Cases reported "Myositis"

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1/36. hepatitis c virus infection and myositis: a polymerase chain reaction study.

    Muscle biopsy tissue from a patient with chronic hepatitis, who was hepatitis c virus (HCV) positive and showed slight weakness of the right arm and leg associated with increased serum creatine kinase levels, was studied using immunocytochemical and polymerase chain reaction (PCR) techniques. Muscle biopsy showed changes compatible with an inflammatory myopathy. Immunohistochemical studies included the use of monoclonal antibodies against human T lymphocytes, macrophages, immunoglobulins, major histocompatibility complex class I molecules (MHC-I), and the neoantigens of the terminal C5b-9 complement membrane attack complex (MAC). In addition to confirming the potential importance of cytotoxic T cells and MHC-I antigen expression in inducing muscle pathology, we demonstrated MAC deposition and the presence of HCV-rna in the muscle of our patient, suggesting that direct involvement of the virus leading to complement activation might be important in inducing muscle damage.
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2/36. mixed connective tissue disease.

    Three patients with mixed connective tissue disease (MCTD) had clinical features that included a high incidence of Raynaud phenomenon, arthritis, myositis, and swollen hands. The diagnostic laboratory test result was the presence of high titers of antibody to extractable nuclear antigen. These antibody titers are notably reduced or abolished in patients with MCTD when the tanned red blood cells that are used in the test are pretreated with ribonuclease. Speckled antinuclear antibodies were present in all patients. patients with MCTD have a low incidence of renal disease, are responsive to treatment with prednisone, and have a good prognosis.
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3/36. Myositis and interstitial lung disease associated with autoantibody to a transfer rna-related protein Wa.

    We describe 2 patients with myositis and interstitial lung disease with the autoantibody to Wa antigen, a 48-kDa transfer rna-related protein. In contrast to the previous description of anti-Wa antibody, our patients lacked systemic sclerosis-related features, but had clinical features consistent with those associated with antibodies to aminoacyl-transfer rna synthetases. The difference in clinical presentation between our patients and patients with systemic sclerosis may be explained by recognition of different epitopes on the Wa antigen.
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4/36. Myositis resulting from disseminated cryptococcosis in a patient with hepatitis c cirrhosis.

    We report a case of myositis that resulted from disseminated cryptococcosis in a patient with hepatitis c cirrhosis. One year after cessation of treatment, the patient remains symptom free with negative results of serum cryptococcal antigen tests and negative culture results.
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5/36. Acquired myopathic intestinal pseudo-obstruction may be due to autoimmune enteric leiomyositis.

    We describe a previously healthy boy who developed intestinal pseudo-obstruction following an episode of gastroenteritis at age 2 years. At presentation, the patient had mildly raised erythrocyte sedimentation rate and c-reactive protein level, and elevated antineutrophil cytoplasmic antibodies, antinuclear anti-dna, and anti-smooth muscle antibodies. His electrogastrography was myopathic with no dominant frequency. First full-thickness intestinal biopsies showed a T lymphocytic myositis, particularly in the circular muscle. Steroid therapy resulted in clinical remission; cessation of steroids, in relapse. Further full-thickness biopsies showed an initial reduction in alpha-smooth muscle actin immunostaining in circular muscle myocytes and later atrophy and disappearance of many myocytes. Vascular and the remaining enteric smooth muscle cells showed HLA-DR and intercellular adhesion molecule 1 expression. These observations demonstrate the ability of enteric myocytes to take part in an inflammatory response and to change their phenotype, allowing them to act as antigen-presenting cells and to activate T cells. This and possible cytokine production by the myocytes play a role in their own destruction. This process responded to immunosuppressive therapy.
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6/36. Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer.

    interleukin-2 is an effective agent against renal cell carcinoma and melanoma, but it has been associated with autoimmune sequelae such as hypothyroidism and vitiligo. A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. After additional therapy with interleukin-2, the patient developed generalized myasthenia gravis (MG) and polymyositis, both of which responded to treatment with corticosteroids and plasmapheresis. To investigate the role of IL-2 in the development of these autoimmune complications, autoantibody titers were assayed from serum obtained before and after IL-2 treatment and after treatment with corticosteroids plus plasmapheresis. Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. acetylcholine receptor antibody levels were normal before starting IL-2. After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. Recovery from the MG and polymyositis was associated with substantial decreases in the acetylcholine receptor and striated muscle antibody titers. These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. This case demonstrates the importance of prompt recognition of IL-2-induced MG and shows how this complication can be successfully managed with aggressive therapy.
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7/36. hepatitis c virus infection and myositis: a virus localization study.

    We report a case of myositis associated with chronic hepatitis c virus infection. Muscle biopsy and immunohistochemistry showed perifascicular atrophy, few necrotic and regenerating fibres, scarce perivascular infiltrates, deposits of immunoglobulin g, C3, fibrinogen and MAC in muscle vessel walls, and non-uniform expression of major histocompatibility complex-I antigens among muscle fibres. hepatitis c virus NS3 antigen and hepatitis c virus rna were detected in infiltrating cells but not within muscle fibres or endothelial cells. Our findings suggest that humoral-mediated immune mechanisms, not directly related to hepatitis c virus infection of muscle structures, may sustain the local inflammatory reaction in this patient.
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8/36. Benign acute myositis associated with rotavirus gastroenteritis.

    Acute myositis developed concomitantly with gastroenteritis in a 2-year-old girl. She had temporary pain and swelling of the calf muscles and transient marked elevation of serum creatine kinase values. rotavirus antigen was detected in stool by latex agglutination, and there was seroconversion of complement-fixation antibody to rotavirus.
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9/36. Acute polymyositis following renal transplantation.

    Myositis is a rare complication following renal transplantation and is most commonly the result of drug-mediated myotoxicity. Other causative disorders include viral infection, electrolyte imbalance and myositis of autoimmune origin. We describe a 60-year-old patient who developed acute polymyositis 4 weeks after a 000 human leukocyte antigen (HLA) mismatch cadaveric renal transplant. Following an uncomplicated transplant course with maintenance triple immunosuppression (prednisolone, mycophenolate mofetil and cyclosporine), the patient presented with severe symmetrical proximal muscle weakness associated with a rise in serum creatine kinase to 46800 U/L. electromyography confirmed myopathic changes and muscle biopsy demonstrated extensive muscle-fiber necrosis with an inflammatory infiltrate. There were no obviously culpable drugs and viral studies were negative. Prompt initiation of high-dose steroid therapy led to clinical and biochemical recovery. Acute polymyositis may occur following renal transplantation. Potential mechanisms include viral antigen transmission or a localized form of graft vs. host disease.
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10/36. Direct evidence for a chronic CD8 -T-cell-mediated immune reaction to tax within the muscle of a human T-cell leukemia/lymphoma virus type 1-infected patient with sporadic inclusion body myositis.

    Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) infection can lead to the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), concomitantly with or without other inflammatory disorders such as myositis. These pathologies are considered immune-mediated diseases, and it is assumed that migration within tissues of both HTLV-1-infected CD4( ) T cells and anti-HTLV-1 cytotoxic T cells represents a pivotal event. However, although HTLV-1-infected T cells were found in inflamed lesions, the antigenic specificity of coinfiltrated CD8( ) T cells remains to be determined. In this study, we performed both ex vivo and in situ analyses using muscle biopsies obtained from an HTLV-1-infected patient with HAM/TSP and sporadic inclusion body myositis. We found that both HTLV-1-infected CD4( ) T cells and CD8( ) T cells directed to the dominant Tax antigen can be amplified from muscle cell cultures. Moreover, we were able to detect in two successive muscle biopsies both tax mRNA-positive mononuclear cells and T cells recognized by the Tax11-19/HLA-A*02 tetramer and positive for perforin. These findings provide the first direct demonstration that anti-Tax cytotoxic T cells are chronically recruited within inflamed tissues of an HTLV-1 infected patient, which validates the cytotoxic immune reaction model for the pathogenesis of HTLV-1-associated inflammatory disease.
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