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 young male patient with myositis associated with Crohn's disease is reported. His serum creatine phosphokinase (CPK) level was markedly elevated, but he had no muscle symptoms. The serum CPK level was not correlated with the activity of Crohn's disease. Muscle biopsy showed myositis with only degeneration of the muscle fibers and infiltration of inflammatory cells. The etiology of myositis in this case was not clear. Diagnosis of myositis based on a muscle biopsy in patients with Crohn's disease showing an elevated serum CPK level without any discernible cause has not been reported previously. Careful attention to the serum CPK and muscle symptoms in patients with Crohn's disease is suggested.
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PMID:Report of a case of Crohn's disease associated with hyper-creatine phosphokinase-emia. 180 46

Infused beta 2 agonists have been shown to cause focal myocardial necrosis. Serum creatine kinase activity was compared in 13 patients with brittle asthma currently being treated with subcutaneous terbutaline and an age and sex matched control group of patients with moderate asthma having inhaled treatment only. The median serum total creatine kinase activity for patients receiving subcutaneous terbutaline (211 units/l) was greater than that for the control group (120 units/l). The cardiac specific isoenzyme component of creatine kinase was not raised in either group, and the electrocardiograms and serum aspartate aminotransferase activity were normal. Electromyograms in five patients receiving subcutaneous terbutaline with high creatine kinase activity showed changes consistent with myositis in two, one of whom was subsequently shown to have a metabolic myopathy, which is thought to be long standing. No pathological changes were seen in the myocardium at necropsy in a patient who died from an acute attack of asthma while taking subcutaneous terbutaline. These results suggest that the raised creatine kinase activity seen in patients receiving this treatment is unlikely to be myocardial in origin.
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PMID:Creatine kinase activity in patients with brittle asthma treated with long term subcutaneous terbutaline. 192 27

A 25-year-old woman with a 2 years history of painful enlargement of the left calf visited our clinic because of ache in the left calf which became severe enough to interfere her walk. She had no history of trauma to the calf, and family history was negative for muscle disease. Physical examination showed an enlarged left calf muscle with pain which was evoked by stretching of the Achilles tendon. There was no muscle weakness or neurological abnormality. Laboratory tests were all within normal limits, including erythrocyte sedimentation rate and serum enzymes such as creatine kinase and aldolase. The CT scan revealed an isolated round-shaped low density area in the left calf muscle, which showed up as a markedly high signal intensity on T2 weighted images of MRI. The lesion was confirmed to be the lateral head of the gastrocnemius muscle. The specimen obtained from the affected muscle demonstrated degenerative and inflammatory changes together with excess fibrosis. There was no sarcoid lesion or malignancy. From the above results, the present case was thought to have isolated focal myositis. Prednisolone 80 mg (40 mg, twice, at 4-day intervals) was given to the left femoral artery without any trouble. Thereafter the patient became free from pain and difficulty in walking, and the lesion demonstrated by CT scan disappeared in 15 days. However, the high signal intensity on T2 weighted images faintly remained until the 54th day after the treatment. In summary, MRI is more sensitive than CT scan for detection of isolated focal myositis, which might be successfully treated by arterial injection of prednisolone within a short period than any other conventional methods.
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PMID:[A case of isolated focal myositis successfully treated by arterial injection of prednisolone--its findings by CT scan and MRI]. 208 34

We report two brothers, aged 68 and 61 years respectively, who had an unclassified familial neuromuscular disease with infiltration of cytotoxic/suppressor T cells in muscle biopsies. The elder brother was in good health and active during child and adulthood until the age of 65 when muscle atrophy in the quadriceps muscle was noted. His muscle weakness and atrophy progressed relatively rapidly in the course of a few years. The muscle symptoms predominated in the under extremities at the initial stage, later to be generalized, sparing the facial muscles. The serum creatine kinase (CK) was 145 mu/ml (normal 5-80 mu/ml). EMG revealed myopathic changes. A biopsy taken from biceps muscle showed extensive inflammatory cellular infiltrations among fibers and in the perimysium. The infiltrated cells were identified to be cytotoxic/suppressor T cells. The younger brother first noticed diminished bulk in quadriceps muscle bilaterally at the age of 59. The muscle symptoms were similar to those seen in his brother. Serum CK was 520 mu/ml. EMG showed myopathic changes except for fibrillation potentials in the biceps. A biopsy taken from quadriceps muscle revealed the similar findings of his brother. The classification of these cases is a controversial subjects. We differentiated quadriceps myopathy, limb-girdle muscular dystrophy and myositis, which we couldn't classify. So at this point we reported these cases as unknown cause of familial neuromuscular disease.
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PMID:[Unknown cause of familial neuromuscular disease with infiltration of cytotoxic/suppressor T cells]. 214 56

Muscle biopsies from 12 patients with systemic lupus erythematosus (SLE) who presented with muscle weakness and myalgias were studied ultrastructurally. Two different alterations were present, myositis (11 cases), and vacuolar myopathy (1 case). The myositis exhibited muscle atrophy, microtubular inclusions, and a mononuclear cell infiltration. In one case, with increased serum creatine phosphokinase, fiber necrosis was evident. Capillary abnormalities included thickening and reduplication of basement membrane, alterations of endothelium and microtubular inclusions. The vacuolar myopathy also showed vacuolated muscle fibers and occasional zebra bodies. The different associations between muscle diseases and SLE are grouped. Our data suggest that SLE myositis is a distinct clinical and pathological entity. The SLE vacuolar myopathy is a pathological entity clinically undistinguishable from SLE myositis.
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PMID:Ultrastructural pathology of skeletal muscle in systemic lupus erythematosus. 231 20

Myositis is recognized as one of several neurologic complications encountered in Kawasaki disease. We report an unusual patient with Kawasaki disease which was complicated by severe myositis and respiratory failure secondary to weakness. Comparison of our patient with previously reported cases leads us to conclude that myositis in Kawasaki disease usually is present within 1-3 weeks of illness; the symptoms usually are mild and probably remain unnoticed by most physicians, but weakness can be severe and respiratory failure may occur. The degree of creatine kinase elevation may be useful in predicting the severity of myopathy and in alerting the physician to the need for close respiratory monitoring. Therapy is supportive and complete recovery is to be expected.
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PMID:Myositis in Kawasaki disease. 234 31

In 25 patients with primary dyslipoproteinemias and severe premature atherosclerosis, during an average combined Lopid-Mevacor treatment span of 12.5 months per patient, our specific aim was to assess safety and efficacy of open-label therapy with diet, gemfibrozil (Lopid), and lovastatin (Mevacor). Because targeted lipid values were not reached on diet alone (low-density lipoprotein cholesterol [LDLC] less than 120 mg/dl, high-density lipoprotein cholesterol [HDLC] greater than 35 mg/dl or total cholesterol [TC]/HDLC less than 4.5), the patients received Lopid, 1.2 gm/day as their initial lipid-lowering drug. Because targeted lipid levels were not reached with Lopid treatment alone after 3 or more months, Mevacor was added, with 17 subjects receiving 20 mg/day, five receiving 40 mg, two receiving 60 mg, and one receiving 80 mg. Outpatient visits were repeated during combined therapy every 6 to 8 weeks, with an average of 6.4 visits per subject, 162 measurements of fasting lipids and liver function tests, and 127 measurements of creatine phosphokinase (CPK). By selection, all patients had normal liver function (gamma-glutamyltransferase, serum glutamic-oxaloacetic transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) levels) and normal CPK levels at baseline. No gamma-glutamyltransferase levels were high during combined therapy. Of the 162 liver function test measurements, five (3.1%) SGOT levels and three (1.9%) SGPT levels were high. Of 127 CPK measurements, three (2.4%) were high; one subject had a high CPK measurement, and one subject had two high measurements for CPK. No symptomatic myositis or myalgias developed in the subjects; none had palpable skeletal muscle tenderness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of combined gemfibrozil-lovastatin therapy for primary dyslipoproteinemias. 234 62

The authors have previously shown that passive daily mobilization of the rabbit hind limb immobilized with the knee in extension leads to necrosis of the deep thigh muscles and myositis ossificans-like periosteal bone formation. In this study the effect of immobilization alone on the rabbit hind limb muscles was examined similarly to that of immobilized limbs. Serum creatine kinase activities increased significantly and intravenously administered Evans blue albumin showed increased vascular permeability in the deep vastus intermedius muscle even on day 1. Necrotic fibers were clearly present in the deep part of the vastus intermedius muscle on day 5 in light and electron microscopy and in enzyme histochemistry. Fibrosis and atrophy were found later. The superficial portion of the vastus intermedius and the deep contralateral nonimmobilized vastus intermedius showed degenerative changes. Bone formation was not noted. The conclusion was that the deep vastus intermedius muscle composed almost exclusively of type I fibers is exceptionally prone to damage when immobilized in a shortened position. Contact of the necrotic muscle with the underlying periosteum is not alone sufficient to induce heterotopic ossification. The additional trauma caused by daily mobilization is needed for the myositis ossificans-like bone formation.
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PMID:Severe degeneration of rabbit vastus intermedius muscle immobilized in shortened position. 235 53

An outbreak of muscle disease affected approximately 20 of 600 ewes in spring 1987 in south-east Scotland. The clinical signs were a flaccid paralysis of the hind limbs and in severe cases collapse. Serum creatine kinase and aspartate aminotransferase activities were increased. Clinically affected sheep had a mean reciprocal serum antibody titre in a sarcocystis immunofluorescence antibody test of 557 whereas 22 sheep from the same flock, sampled one year earlier, showed a mean reciprocal titre of only 51. Histologically a heavy infestation of sarcocysts, myodegeneration and a non-suppurative myositis centred on degenerating sarcocysts were observed in a wide range of skeletal muscles and myocardium from four affected sheep. Monensin sodium had been inadvertently included in the protein pellet used in the feed for one week before the onset of the disease.
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PMID:A myopathy of sheep associated with sarcocystis infection and monensin administration. 250 29

Polymyositis and myasthenia gravis-like syndromes have been seen in patients with GVH disease following bone marrow transplantation. We therefore investigated the histopathology of muscle in mice with acute graft-versus-host disease in order to determine whether these conditions are caused by injury from the GVH reaction itself or are due to radiation and drugs used to prepare the host for transplantation. GVH reactions were induced by intravenously infusing 50 x 50(6) lymph node and spleen cells from A/J-strain donors into (C57BL/6 x A/J)F1-hybrid recipients. These mice developed an active inflammatory myopathy beginning 15 days after engraftment. The inflammatory infiltrates were focal in distribution, initially around perimysial blood vessels, and later around muscle fibers. The infiltrating cell population was composed of lymphocytes, plasmacytoid cells, and macrophages. Muscle cell necrosis was observed and was temporally related to elevations in serum creatine kinase. Similar histologic changes were present in the myocardium. Our findings support the notion that muscle involvement in patients with GVH disease is caused by the disease itself. Myositis accompanying experimental GVH disease in mice may hold promise as a model of autoimmune inflammatory myopathy.
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PMID:Inflammatory myopathy in F1 hybrid mice with acute graft-versus-host reactions. 275 59


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