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

The DA strain of Theiler's murine encephalomyelitis virus, a member of the cardiovirus genus of picornaviruses, induces a restricted and persistent infection associated with a demyelinating process following intracerebral inoculation of mice; both virus infection and the immune response are believed to contribute to the late white matter disease. We now report that intraperitoneal inoculation with DA produces an acute myositis that progresses to a chronic inflammatory muscle disease in CD-1 mice as well as several inbred mouse strains. Some mouse strains also develop central nervous system white matter disease and a focal myocarditis. Infectious virus in skeletal muscle falls to undetectable levels 3 weeks postinoculation (p.i.), although viral genome persists for at least 12 weeks p.i., the longest period of observation. Severe combined immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting that DA virus is capable of inducing chronic muscle disease in the absence of an immune response. The presence in immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus suggests that the immune system also contributes to the pathology. T lymphocytes are the predominant cell type infiltrating the skeletal muscle during the chronic disease. This murine model may further our understanding of virus-induced chronic myositis and help to clarify the pathogenesis of human inflammatory myopathies.
J Virol 1996 Dec
PMID:Theiler's murine encephalomyelitis virus-induced cardiac and skeletal muscle disease. 897 Oct 22

An experimental autoimmune myositis (EAM) was produced by immunizing SJL/J mice with the myosin B (MB) fraction of the syngeneic muscle. Immunoblot analysis of the IgG of the EAM mice demonstrated antibodies against a variety of muscle proteins. The condition was then transferred to normal mice by both injecting immunoglobulin G or T cells from the EAM mice. This is the first model of transferrable EAM caused by syngeneic muscle fraction, and it has an unique resemblance to human inflammatory myopathies involving both humoral and cellular immune mechanisms.
J Neurol Sci 1996 Dec
PMID:Experimental autoimmune myositis in SJL/J mice produced by immunization with syngeneic myosin B fraction. Transfer by both immunoglobulin G and T cells. 899 20

Idiopathic hypereosinophilic syndrome (HES) is a rare disorder marked by a sustained overproduction of eosinophils and a predilection for damage to multiple organ systems. Its neurologic involvement ranges from the central to the peripheral nervous system, and can be associated with eosinophilic myositis. We report a 68-year-old woman who had eosinophilia, eosinophilic dermatitis and eosinophilic pneumonia. She also suffered from numbness and weakness of the lower limbs. Because of long-lasting (> 6 mo) eosinophilia (> 1.5 x 10(9)/L) in the peripheral blood and the fact that no other underlying causes of eosinophilia and neurologic involvement could be identified, a diagnosis of idiopathic hypereosinophilic syndrome was made. The muscle biopsy showed infiltration of inflammatory cells, including a few eosinophils (Liu's stain). Magnetic resonance images, motor evoked potentials, somatosensory evoked potentials and nerve conduction velocities also showed abnormalities in the central and peripheral nervous systems. The pathogenesis and treatments of HES are discussed in this report.
J Formos Med Assoc 1996 Dec
PMID:Idiopathic hypereosinophilic syndrome with eosinophilic myositis, peripheral neuropathy and central nervous system involvement. 900 Aug 11

Sporadic inclusion body myositis and the hereditary inclusion body myopathies are severe, progressive muscle diseases, characterized pathologically by vacuolated muscle fibers containing paired helical filaments. We immunostained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion body myopathy, disease control, and normal patients with several antibodies against apolipoprotein E (ApoE). Approximately 80 to 90% of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined, strongly immunoreactive ApoE inclusions. In hereditary inclusion body myopathy, only rare vacuolated fibers had immunoreactive inclusions, whereas most had diffuse cytoplasmic ApoE immunoreactivity. Ultrastructurally, ApoE immunoreactivity in sporadic myositis was localized mainly to the paired helical filaments. By contrast, in the hereditary form, ApoE immunoreactivity occurred on material in close proximity to the paired helical filaments, but never was on the paired helical filaments. In both muscle diseases, ApoE was also on the 6- to 10-nm filaments and amorphous material. In the sporadic form, ApoE-immunoreactive deposits colocalized with Congo red-positive deposits; however, in muscle fibers from patients with hereditary disease there was no congophilia. ApoE messenger RNA was not detectable in muscle fibers from patients with hereditary or sporadic disease but was expressed abundantly in muscle macrophages. In all control and inclusion body myositis or myopathy biopsy specimens, ApoE immunoreactivity was strong at the postsynaptic domain of neuromuscular junctions; nonjunctional regions of normal fibers were negative for ApoE. ApoE immunoreactivity occurred diffusely in regenerating muscle fibers, a subset of which had detectable ApoE messenger RNA.
Ann Neurol 1996 Dec
PMID:Apolipoprotein E and apolipoprotein E messenger RNA in muscle of inclusion body myositis and myopathies. 900 91

The third case in the literature is reported of an infection produced by Pleistophora. The clinical detail of the three cases are discussed. Two of the patients-including the reported one-were infected by HIV. All patients suffered from myositis with fever, resting and at palpation myalgia, and progressive weakness. Blood tests showed anaemia and high levels of muscle enzymes. Necrotic muscle fibrosis induced disabling contractures. Diagnosis was obtained by detecting the protozoon in a muscle biopsy. The spores may be detectable by means of different staining methods at light microscopy although electron microscopy remains the most reliable technique. Since this is such a rare condition there is no known treatment. Whether the albendazole could be as useful as occurs in patients infected by other genera of microsporidia in still uncertain.
Med Clin (Barc) 1996 Dec 07
PMID:[Myositis caused by Pleistophora in a patient with AIDS]. 901 6

To investigate the possible role of nitric oxide (NO)-induced 'oxidative stress' in the pathogenesis of inclusion-body myositis (IBM), we immunostained muscle biopsies of 12 patients with IBM with isoform-specific antibodies against the neuronal and inducible forms of nitric oxide synthase and with antibodies against nitrotyrosine. Between 70 and 80% of IBM vacuolated muscle fibers contained inclusions strongly immunoreactive with all three antibodies, which by immuno-electronmicroscopy co-localized mainly to cytoplasmic paired-helical filaments, and also to amorphous structures and floccular material. Excess intracellular NO can combine with superoxide to produce highly reactive peroxynitrite which can nitrate tyrosines of proteins. The presence of nitrotyrosine is indicative of NO-induced "oxidative stress'. Our data suggest that this mechanism may play a pathogenic role in IBM.
Neuroreport 1996 Dec 20
PMID:Increase of nitric oxide synthases and nitrotyrosine in inclusion-body myositis. 905 71

We present two cases of interstitial pneumonia (IP) whose sera contain autoantibodies to PL-12 (alanyl tRNA synthetase). The first patient is a 47-year-old female who was diagnosed as IP and treated with corticosteroid at another hospital. She was admitted to Keio University Hospital due to worsening of dyspnea and polyarthritis. Laboratory studies revealed elevation of LDH and CRP, and her chest radiography showed interstitial fibrosis. Because of clinical deterioration, the dose of corticosteroid was increased (prednisolone 40 mg/day) and her symptom was stabilized. The second patient, a 55 year-old female, was admitted to Tokyo Metropolitan Ohtsuka Hospital because of dyspnea on exertion and polyarthritis. She did not show any symptom of myositis and was diagnosed as IP with arthritis on the basis of her clinical and chest radiography. She was treated with oral corticosteroid (prednisolone 30 mg/day), which resulted in improvement of her respiratory symptom and arthritis. Both patients were found to have autoantibodies to the PL-12. Autoantibodies to aminoacyl tRNA synthetases have been recognized as having a linkage with myositis mainly because of observations of the Jo-1 specificity. There was one report on a North American population that most but not all patients with anti-PL-12 antibodies had myositis. However, the clinical significance of anti-PL-12 has not been examined in Japanese patients. These patients suggested that anti-PL-12 antibodies have a stronger association with IP than myositis in Japanese patients.
Ryumachi 1996 Dec
PMID:[Two cases of interstitial pneumonia with anti-PL-12 (alanyl tRNA synthetase) antibodies]. 912 26

Three new cases of reactivation of Chagas' disease in patients with AIDS, with central nervous system and/or cardiac involvement, are reported. One patient had histological evidence of acute esophageal and gastric Trypanosoma cruzi myositis, a previously unrecognized finding in patients with reactivated Chagas' disease. The patients had a low CD4 lymphocyte count and had other AIDS-defining opportunistic infections. One patient's condition improved with benznidazole therapy. Analysis of these three cases and review of the 13 others published in the literature revealed that the central nervous system is the most commonly involved site (75%), followed by the heart (44%). Early diagnosis and treatment with benznidazole or nifurtimox probably improve the survival rate. Long-term secondary prophylaxis should be recommended for patients who respond to therapy, although it is uncertain which drug to use for this purpose. T. cruzi should be included in the list of opportunistic pathogens causing infection in severely immunocompromised patients with AIDS.
Clin Infect Dis 1997 Dec
PMID:Reactivation of Chagas' disease in patients with AIDS: report of three new cases and review of the literature. 943 85

Myositis ossificans traumatica of the masseter muscle is uncommon. The condition is benign and results in reactive heterotopic bone formation, usually producing limitation of opening of the jaws. Radiographic and microscopic examination can confirm the diagnosis. Treatment of myositis ossificans traumatica of the masseter muscle is surgical, with other modalities used when occurring in other muscles of the body.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997 Dec
PMID:Myositis ossificans traumatica of the masseter muscle: review of the literature and report of two additional cases. 943 43

While the plain film and nuclear medicine bone scan are still the traditional imaging modalities used in the evaluation of musculoskeletal infection, the cross-sectional imaging modalities, computed tomography (CT) and magnetic resonance imaging (MRI), have become critical in the delineation of many types of musculoskeletal infection. In particular, the evaluation of soft tissue infections, including cellulitus, myositis, fasciitis, abscess, and septic arthritis are often best evaluated by MRI or CT due to their excellent anatomic resolution and soft tissue contrast. Even in osseous infection, CT and MRI can give better anatomic delineation of the extent of infection. In cases where the plain film and nuclear medicine bone scan findings are complicated due to previous surgery, trauma, or underlying illness, the anatomic resolution and soft tissue contrast provided by MRI and CT are often necessary to determine if underlying infection exists. MRI's visualization of the bone marrow allows for the sensitive detection of osteomyelitis, although specificity for the diagnosis of osteomyelitis is aided by other findings, including cortical destruction. The CT and MRI findings in the spectrum of musculoskeletal infections are discussed and contrasted, and pitfalls in their evaluation of musculoskeletal infection are described.
Crit Rev Diagn Imaging 1997 Dec
PMID:CT and MRI evaluation of musculoskeletal infection. 944 78


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