Eosinophilia-Myalgia Syndrome
L-tryptophan contaminant 'peak E' induces the release of IL-5 and IL-10 by peripheral blood mononuclear cells from patients with functional somatic syndromes. (1/10)
In 1989, the development of eosinophilia myalgia syndrome (EMS) was observed in some patients after the intake of l-tryptophan containing several contaminants, including 1,1'-ethylidenebis[l-tryptophan] ('peak E'). Since l-tryptophan has been taken particularly by individuals suffering from functional somatic syndromes (FSS), such as fibromyalgia syndrome (FMS), we put forward the hypothesis that EMS may have developed preferentially in patients with FSS as an allergic reaction towards the contaminant peak E. We therefore studied the immunological reactivity towards l-tryptophan and peak E in these individuals (n = 12) and compared these data with those obtained in 12 healthy controls and 12 patients with other chronic disorders. Peripheral blood mononuclear cells (PBMC) were cultured for 7 days with pure l-tryptophan and peak E. Supernatant fluids were collected at day 7. The type 2 cytokines IL-4, IL-5 and IL-10, and the type 1 cytokines IL-2 and IFN-gamma, were determined by a double sandwich ELISA. PBMC from seven of the 12 FSS patients, but only three of the 24 controls, produced cytokines after incubation with peak E (P < 0.05). Interestingly, six of the seven FSS patients reacting with peak E produced IL-5 and/or IL-10. In contrast, PBMC from only one patient with other chronic disorders and one healthy control secreted type 2 cytokines in response to peak E. The observed heightened type 2 reactivity towards the more immunogenic contaminant 1,1'-ethylidenebis[l-tryptophan] in FSS patients may therefore be taken as an additional argument for our concept that EMS may have developed as a kind of drug-induced allergic disease. (+info)Chronic demyelinating polyneuropathy associated with eosinophilia-myalgia syndrome. (2/10)
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. (+info)Detection of antineutrophil cytoplasmic antibody in a patient with L-tryptophan induced eosinophilia-myalgia syndrome. (3/10)
The Center for Disease Control has received numerous reports of an eosinophilia-myalgia syndrome related to products containing L-tryptophan. The case is reported of eosinophilia-myalgia syndrome and polyneuropathy associated with myeloperoxidase specific antineutrophil cytoplasmic antibody. (+info)Immunogenetic risk and protective factors for the development of L-tryptophan-associated eosinophilia-myalgia syndrome and associated symptoms. (4/10)
(+info)Post-epidemic eosinophilia-myalgia syndrome associated with L-tryptophan. (5/10)
(+info)Effects and side effects associated with the non-nutritional use of tryptophan by humans. (6/10)
(+info)Enhanced collagen synthesis and transcription by peak E, a contaminant of L-tryptophan preparations associated with the eosinophilia myalgia syndrome epidemic. (7/10)
The pathogenesis of the eosinophilia myalgia syndrome (EMS) remains unclear. Several abnormal constituents have been found in the L-tryptophan lots responsible for the illness, particularly, 1,1-ethylidenebis[L-tryptophan], also called peak E or EBT, and 3-phenylamino-alanine or peak 5. However, the role of these contaminants in the pathogenesis of EMS and in the development of fibrosis is unknown. We now report that peak E, a dimer of L-tryptophan, is a potent stimulus for human dermal fibroblast DNA and collagen synthesis. Peak E (0.1-1.0 microM) increased DNA synthesis up to four-fold (P = 0.0001) in a dose-dependent manner (r = 0.987). When added to monolayer cultures for 2 to 24 h, peak E (0.5 to 100 microM) caused a progressive, more than threefold increase in alpha 1(I) procollagen mRNA levels and collagenous protein. No increase in procollagen mRNA levels was found after the addition of another major L-tryptophan contaminant, peak 5, or with L-tryptophan itself. Transient transfection with a 2.5-kb alpha 1(I) procollagen promoter-luciferase construct showed that peak E causes a twofold upregulation of promoter activity (P = 0.022). Contraction of collagen gels, consisting of human dermal fibroblasts incorporated into a type I collagen lattice, was enhanced two-fold by exposure to peak E (P = 0.001). We conclude that a major constituent of contaminated batches of L-tryptophan, peak E, is a potent stimulus for fibroblast activation and collagen synthesis. This stimulatory action of peak E may provide a direct mechanism for the development of fibrosis in EMS. (+info)A murine model of the eosinophilia-myalgia syndrome induced by 1,1'-ethylidenebis (L-tryptophan). (8/10)
The eosinophilia-myalgia syndrome (EMS) is a recently described disease that has been associated with the ingestion of L-tryptophan containing trace amounts of several impurities. The first such contaminant to be identified and linked epidemiologically to the EMS epidemic was 1,1'-ethylidenebis(L-tryptophan) (EBT), but its role in the etiology and pathogenesis of the syndrome has been controversial. We report the development of inflammation and fibrosis affecting the dermis and subcutis, including the fascia and perimyseal tissues, after the daily intraperitoneal administration of EBT to female C57BL/6 mice. Such changes are accompanied by increased numbers of mast cells, many of which appear to be degranulating. Plasma levels of quinolinic acid, a metabolic product of L-tryptophan via the kynurenine pathway, are reduced initially, and then become elevated when inflammation and fibrosis are more pronounced. The nature and location of the inflammatory cell infiltrate and fibrosis, as well as the presence of mast cells and alterations of L-tryptophan metabolism, are consistent with findings reported in patients with EMS. This murine model suggests that EBT may have been one of the mediators of EMS and should facilitate studies of the pathogenesis of EMS. (+info)Eosinophilia-myalgia syndrome (EMS) is a rare disorder characterized by severe muscle pain (myalgia) and increased levels of eosinophils, a type of white blood cell, in the blood. The exact cause of EMS is not fully understood, but it has been associated with the ingestion of L-tryptophan, an amino acid supplement, and contaminants found in some batches of this supplement.
The symptoms of EMS can vary widely, but often include:
* Severe muscle pain and stiffness, particularly in the arms, legs, and back
* Weakness and fatigue
* Swelling of the hands and feet
* Skin rashes or other skin changes
* Difficulty swallowing or breathing
In addition to these symptoms, people with EMS often have elevated levels of eosinophils in their blood, which can be detected through a complete blood count (CBC) test. Other diagnostic tests, such as muscle biopsies and imaging studies, may also be used to help confirm the diagnosis.
The treatment of EMS typically involves a combination of medications to manage symptoms and reduce eosinophil levels. Corticosteroids, immunosuppressive drugs, and anti-inflammatory agents are commonly used to treat the muscle pain, swelling, and other symptoms associated with EMS. In severe cases, plasma exchange or intravenous immunoglobulin therapy may be necessary.
It is important to note that L-tryptophan supplements have been banned in the United States since 1990 due to their association with EMS. People who experience symptoms of EMS should seek medical attention promptly and avoid taking any dietary supplements containing L-tryptophan.
Eosinophilia is a medical condition characterized by an abnormally high concentration of eosinophils in the circulating blood. Eosinophils are a type of white blood cell that play an important role in the immune system, particularly in fighting off parasitic infections and regulating allergic reactions. However, when their numbers become excessively high, they can contribute to tissue damage and inflammation.
Eosinophilia is typically defined as a count of more than 500 eosinophils per microliter of blood. Mild eosinophilia (up to 1,500 cells/μL) may not cause any symptoms and may be discovered during routine blood tests. However, higher levels of eosinophilia can lead to various symptoms such as coughing, wheezing, skin rashes, and organ damage, depending on the underlying cause.
The causes of eosinophilia are varied and can include allergic reactions, parasitic infections, autoimmune disorders, certain medications, and some types of cancer. Accurate diagnosis and treatment of eosinophilia require identification and management of the underlying cause.