motor and maximal in the lower extremities. Two patients were confined to a wheelchair and one was ventilator-dependent and bedridden. Sensory loss predominantly involved small fiber modalities. Electrophysiological studies showed multifocal marked conduction slowing and conduction block indicating segmental demyelination, with associated axonal degeneration that was accentuated distally. Examination of sural nerve biopsy specimens demonstrated axonal degeneration in all 3 patients and perivascular infiltrates in 2. Levels of quinolinic acid, a neurotoxic metabolite of L-tryptophan, were elevated in the cerebrospinal fluid in the 2 patients in whom it was measured. The cause of the neuropathy is unknown but may include immune mechanisms or toxicity of eosinophils, L-tryptophan, its metabolic products, or contaminants within L-tryptophan preparations.
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PMID:Peripheral neuropathy associated with eosinophilia-myalgia syndrome. 217 66


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