Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 16-year-old girl, one of dizygotic twins, presented in 1976 complaining of a 1-year history of a lack of coordination and an inability to run. The results of biochemical tests confirmed the diagnosis of classic abetalipoproteinemia. In addition to the recognized neurologic features of this disorder, she had a reduced evoked motor unit potential and markedly elevated serum levels of muscle enzymes, which suggested myositis. The serum vitamin E level was markedly decreased. Oral therapy with vitamin E, 800 mg daily, was begun, and in 1981 the dosage was increased to 3200 mg daily. Over the 7 years of follow-up she improved clinically, there was an increase in the evoked motor unit potential, the serum levels of some of the muscle enzymes decreased to normal, and the serum and tissue vitamin E levels increased significantly. It was concluded that treatment with high doses of vitamin E was responsible for the arrest of the usually progressive neuropathy and myopathy.
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PMID:Arrest of neuropathy and myopathy in abetalipoproteinemia with high-dose vitamin E therapy. 298 Nov 35

We report a patient with late-onset celiac disease and neurological manifestations including myopathy, polyneuropathy, and ataxia. Laboratory investigations showed anti-gliadin antibodies and severe vitamin E deficiency. Muscle biopsy revealed inflammatory infiltrates and rimmed vacuoles, similar to those found in inclusion-body myositis. A gluten-free diet and vitamin E supplementation reversed both the clinical neurological manifestations and the abnormalities in the muscle biopsy. Anti-gliadin antibodies were no longer present. This case illustrates the spectrum of neurological complications of celiac disease and documents the occurrence of reversible pathology resembling inclusion-body myopathy in the muscle.
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PMID:Reversible inflammatory and vacuolar myopathy with vitamin E deficiency in celiac disease. 1538 48

This report describes necrotizing and eosinophilic myositis affecting the masticatory muscles of a group of mink. Affected animals demonstrated sudden death with marked subcutaneous oedema over the dorsal head. The temporalis and masseter muscles were pale, swollen and friable. Histologic changes consisted of varying degrees of myodegeneration, myonecrosis and inflammation. Eosinophils were prominent in the inflammatory infiltrate. Similar to dogs, masticatory muscles in mink were found to contain unique type 2M fibres, suggesting a possible target for an immune response. Aerobic and anaerobic tissue cultures of the affected musculature revealed no significant pathogens. Histological and nutritional analyses were not typical of vitamin E/selenium deficiency. This case series supports the existence of a novel disease entity in mink with some features comparable with masticatory muscle myositis in dogs.
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PMID:Necrotizing and eosinophilic masticatory myositis in farmed mink: a preliminary description. 2501 23