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 author reports a case of eosinophilia-myalgia syndrome (EMS), not associated with the use of tryptophan. Other nutritional supplements should be considered as possible etiologic agents in EMS. Further research in this area is needed.
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PMID:Eosinophilia-myalgia syndrome not associated with L-tryptophan. 160 35

Actinomycetal infections by Actinomyces, Nocardia, and Streptomyces appear to be increasing in incidence. Clinical and laboratory data from twelve patients believed to have subclinical actinomycete-streptomycete infections (ASI)* are presented. It is proposed that the recent epidemic of eosinophilia-myalgia syndrome (EMS) may have been caused by pre-existing host ASI that generated toxic agents when individuals ingested supplemental L-tryptophan (LT). LT is the substrate used by streptomycetes to synthesize actinomycins, extremely cytotoxic metabolites that could have accounted for symptoms seen in EMS. Actinomycins inhibit CoA activity and interfere with the synthesis and utilization of amino acids. LT also provides streptomycetes with additional NAD, a substance of great importance to their DNA synthesis and metabolic activity. With increased activity, streptomycin, chloramphenicol, adriamycin or any one of the many secondary metabolites (antibiotics) produced by Streptomyces could be endogenously generated in greater quantities. The clinical result would be increased host toxicity. A contaminant that has been isolated from case associated lots of LT may have simply provided additional tryptophan for an ASI. It is also possible that a nucleotide or similar substance in the case associated LT products caused increased activation of tryptophan-2,3-dioxygenase, the rate-limiting enzyme required for the production of NAD and/or actinomycin. Potential reasons for ASI, atypical forms of actinomycete-streptomycete micro-organisms, and the possibility of involvement in other diseases are discussed.
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PMID:Early impressions concerning actinomycetal infections that may play a role in the pathogenesis of eosinophilia-myalgia syndrome (EMS) and other 'new illnesses'. 161 56

The ingestion of L-tryptophan (LT)-containing products has recently been associated with a newly diagnosed disorder known as eosinophilia-myalgia syndrome (EMS). This article reviews the pertinent research concerning the association between LT-containing products and EMS, including (a) the incidence and clinical course of EMS; (b) characteristics (eg, age and sex) of patients with EMS; (c) LT intakes (eg, dose, duration of intake) associated with EMS; (d) tracing of implicated LT-containing products to one raw material manufacturer, (e) theories related to the association, for example, the contamination theory; and (f) regulatory issues surrounding LT-containing products. The importance of this information to the dietitian is twofold. First, because LT is an essential amino acid, questions concerning LT-containing products and EMS are often directed to dietitians. Second, dietitians should be aware of the association to help facilitate the identification and care of patients with EMS.
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PMID:Review of L-tryptophan and eosinophilia-myalgia syndrome. 162 54

Since some patients with eosinophilia-myalgia syndrome ingested tryptophan along with benzodiazepines, we investigated whether demoxepam, the N-desalkylated compound of chlordiazepoxide, would influence the binding of tryptophan to hepatic nuclei. L-Tryptophan has been shown to bind (saturable, stereospecific, and of high affinity) to rat hepatic nuclei and nuclear envelopes. We report that demoxepam has an inhibitory effect on in vitro [3H]tryptophan binding to rat hepatic nuclei and has an apparent KD approximately 22 microM.
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PMID:Inhibitory effect of demoxepam on tryptophan binding to rat hepatic nuclei. 162 59

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

On October 1989, eosinophilia and incapacitating myalgia, together with arthralgia, dyspnea, cough and edema of the extremities, were shown to be associated with L-tryptophan ingestion. Since then, 1531 cases of eosinophilia-myalgia syndrome have been reported in United States and 22 in Belgium. We report here the unusual pulmonary presentation of this syndrome with a dramatic response of eosinophilia to corticotherapy. The cardio-pulmonary symptoms of eosinophilia-myalgia syndrome and its pathophysiology, which remains unclear, are discussed. The withdrawal of the substance and corticotherapy generally lead to complete recovery although several deaths have been reported.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan. A case report with pulmonary manifestations and review of the literature. 165 79

Eosinophilia-Myalgia-Syndrome (EMS), a newly recognized illness, was described first in October 1989, when it formed an epidemic in the USA and later also in Europe. In the meantime, ingestion of L-tryptophan containing products has been recognized to trigger this syndrome, but the pathophysiological basics are still subject to speculation. Often starting with a flu-like period, the disease is dominated by dermatologic (fasciitis) and neurologic (neuropathy, myopathy) symptoms in the subsequent stages. Reporting on an own case and reviewing the literature, clinicopathological aspects and the problems of treatment are discussed. In contrast with the majority of published cases, which showed predominance of axonal damage, our patient displayed the clinical and electro-physiologic characteristics of demyelinating neuropathy.
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PMID:[Polyneuropathy and fasciitis in eosinophilia-myalgia syndrome]. 166 83

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

Several developments in serotonin neuropharmacology have implications for psychiatric disorders and have already begun to impact their treatment. Selective inhibitors of serotonin uptake, which enhance serotonergic function by preventing the removal of serotonin from the synaptic cleft via the membrane transporter, have been introduced for the treatment of depression and may be effective in other disorders. Precursor loading can increase serotonin concentrations in the synaptic cleft, and tryptophan--which has been available in health food stores and drug stores--had become increasingly used for self-medication of depression, insomnia, and premenstrual syndrome. Conversion to serotonin is not the major metabolic pathway for tryptophan, and large increases in other tryptophan metabolites (such as quinolinic acid, a substance that is excitotoxic at high concentrations) accompany small increases in extracellular serotonin. The recent epidemic of the eosinophilia-myalgia syndrome associated with tryptophan now appears due to a trace contaminant in the product from a single manufacturer. A major advance in serotonin pharmacology has been the elucidation of serotonin receptor heterogeneity. At least seven receptor subtypes (5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, 5-HT2, 5-HT3, 5-HT4) have been identified in brain. Direct-acting agonists and antagonists can have selective affinity for specific receptor subtypes. Selective activation of 5-HT1A receptors seems to cause anxiolytic and possibly antidepressive effects. Selective antagonists of 5-HT2 or 5-HT3 receptors may be useful in treating anxiety and schizophrenia. Drugs that enhance serotonergic function suppress aggression in animals, but the specific receptor subtypes involved are not known. The advances being made in serotonin pharmacology will help define the role of this brain neurotransmitter in psychiatric and other disorders and can be expected to lead to further therapeutic advances.
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PMID:Role of serotonin in therapy of depression and related disorders. 167 51

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. 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:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25


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