Eosinophilia-myalgia syndrome

Eosinophilia myalgia syndrome was first recognized in 1989 from a patient's unique clinical picture epzinofilie including severe myalgia and peripheral blood. All patients ingested supplements containing L-tryptophan induced sleep.
The disease is chronic and characterized by itching, skin lesions, edema, changes in scleroderma and pain, with dramatic and eosinophilia myalgia. In the early stage of the disease all patients have muscle cramps, cough, dyspnea and weight loss. This phase lasts several weeks and is followed by a chronic changes characterized by scleroderma, neuropathy, neurocognitive deficits, and muscle spasms. The exact cause of the disease is still unknown. Histological feature is the extensive inflammatory reaction.
Most patients with eosinophilia-myalgia syndrome continue to have symptoms 4 years after onset of infarction. This is due to tissue destruction permamente acute phase of disease. Only 10% of patients reported complete remission. Muscle pain, fatigue and muscle spasms are the most frequent accusations of waste.Subjective memory loss and difficulties of finding cuvitelor are also reported. These symptoms do not respond to any treatment.Patients who had disease onset with severe internal organ damage, neuropathy and thickening of the skin tend to show a negative prognosis.
PathogenesisEosinophilia-myalgia syndrome pathogenesis is unknown. The three major diseases found in patients include:Capillary endothelial-cell hyperplasia with swelling and necrosis-Infiltrating inflammatory monocytes histiocite, lymphocytes and macrophages in nerves, muscles and connective tissue adjacentIncreased fibrosis of the fascia, and skin.The risk factors considered nonnecesara ingestion of tryptophan inhibit histamine degradation and increasing the formation of indole metabolites, which will block the degradation of histamine in the new po-I effects. Increased activity of histamine is known to induce eosinophilia in peripheral blood and myalgia. Patients with adjustment disorders pituitaro-hypothalamic-adrenal axis, which does not have this syndrome show high sensitivity to the ingestion of tryptophan and histamine. Histamine imbalance seems to be a common pathogenesis for syndromes characterized by eosinophilia and myalgia.
Toxic metabolites hypothesis:L-tryptophan is metabolized through two different ways. The first is cleaved into serotonin, and in the latter is degraded to kinurenina.Kirunenina can be metabolized to quinolinic acid, which is an endogenous neurotoxin involved in the pathogenesis of several neurological diseases and emtabolice. Metabolites of both pathways are associated with connective tissue disease.Supraproducerea serotonin by carcinoid tumors is associated with myalgia and arthralgia, with sclerodermalike changes.Contamination theory:Due to the nature of the epidemic syndrome, inherited altered sensitivity to tryptophan can not be only the pathogenesis of the syndrome. It has been suspected as the cause of a contaminant. In fact L-tryptophan produced by different brands shows various impurities which would trigger the syndrome.
Signs and symptomsVariz clinical manifestations of the syndrome in general. Typically there is an abrupt onset of incapacitating myalgia, muscle cramps, dyspnea, peripheral edema, mild fever, fatigue and skin rashes.The acute inflammatory symptoms subside in 3-6 months and is installed varying degrees of neuropathy, myopathy and thickening of the skin. At four days after the acute phase, patients reported persistent chronic fatigue, intermittent myalgia, muscle cramps, but no new episodes after this period.Early clinical manifestations observed in the first four months of illness include:Myalgia:Patients experience pain incapacitating muscle, generalized severe that tends to worsen in a few weeks. Muscle weakness is not observed in this state. Shoulders, back and legs are affected most often. Relapses are common after a full resolution. Leg cramps involving abdominal muscles appear to persist for several weeks and a few years. Movement, exercise or change position triggers muscle spasms.
Edema:Affecting the extremities, peripheral edema, facial edema and periorbital appear at more than half of patients, typically at 4 weeks after onset.
Arthralgia: pain in large joints is common, but arthritis is rare.
Alopecia: hair loss on the scalp, without scarring is frequently observed during acute disease gradually resolves.
Skin eruptions:Cutaneous manifestations develop 3 weeks after onset of myalgia and are maintained for 3 months. The type of eruption observed in patients include macules varying from small and large purple and brown till, urticaria, mucinous yellow cards, dermatografism, erythematous lesions serpiginoase and boards. Severe itching is prominent in some patients.
Thickening of skin:This change occurs in one third of patients. It is similar to that of Eosinophilic fasciitis with subcutaneous induration affecting the forearms, arms and legs. Thickened patches of skin are occasionally seen similar morphea. In contrast to systemic sclerosis, digital skin thickening and Raynaud's phenomenon are rare.
Pulmonary symptoms:Nonproductive cough, dyspnea is observed especially at 3 weeks after onset of myalgia. These accusations are self-limiting in most patients and are maintained three months.
Neurological symptoms:Paresthesia, tingling, burning sensation are present in one third of patients.
Gastrointestinal symptoms:Dyspepsia, dysphagia, diarrhea are problems described in some patients.Clinical one year after onset of illness - patients have persistent chronic symptoms:With remission and relapse-myalgia-Muscle weaknessDescribed as deep-fatigueMuscle cramps, spontaneous or induced activityJoint pain and stiffness,-Tingling and burning sensation-Memory loss, difficulty concentrating-Difficulty in communication, changes similar to scleroderma-Exercise dyspnea.