PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MYOSITIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMedDate not supplied

Penicillamine-induced myositis in rheumatoid arthritis.

A patient with rheumatoid arthritis who developed multiple mononeuropathies multiplex was shown to have vasculitis in nerve biopsy, but no evidence of inflammatory muscle disease in muscle biopsy. Treatment with penicillamine caused the rare complication of polymyositis, documented clinically, electrophysiologically, and by light and electron microscopy in a second muscle biopsy. The evidence presented supports the concept that penicillamine may induce polymyositis or aggravate a pre-existing low-grade myositis.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Canine muscle fiber types and susceptibility of masticatory muscles to myositis.

The myofiber type composition was studied in 42 different muscles of the dog to determine if there are unique features that might explain the preferential involvement of the muscles of mastication by inflammatory myopathies. The principal myofiber types for most muscles studied were type 1 and type 2A and, to a lesser extent, type 2C, whereas the dorsal group of muscles innervated by the mandibular nerve (Mm. temporalis, and tensor veli palatini) was composed only of type 2C myofibers and a variant of the type 1 myofiber whose staining intensity was not fully reversed after preincubation in acid media. The distribution of this myofiber type composition was associated with the innervation and embryologic development of the dorsal muscles innervated by the mandibular nerve. This unique myofiber type composition could provide the basis for the preferential susceptibility of these muscles to agents (e.g., immune and/or infectious) that produce myositis; however, further studies are required to assess that possibility.

Animals↗
PubMedDate not supplied

Fiber type-specific autoantibodies in a dog with eosinophilic myositis.

Serum from a 2-year-old male Belgian sheepdog with eosinophilic myositis, which particularly affects the masticatory muscles, was tested for the presence of muscle-specific autoantibodies. Control type 2 temporalis muscle fibers were selectively stained following incubation with the patient's serum and staphylococcal protein A conjugated to horseradish peroxidase (SPA-HRPO). Likewise, type 2 fibers in the patient's temporalis muscle were selectively stained with SPA-HRPO. The same staining procedures applied to limb muscle did not result in fiber staining. Proteins isolated from the temporalis and triceps brachii muscles of a normal dog were separated under denaturing conditions by one-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The separated proteins were transferred onto nitrocellulose paper and incubated with either sera from the patient, normal dogs, or neuromuscular disease controls. Subsequent incubation with peroxidase-conjugated goat anti-dog IgG demonstrated antibodies to at least four proteins of the temporalis muscle (myosin heavy chain and three unidentified proteins) when incubated with the patient's serum but not with the controls. Under all conditions, antibodies to the proteins of the triceps brachii were not detected. These findings establish the presence of autoantibodies to specific temporalis muscle proteins that may initiate the myonecrosis and inflammatory response as well as limit the distribution of the response.

Animals↗
PubMed1990

Electrophysiological spectrum of inclusion body myositis.

We present electrodiagnostic data on 30 patients with inclusion body myositis (IBM) in order to better delineate its electrophysiological features. Comprehensive electromyography (EMG) and nerve conduction studies (NCS) were performed in all cases. Twelve patients had single fiber electromyography (SFEMG). EMG showed abundant short-small motor unit potentials (MUP) with fibrillations and positive sharp waves in 56.6% of patients, and a mixed pattern of large and small MUP in 36.7%. In 6.7%, only "neurogenic" features were seen. NCS were slow in 33.3%. SFEMG revealed a mildly abnormal jitter and a slightly increased fiber density. IBM demonstrates a heterogeneous EMG profile. A pattern of large and small MUP is highly suggestive of IBM but is seen in only about one third of cases.

Action Potentials↗
PubMed1993

Focal myositis of the temporal muscle.

Focal myositis is a rare inflammatory disease of the skeletal muscle that may involve any part of the body. We present a 19-year-old man with a short history of a painful pseudotumor in the right temporal region. MRI pictures showed a swollen right temporal muscle and muscle biopsy revealed the characteristic histological and immunocytochemical findings of polymyositis.

Adult↗
PubMed2002

The muscular dystrophy with myositis (mdm) mouse mutation disrupts a skeletal muscle-specific domain of titin.

Muscular dystrophy with myositis (mdm) is a recessive mouse mutation that causes severe and progressive muscular degeneration. Here we report the identification of the mdm mutation as a complex rearrangement that includes a deletion and a LINE insertion in the titin (Ttn) gene. Mutant allele-specific splicing results in the deletion of 83 amino acids from the N2A region of TTN, a domain thought to bind calpain-3 (CAPN3) the product of the human limb-girdle muscular dystrophy type 2A (LGMD2A) gene. The Ttn(mdm) mutant mouse may serve as a model for human tibial muscular dystrophy, which maps to the TTN locus at 2q31 and shows a secondary reduction of CAPN3 similar to that observed in mdm skeletal muscle. This is the first demonstration that a mutation in Ttn is associated with muscular dystrophy and provides a novel animal model to test for functional interactions between TTN and CAPN3.

Animals↗
PubMed1994

The alpha beta T-cell receptor repertoire in inclusion body myositis: diverse patterns of gene expression by muscle-infiltrating lymphocytes.

Inclusion body myositis (IBM) is one member of a group of disorders known as idiopathic inflammatory myopathies (IIM) in which autoreactive T cells directed against muscle are thought to play a primary role in disease pathogenesis. We have utilized the polymerase chain reaction to determine the pattern of alpha beta T-cell receptor (TCR) variable (V) gene expression in muscle biopsies from 13 IBM patients. In the majority of biopsies, we detected oligoclonal patterns of TCR V gene expression by muscle-infiltrating lymphocytes; an average of six out of the 22 TCR V alpha gene families surveyed and seven out of 24 TCR V beta gene families surveyed were detected per biopsy. While no TCR V alpha gene families were over-represented in our survey, TCR V beta 3 and V beta 6 gene usage was a prominent feature of IBM muscle biopsies. TCR gene expression was characterized further by analysing the junctional sequence composition of both V beta 3 and V beta 6 clones from muscle biopsies of the IBM patients. A large number of structurally diverse V beta 3 and V beta 6 clonotypes were identified from these patients demonstrating a polyclonal pattern of T cell infiltration. These data, while describing prominent TCR V beta 3 and V beta 6 gene detection, do not suggest that a common antigen-driven T-cell response promotes chronic inflammation in muscle of IBM patients.

Adult↗
PubMed1981

Inclusion body myositis.

The histochemical and ultrastructural study of muscle biopsies of two patients with a chronic muscle weakness and wasting showed particular changes in muscle fibers: (1) peripheral lined vacuoles, containing whorls of membranes and cytoplasmic debris; (2) collections of intranuclear and intrasarcoplasmic tubular filaments (16-18 nm in external diameter and 6.5 nm in inner diameter). These changes are characteristic of a rare muscle disorder termed inclusion body myositis; its individuality is favoured by the present study. The resemblance of the tubular filaments to myxovirus nucleocapsid has been suggested by various authors but attempts to isolate the virus were unsuccessful in several reported cases as well as in those here presented. This does not exclude a viral origin of the disease. The similarity of the tubular filaments to thick myofilaments has been invoked by others, but has not been demonstrated. At the present the nature of the abnormal filaments remains unknown.

Adult↗
PubMed1993

Inclusion body myositis: clinical and histopathological features of 36 patients.

Thirty-six patients (15 females, 21 males) with inclusion body myositis (IBM) were studied. The diagnosis was established according to clinical and histopathological criteria. Clinical features were insidious onset of slowly progressive muscle weakness and wasting with depressed or absent tendon reflexes especially in the lower limbs. The pattern of muscle weakness was variable. The majority of patients (58%) showed proximal and symmetrical weakness usually most prominent in the legs. Isolated distal (6%) and asymmetrical weakness (19%) was less frequently observed. Myalgia occurred in 42% of the patients. The age at onset of symptoms ranged from 20 to 73 years (mean 47 years). Serum creatine kinase levels were normal (11%) or mildly elevated (89%). Needle electromyography revealed myopathic features in about 80% of the patients, and results of nerve conduction studies were normal in most of the cases. The predominant histopathological findings were numerous muscle fibers with rimmed vacuoles (100% of the patients), groups of atrophic fibers (92%), and inflammatory infiltrates (89%). The inflammatory infiltrates were located predominantly at endomysial sites and were composed mainly of T8 cells. Electron microscopy showed characteristic intracytoplasmic filamentous inclusions in all 36 cases. Immunosuppressive treatment in 16 patients failed to prevent disease progression in all but one patient with an associated Sjögren's syndrome. It is concluded that the consistent combination of typical histopathological findings and characteristic clinical features offers a firm basis for the diagnosis of IBM. IBM should be suspected in any adult patient presenting with clinical signs of a chronic polymyositis unresponsive to immunosuppressive therapy. The etiology and pathogenesis of IBM remain to be established.

Adult↗
PubMed1995

Acute myositis ossificans.

We have described the pre- and postgadolinium MR appearance in one case of acute myositis ossificans. The unenhanced sequences can be helpful in excluding malignancy, particularly when viewed serially. While use of gadolinium allowed primary sarcoma to be ruled out in this case, it was not useful in the exclusion of early abscess formation or necrotic metastasis.

Acute Disease↗
PubMed1993

Experimental allergic myositis in SJL/J mice immunized with rabbit myosin B fraction: immunohistochemical analysis and transfer.

Experimental allergic myositis (EAM) was produced in SJL/J mice by inoculation with the myosin B fraction of the rabbit skeletal muscle, and the pathological changes were quantified. The myosin B fraction contains actin, myosin, tropomyosin and many other proteins, and has been known to induce severe EAM in guinea pigs. In the present model, macrophages and CD4+ lymphocytes predominated among the infiltrating cells. On the surface of muscle fibers and in the regions of cell infiltration deposition of the immunoglobulin G (IgG) and complement factor 3 was observed. EAM was transferred to normal mice by injecting the serum IgG of EAM. Depleting the recipients of complement before the transfer resulted in less-severe pathological changes. Morphologically, the EAM IgG showed an affinity for the nuclei, myofilaments, sarcolemma and blood vessels of mouse skeletal muscle. Biochemically EAM IgG contained antibodies against myosin, actin, troponin, M protein and other muscle proteins. These results indicated that IgG and complement play important roles in this model.

Animals↗
PubMed1992

Inclusion body myositis with abundant ring fibers.

A 37-year-old male presenting with a 7-year history of leg weakness was found to have moderate weakness confined to the quadriceps and myopathic changes on electromyography. Serum creatine phosphokinase was 2130 units/liter. Biopsy of the quadriceps muscle revealed an inflammatory myopathy with cytoplasmic and nuclear filamentous inclusions characteristic of inclusion body myositis. An unusual finding was the large proportion of ring fibers along with severe atrophy and fibrosis. The pathogenesis of the ring fibers in this setting is discussed.

Adult↗
PubMed1993

Strong immunoreactivity of alpha 1-antichymotrypsin co-localizes with beta-amyloid protein and ubiquitin in vacuolated muscle fibers of inclusion-body myositis.

In 10 of 10 inclusion-body myositis (IBM) patients, including 1 hereditary case, vacuolated muscle fibers contained large or small cytoplasmic inclusions immunoreactive for alpha 1-antichymotrypsin (alpha 1-ACT). All IBM muscle biopsies had characteristic cytoplasmic tubulo-filaments by electron microscopy. None of 17 control muscle biopsies contained the alpha 1-ACT immunoreactive inclusions characteristic of IBM. In vacuolated muscle fibers, alpha 1-ACT immunoreactive inclusions colocalized with beta-amyloid protein and ubiquitin immunoreactivities. Our study provides the first demonstration of alpha 1-ACT accumulations in abnormal human muscle, and it suggest that, as in Alzheimer's disease and Down's syndrome, alpha 1-ACT may be involved in the pathogenesis of IBM.

Adolescent↗
PubMed1981

Myositis ossificans in hemophilia.

A review of the radiographs of 60 hemophilia patients showed nine (15%) with ectopic new bone formation. Three of these patients had multiple sites of involvement. The high frequency discovered in this series contrasts with the paucity of descriptions to be found in the literature. This process of myositis ossificans affects the lower half of the body and probably represents dysplastic metaplasia developing at the site of an intramuscular hematoma when remote from bone, as well as ossification of hemorrhagic lesions related to the periosteum. In conventional radiographs anatomic localization of bone foci is difficult, but use of computed tomography permits precise identification of the affected muscle. There is negligible disability associated with this condition.

Adolescent↗
PubMed1979

Ultrasound appearance of myositis ossificans.

Ultrasonic evaluation of a soft tissue mass of the thigh was performed and suggested the diagnosis of myositis ossificans. Correlation with routine radiographic studies is made, as well as with the follow-up radiographic examination.

Adult↗
PubMed1988

Equine postanaesthetic myositis: thromboxanes, prostacyclin and prostaglandin E2 production.

Arachidonic acid cyclooxygenase metabolites, thromboxane B2 (TXB2), prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 (6-keto-PGF1) were measured in horses where anaesthesia was maintained with halothane. Two horses suffering from postanaesthetic myositis were compared with four normal horses. TXB2 and PGE2 levels were higher in mixed venous blood drawn from the myopathic horses. An increase of TXB2 and PGE2 levels appeared when myopathic horses were rolled into dorsal recumbency after a prolonged period of lateral recumbency. One hour after the end of anaesthesia, TXB2 had continued to increase whereas PGE2 decreased. By measurements on blood samples drawn from the brachial vein, we have shown that the rising level of TXB2 in mixed venous blood is mainly due to the increase of TXB2 in blood draining the dependent leg. The origin of the rise in PGE2 is not demonstrated in this study. 6-keto-PGF1 did not change during anaesthesia. An explanation of this imbalance between TXB2 and 6-keto-PGF1 production is considered.

6-Ketoprostaglandin F1 alpha↗