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)

In late October 1989, over 1,500 cases of an unusual illness involving severe myalgia and striking peripheral eosinophilia were reported in the United States and several other countries. Other clinical manifestations included pulmonary involvement (interstitial infiltrates and pleural effusions), skin rash and edema, axonal polyneuropathy, perimyositis, and possible adverse neurocognitive effects. Because of the primary manifestations of the illness, it was named "eosinophilia-myalgia syndrome" (EMS) by the Centers for Disease Control. Epidemiologic studies clearly linked illness to the ingestion of tryptophan produced by a single manufacturer in Japan, and the time course of the epidemic was most consistent with its being caused by a product contaminant. Epidemiologic analysis of plant operating conditions and data obtained from chemical analyses of case- and control-associated lots implicated 1,1'-ethylidene-bis(tryptophan) (EBT) as a candidate for the compound that causes EMS. However, the etiologic significance of EBT is still uncertain. Factors found to increase a person's risk for EMS included higher tryptophan dose and older age. Although cases occurred predominantly in women and patients had frequently been taking other medications concurrently with tryptophan, sex and use of several categories of other medications were not shown to influence the risk of illness. Few patients recovered rapidly and fully from the disease. Many were treated with glucocorticoid medications, and although they may have benefited from therapy in the short term, the development of chronic sequelae of EMS appears not to have been prevented. Public health practitioners currently depend on the reports of alert clinicians to detect this type of outbreak. In this case, state and federal government epidemiologists, once they were notified, were able to develop substantial basic information about the epidemic in a relatively short time. Control measures were introduced rapidly, effectively stopping the epidemic.
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PMID:Eosinophilia-myalgia syndrome: coming to grips with a new illness. 128 11

Polyneuropathy may complicate eosinophilia-associated connective tissue disease. We report a multi-focal neuropathy in a patient with eosinophilic fasciitis proven by demonstrating an eosinophilic cellular infiltrate in a fascial biopsy specimen from the forearm. Sural nerve biopsy revealed lymphocytic cuffing of epineural arterioles. Although described in the L-tryptophan-related eosinophilia-myalgia syndrome, peripheral neuropathy with these features has not been previously noted in a patient with eosinophilic fasciitis who had not consumed L-tryptophan.
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PMID:Multifocal peripheral neuropathy in eosinophilic fasciitis. 131 79

Eosinophilia-myalgia syndrome (EMS) is a newly recognized disorder, characterized by myalgia, weakness, scleroderma-like changes, and eosinophilia. EMS is associated with lots of L-tryptophan allegedly contaminated with byproducts of the manufacturing process. We describe 3 patients with EMS who presented with a severe demyelinating sensorimotor polyneuropathy. Electrodiagnostic studies revealed multifocal conduction block, slowing and temporal dispersion of motor responses, and prolonged or absent F-responses. Despite plasmapheresis; corticosteroids; and, in 1 patient, cyclophosphamide, 2 patients died and the remaining patient experienced minimal recovery. Pathology revealed patchy perivascular infiltrates and fibrosis in the connective tissue of muscle and nerve. Autopsy of the central nervous system in 2 patients did not reveal changes unique to EMS. In addition to other organ involvement, EMS may manifest as a potentially fatal polyneuropathy, which initially appears to have prominent demyelinating features.
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PMID:Demyelinating polyneuropathy in eosinophilia-myalgia syndrome. 132 57

A 59-year-old woman was admitted to our hospital with acute onset of chest pain. She had experienced high fever, weight loss, polyarthralgia, myalgia, polyneuropathy and hallucinations for 3 years before admission. The diagnosis of polyarteritis nodosa with hepatitis B surface antigenemia was made by muscle biopsy and serological examinations, and administration of prednisolone induced remission of all the manifestations. After developing the acute attack of severe chest pain, she died suddenly. At autopsy, a DeBakey type 1 aortic dissection was found and the immediate cause of death was found to be cardiac tamponade secondary to rupture of the aortic dissection. Microscopically, necrotizing inflammatory lesions were present in the medium sized vascular arteries throughout her body. Furthermore, necrotizing vasculitis was also found in the vasa vasorum of the adventitia and media of the thoracic aorta. The dissecting lesion was seen in the outer layer of the media. Our results suggest that spontaneous dissection of the aorta may be attributed to necrotizing vasculitis of the vasa vasorum.
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PMID:Polyarteritis nodosa with aortic dissection: necrotizing vasculitis of the vasa vasorum. 136 Dec 5

The eosinophilia-myalgia syndrome is a newly recognized illness that has been associated with the consumption of tryptophan products. We describe the clinical and histopathological findings and the results of biochemical analyses of tryptophan metabolism in patients with this syndrome and the toxic-oil syndrome which took place in 1981 in Spain. Symptoms and laboratory findings are similar. Chronic phase of EMS is characterised by long-term disability, sclerodermatous skin thickening, sensorimotor polyneuropathy and severe episodic myalgias. The development of the syndrome may result from a confluence of several factors including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:[Eosinophilia-myalgia: new syndrome]. 136 28

Eosinophilia-myalgia syndrome (EMS) is a newly described syndrome associated with use of L-tryptophan. A neuropathy with features of axonal degeneration has also been described in conjunction with EMS. Demyelinating polyneuropathy is not a well recognised association of the syndrome. The two patients with EMS reported presented with profound weakness and sensory loss and were found to have clinical, electrophysiological and pathological evidence of a chronic demyelinating polyneuropathy. The concurrence of this neuropathy with EMS, as well as several other features of their illness, is suggestive of an immune mediated mechanism in the pathophysiology of EMS.
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PMID:Chronic demyelinating polyneuropathy associated with eosinophilia-myalgia syndrome. 153 36

In 1981 epidemic poisoning with adulterated cooking oil occurred in Spain, affecting more than 20,000 people. The condition caused has since become known as the toxic oil syndrome (TOS). About 10-15% of the patients with acute symptoms developed a chronic disease with scleroderma-like skin manifestations, polyneuropathy and myositis. While the acute phase of the TOS was characterized by eosinophilia and elevated IgE, the chronic stage involved humoral autoimmune phenomena, such as antinuclear and antinucleolar antibodies, in many cases. In women with the chronic phase of TOS there was a possible prevalence of HLA-DR3 and HLA-DR4. The recently characterized eosinophilia-myalgia syndrome (EMS), which is thought to have been induced by contaminated L-tryptophan preparations, is similar to the TOS in some particulars. Understanding of the toxicological, immunological and genetic pathways leading to these diseases might give us some insight into the pathogenesis of spontaneously occurring autoimmune diseases, such as systemic scleroderma.
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PMID:[Toxic oil syndrome--an example of an exogenously-induced autoimmune disease]. 162 65

A 53-year-old woman with non-productive cough of unexplained aetiology for two years, developed a sub-acute symmetrical polyneuropathy involving all four limbs, accompanied by fever, cutaneous rash and myalgia in lower limbs. Laboratory studies revealed a leukocytosis with 70% eosinophils and excluded any cause for the hypereosinophilia. An echocardiogram showed increase in thickness of the atrial septum. Motor and sensory conduction velocity were reduced in ulnar and median nerve and unrecordable in peroneal and tibial nerves. A sural nerve biopsy showed an axonal degeneration involving myelinated and unmyelinated fibers as well as a vasculitis with fibrinoid necrosis and perivascular infiltration of eosinophils. There was considerable clinical and laboratory improvement with the use of steroids. The differential diagnosis between idiopathic hypereosinophilic syndrome and other disorders known to course with vasculitis and hypereosinophilia is discussed.
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PMID:Peripheral neuropathy in hypereosinophilic syndrome with vasculitis. 166 82

31 patients with L-tryptophan-associated eosinophilia-myalgia syndrome (EMS) that developed during the United States outbreak in 1989 were followed up prospectively at a university hospital outpatient rheumatology clinic for 16 to 24 months from the onset of their illness. Another patient with EMS associated with L-tryptophan in 1988 was followed up for 30 months. 93% of the 28 survivors from the 1989 cohort continue to have symptoms affecting 1-4 organ systems (median 3) and 3 have died, so the disorder produces considerable morbidity and mortality. The chronic sequelae most often associated with long-term disability are sclerodermatous skin thickening (54%), sensorimotor polyneuropathy (61%), proximal myopathy (36%), and severe episodic myalgias (64%). Thrombocytopenia developed in 1 patient. HLA-class II typing revealed a non-significant trend towards an association with HLA-DR4. Early therapy with corticosteroids did not seem to prevent the development of chronic manifestations.
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PMID:Clinical follow-up and immunogenetic studies of 32 patients with eosinophilia-myalgia syndrome. 167 35

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


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