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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A survey of skeletal muscle pathology in 92 autopsied cases of AIDS revealed microscopic alterations in 64 cases. There were 40 cases of disuse atrophy, 8 of denervation atrophy, 2 of cryptococcal myositis, 1 of Mycobacterium avium intracellulare (MAI) infection and 2 of necrotizing myopathy associated with hyperkalemia. A second group of cases with changes of unknown etiology was found. These were tentatively ascribed to the direct or indirect action of HIV. This category includes 8 cases of inflammatory myopathy, 8 of necrotizing myopathy in absence of a known etiological factor, 3 of extreme atrophy and 4 of "regenerating" myopathy.
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PMID:Skeletal muscle pathology in AIDS: an autopsy study. 236 23

Twenty-two chronic alcoholic patients were assessed by neurologic examination and muscle biopsy. The patients manifested proximal muscular weakness to a variable extent. One case presented as an acute bout of myopathy, according to the Manual Muscle Test, MMT. The most prominent histologic feature observed was muscle atrophy (95.3%) better evidenced through the ATPase stain with the predominance of type II A fibers (71.4%). Lack of the mosaic pattern (type grouping) seen in 76% of the cases and an important mitochondrial proliferation with intrasarcoplasmatic lipid accumulation in 63% of the patients. In case of acute presentation of muscle weakness the pathological substrate is quite different, i.e. presence of myositis mainly interstitial characterized by lymphoplasmocytic infiltrate and several spots of necrosis like Zencker degeneration. Based on histologic criteria, our data suggest that: the main determinant of muscle weakness seen in chronic alcoholic patients is neurogenic in origin (alcoholic polyneuropathy); the direct toxic action of ethanol under the skeletal muscle is closely related to the mitochondrial metabolism; the so-called acute alcoholic myopathy has probably viral etiology.
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PMID:[Histochemical study of the skeletal muscle in chronic alcoholism]. 248 Jul 68

Two techniques to measure muscle fiber conduction velocity (MFCV) were compared. First, muscle fibers of biceps muscle were directly stimulated with needle electrodes, and the latency of the evoked muscle fiber action potentials was measured at a distance of 5 cm. Subsequently, the MFCV was measured at the same place with surface electrodes using the cross-correlation method. Fourteen controls were studied and illustrative results of the measurements of 6 myopathy patients are given. A clear correlation between the mean values of the two methods was found. The surface EMG technique resulted in a systematically higher MFCV (mean 1.0 m/sec); the variability of MFCV was much higher with the invasive technique. The reasons for these differences are discussed. MFCV measurements are shown to be of diagnostic value in some myopathies, for example myositis. In myopathies with a global reduction of the MFCV the two methods are of equal value; in some cases of longstanding myositis the needle method demonstrated some very slowly conducting fibers which were not detected with the surface method.
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PMID:Evaluation of the estimation of muscle fiber conduction velocity. Surface versus needle method. 248 Aug 88

Aetiologic conditions for enlargement of extra ocular muscles are graves' orbitopathy, acute or subacute myositis as a subgroup of inflammatory orbital pseudotumor, and sometimes lymphoid or metastatic tumor. The distinction of these aetiologies can be made on clinical versus CT Scan or IRM grounds with two different patterns of oculomotor disfunction. Restrictive extensibility, which found expression in the antagonist field, is typical of grave's myopathy, sequelae of subacute myositis or acute myositis of the superior oblique. Deficiency of the enlarged muscle's contractibility is typical of a recent and transient myositis involving a rectus muscle or of a rare tumor of an extraocular muscle.
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PMID:[Oculomotor disorders and enlargement of the extraocular muscles]. 264 Nov 1

We recently described the induction of an inflammatory myopathy in SJL/J mice after injection of skeletal muscle Ag and adjuvant that is characterized by necrosis of muscle fibers associated with infiltrating mononuclear cells. In the present study, an immunohistologic analysis was performed to examine the phenotype of these infiltrating cells and to determine changes in cell-surface Ag expression in involved muscle. The predominant cells infiltrating muscle after induction of experimental autoimmune myositis (EAM) were found to be Mac-1+/I-A+ macrophages, representing 80 to 90% of all infiltrating cells, and CD4+ T lymphocytes, representing 10 to 15% of all infiltrating cells. Few CD8+ T cells, and no B cells, were seen in the involved muscles. Interestingly, endothelial cells in involved muscles were also noted to express class II MHC Ag. Aberrant I-A Ag expression was not observed on endothelial cells in other tissues examined, including kidney, liver, cardiac muscle, and lung. I-A Ag expression appeared to correlate with susceptibility to disease in that muscle endothelial cells remained negative after attempts to induce EAM in a nonsusceptible strain. Together, the data suggest that aberrant organ-specific class II MHC Ag expression and a response by CD4+ T cells may be pathogenetically involved in the muscle injury of EAM. In addition, the predominance of infiltrating macrophages suggests that these recruited cells may also be important in the immune-mediated muscle damage.
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PMID:Aberrant expression of class II MHC antigens by skeletal muscle endothelial cells in experimental autoimmune myositis. 265 63

Idiopathic inflammatory myopathy, a category encompassing polymyositis, dermatomyositis, and a number of other disorders, is very uncommon, but has been the focus of intense study in the Arthritis and Rheumatism Branch of the National Institute of Arthritis and Musculoskeletal and Skin Diseases for the past several years. We describe the clinical picture, stressing the need for biopsy to ensure correct diagnosis. It is especially important to recognize the treatment-resistant variant, inclusion body myositis. The extraskeletal manifestations, particularly the cardiopulmonary, oropharyngeal, gastrointestinal, and endocrine involvement, are described. The cardiopulmonary involvement, especially interstitial lung disease, arrhythmias, and cardiac failure, may dominate the clinical picture. The known causes are varied, and include drugs, toxins, and some infectious agents, however, in most cases a cause cannot yet be identified. Circumstantial evidence suggests that picornaviruses may initiate some cases in humans, and a very similar disease in mice caused by a picornavirus is actively under study. Studies of autoantibodies and cellular immune function support a central role for disordered immunity in the pathogenesis. The myositis-specific autoantibodies, especially those directed at certain enzymes important in protein synthesis (the aminoacyl-transfer RNA synthetases), are found in a clinically distinct subset of patients. Although most patients respond initially to corticosteroids, cytotoxic drugs are sometimes added when steroid toxicity or refractoriness develops. We describe several newer therapies under study for such cases and outline future directions in research.
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PMID:Current concepts in the idiopathic inflammatory myopathies: polymyositis, dermatomyositis, and related disorders. 266 48

We report the case of a 69 year old female, who in 1979 presented with a granulomatous myositis confirmed by muscular biopsy. The histology is typical for sarcoidosis, but tests on other organs remained negative for eight years. Up to 1987, 79 cases of sarcoid myopathy have been published in medical journals, of which 44% had an isolated muscular involvement. We discuss the differential diagnosis, the histology, pathology, etiology and the manifestations shown by the EMG of this rare illness, as well as our patient's peculiar signs.
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PMID:[Sarcoidosis: apropos of a case of isolated myopathy]. 274 Jun 74

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

Routine methods of monitoring treatment responses in polymyositis patients, such as clinical strength assessments and measurements of ESR and serum creatine kinase, have been compared with functional strength measurements and assay of serum myoglobin levels, in a prospective study of nine cases followed for up to five years. Seven patients also underwent serial muscle biopsies during the first year of treatment in order to document the nature and chronology of histological changes during therapy. Inflammatory and necrobiotic changes indicating active myositis resolved within six months in all cases and no patient developed histological evidence of steroid myopathy. Scores on functional muscle strength assessments improved more slowly than static manual muscle strength test results, reflecting morphometric and architectural abnormalities in the biopsies which persisted throughout the period of observation. Serum creatine kinase levels returned to normal more rapidly than serum myoglobin. No statistical relationship was found between muscle strength measurements and biochemical or histological changes within the patients as a group, but variations in these indices in individual subjects reflected changes in clinical state.
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PMID:Clinical, biochemical and histological responses to treatment in polymyositis: a prospective study. 281 Mar 11

Methionine sulfoximine (MSO) is a centrally acting neurotoxin which inhibits the glutamate metabolism enzymes and has convulsive properties. Administration of a small dose of MSO to rabbits, either intravenously or intracerebroventricularly, except for the already known convulsive effects, may also be responsible for hind leg myopathy (rigid paralysis with histological findings resembling myositis) which sets in by the 4th day after MSO administration.
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PMID:Long-term effects of the administration of the convulsive substance DL-methionine-DL-sulfoximine to the rabbit. 281 83


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