What Is Eosinophilia-Myalgia Syndrome?

Eosinophils in normal humans range from 0% to 7% of the number of white blood cells. Exceeding the normal value is called eosinophilia. Eosinophils have a defensive function in the body, but their increase also causes damage to their own tissues. Eosinophilia-myalgia syndrome is a disease caused by eosinophils to muscles.

Basic Information

English name
eosinophilia-myalgia syndrome
Visiting department
Internal medicine
Multiple groups
female
Common causes
Early low fever, fatigue, dyspnea, cough, joint pain, arthritis, red skin rash, but it disappears quickly, with obvious muscle pain and muscle spasms, etc.

Causes of eosinophilia-myalgia syndrome

Studies have found that L-tryptophan contains a small amount of tryptophan dimer. Is this chemical a causative agent of eosinophilia-myalgia syndrome or another unidentified substance is on the rise? The role is unclear.

Clinical manifestations of eosinophilia-myalgia syndrome

The onset of eosinophilia-myalgia syndrome can be sudden or insidious, more common in women. Early manifestations are low fever, fatigue, dyspnea, cough, joint pain, arthritis, and red spots on the skin, but it disappears quickly, the patient may have obvious muscle pain and muscle spasm, and invasive lesions in the lung may appear. Scleroderma-like skin changes occurred after 2 to 3 months, but there was no Raynaud phenomenon. Patients may have myocarditis and arrhythmia, a small number of patients may have pulmonary hypertension, and one third of patients have the manifestation of eosinophilic fasciitis. Some patients experience persistent peripheral nerve atrophy, and ascending multiple nerve atrophy can lead to paralysis and respiratory failure. Patients may have decreased cognitive recognition, manifested by memory loss, inability to concentrate, etc.
After stopping L-tryptophan, the clinical symptoms of eosinophilia-myalgia syndrome cannot disappear immediately, and need to go through a chronic process. Patients were followed up for 2 years and found that most of the symptoms and signs could be improved or disappeared except for the decrease in recognition ability, but one third of the patients became more ill and peripheral neuropathy was not improved.

Eosinophilia-myalgia syndrome diagnosis

The disease can be diagnosed based on the clinical manifestations of skin lesions, increased eosinophils in the surrounding blood, and characteristic histopathology.

Differential diagnosis of eosinophilia-myalgia syndrome

Adult scleredema
This disease sometimes needs to be distinguished from adult scleredema, which often starts in the neck, then spreads to the face and trunk, and eventually affects the upper and lower limbs. The lesions were diffuse non-depressive swelling and stiffness. There is often a history of upper respiratory infections before onset. Histopathology showed swelling and homogenization of collagen fibers, and the gaps were filled with an acidic mucopolysaccharide matrix.
2. Dermatomyositis
Dermatomyositis involves muscles mainly in the scapular belt and the proximal extremities. The upper eyelid has edema purple spots and the Gottron sign on the back of the hand and knuckle. Serum muscle enzymes such as CK, ALT, and AST, and 24-hour urine creatine excretion were significantly increased.
3. Systemic scleroderma
It is not difficult to distinguish systemic scleroderma from this disease. This disease has no Raynaud phenomenon, visceral involvement (especially lung and gastrointestinal tract) is rare, no telangiectasia, no anti-Scl-70 antibody and anti-centromere antibody appear. In addition, eosinophils were elevated in systemic scleroderma without blood, and histopathological manifestations were also different.

Eosinophilia-myalgia syndrome complications

Patients may have myocarditis and arrhythmias, a small number of patients may have pulmonary hypertension, and some patients have persistent peripheral nerve atrophy. Ascending polyneuropathy can lead to paralysis and respiratory failure.

Eosinophilia-Myalgia Syndrome Treatment

When there are obvious symptoms, treat symptomatic treatment, and glucocorticoid should be given at the same time. The commonly used medicine is Bonisson, which is reduced after 1 to 1.5 months. If necessary, add immunosuppressants (methotrexate, cyclophosphamide, etc.).

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