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

Several infectious agents can cause chronic or acute myopathy. Most current investigations into possible infectious causes of the idiopathic inflammatory myopathies have focused on retroviruses, including HIV and human T-cell leukemia-lymphoma virus type I. In both cases, viruses likely do not directly infect muscle fibers but instead induce an immunologically mediated myositis. Other interest has focused on enteroviruses as potential etiologic agents of idiopathic inflammatory myopathy, but their relationship to human myositis is less clear. In addition to chronic muscle disease, several infectious agents can cause acute myositis, including pyomyositis, which is being recognized in temperate climates with increasing frequency, and rhabdomyolysis.
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PMID:Infectious agents associated with myopathies. 901 53

We report on a patient of Ki-1 lymphoma-associated hypereosinophilic syndrome and eosinophilic polymyositis. A 22-year-old male was admitted to a hospital because of anterior chest pain, when he had a white cell count of 12,000 with 33% of eosinophils. He first noticed muscle weakness in the right shoulder at age 23 years. At the age of 25, he experienced marked muscle weakness in his arms and neck, which brought him to our hospital. Neurological examination on admission revealed moderate muscle atrophy and weakness in the neck flexors and both upper extremities, and marked muscle hypertrophy in the sternocleidomastoideus and trapezius muscles. Laboratory studies showed a white blood cell count of 17,700 with 56% of eosinophils. His serum creatine kinase (CK) level was elevated to 347 units. A muscle biopsy specimen showing active myositis infiltrated by eosinophils confirmed the diagnosis of eosinophilic myositis. Although eosinophilia and serum CK activity decreased markedly with corticosteroid treatment, his muscle weakness was unchanged. At the age of 27 years, lymphadenopathy developed. Immunocytochemical examination on a biopsied neck lymph node indicated Ki-1 lymphoma with positive Ki-1, CD45 and epithelial membrane antibodies. In spite of chemotherapy and local irradiation treatment, he died four months after the emergence of Ki-1 lymphoma. We discussed the relationship between hypereosinophilic syndrome, eosinophilic polymyositis and Ki-1 lymphoma on pathogenetic mechanism.
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PMID:[A case of Ki-1 lymphoma-associated eosinophilic polymyositis]. 924 41

Fibroinflammatory disorders constitute heterogeneous clinical conditions whose cause and pathogenesis are largely unknown. Inflammatory pseudotumor has been applied in a generic sense to several of these disorders, which present as a mass displacing surrounding anatomic structures or leading to organ dysfunction secondary to compressive growth around the ureter(s), common bile duct, or great vessels in the mediastinum. The fibrosclerosing disorders of retroperitoneal fibrosis, sclerosing mediastinitis, sclerosing cholangitis, orbital pseudotumor, and Riedel thyroiditis are seemingly related in a clinical sense because there are well-documented cases of patients with two or more of these conditions and reports of these disorders presenting in family members. Although the pathogenesis of the fibrosclerotic disorders has not been elucidated, autoimmunity in the context of an established collagen vascular disease or the setting of inflammatory periaortitis in retroperitoneal fibrosis has been one suggested mechanism. In the course of the diagnostic evaluation of an individual with a suspected fibrosclerotic disorder, it is imperative to exclude an underlying infection or malignancy. This caveat is especially relevant to sclerosing mediastinitis as a presentation of histoplasmosis or to retroperitoneal fibrosis secondary to a sclerosing large cell lymphoma. Sclerosing mesenteritis has some clinical and pathological overlap with the fibrosclerotic disorders, but its nosologic and pathogenetic relationship is uncertain at this time. There are several other fibroinflammatory processes, such as focal myositis, inflammatory fibroid polyp of the gastrointestinal tract, calcifying fibrous pseudotumor, and sclerosing peritonitis, which are probably unrelated to inflammatory myofibroblastic tumor or the primary fibrosclerotic disorders.
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PMID:Idiopathic fibrosclerotic disorders and other inflammatory pseudotumors. 960 7

A rapidly enlarging lump in the neck of an adolescent, is a cause for concern. Amongst the various clinical differential diagnoses, including lymphoma and other malignant lesions, focal myositis is an unusual cause. To date, only two such cases affecting the sternomastoid have been reported worldwide. We report a further similar case.
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PMID:Rapidly enlarging lump in the neck: is it a tumour? 1107 85

OBJECTIVE. We looked for the development of specific systemic disease or malignant lymphoma in patients whose initial diagnosis was idiopathic inflammatory pseudo-tumor of the orbit (IOPT). PATIENTS AND METHODS. IOPT was diagnosed in 24 patients on the basis of imaging findings and surgical biopsies (70%). Nineteen of these 24 patients (10 men and 9 women, age range 19- 83 years) were reassessed 1-12 years after the initial diagnosis. RESULTS. The initial diagnosis described diffuse inflammation (33%), dacryoadenitis (20%) or myositis (47%). At reassessment, 4 patients had developed a specific disease: generalized lymphoma, Wegener's disease, necrotizing vasculitis, and Crohn's disease. All four were recognized within one year of the IOPT diagnosis. A biopsy was obtained in these four patients and was not contributive. One case of non-specific granulomatous proliferation was found 6 years after the initial diagnosis. One case of orbital meningioma occurred 10 years after radiotherapy of the orbit and could not be attributed to a definite cause. The other patients had a common non-specific clinical course; recurrent inflammation required corticosteroid therapy in 55% and complementary external radiotherapy of the orbit in 22%. DISCUSSION AND CONCLUSION. Specific diseases that developed after an initial diagnosis of inflammatory pseudo-tumor of the orbit occurred early and appeared more often in diffuse forms, suggesting the need for more extensive histopathological diagnostic procedures. The clinical course tended to be more quiescent in patients who passed the critical period of the first year.
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PMID:What has become of our idiopathic inflammatory pseudo-tumors of the orbit? 1204 80

The authors describe the case of a patient with NHL, who had undergone a series of clinical and laboratory investigations for the presence of pain, oedema and functional deficiency of the lower limbs associated with generalized weakness. From the data of the literature in cases of myositis, labelled as paraneoplastic disorders, no histological classification or phenotypic characterization have been provided, with exception of a case diagnosed as K1 positive lymphoma. A meta-analysis of case control studies and cohort of myositis and neoplasia do not show an increased incidence of cancer before a diagnosis of polymyositis (PM), although it seems to be an increased risk following diagnosis. The association of PM with a neoplasia, compared with that of dermatomyositis (DM) with a neoplasia, seems less frequent. In view of these considerations, of the usefulness of a diagnosis of neoplasia concurrently or in association with a neoplasia with a PM/DM, and furthermore in order to better define the frequency of a particular phenotype in the subsequent lymphoproliferative disorders, we have described a case of polymyositis, admitted in one hospital and subsequently recognized as being associated with a diffuse follicular non-Hodgkin lymphoma with small B lymphocytes.
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PMID:[Polymyositis as a paraneoplastic syndrome in a case of non-Hodgkin lymphoma]. 1267 87

Orbital inflammatory disease (OID) broadly describes a variety of pathologic processes and clinical presentations. OID may be idiopathic or may be secondary to a systemic inflammatory disease, retained foreign body, or infectious disease. OID includes the spectrum of bacterial or fungal infections, diffuse inflammation of multiple tissues (e.g., sclerosing orbititis or diffuse anterior OID), and preferential involvement of specific orbital structures (e.g., orbital myositis or optic perineuritis). Mimics of OID include congenital orbital mass lesions or orbital neoplastic disease such as lymphoma or rhabdomyosarcoma. The ultimate diagnosis and treatment plan relies on a careful history and detailed clinical examination followed by the judicious use of ancillary diagnostic testing and a comprehensive treatment plan. The purpose of this review is to provide an overview of the spectrum of diseases known as OID, with emphasis on specific diagnostic challenges in the evaluation and management of patients with idiopathic OID.
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PMID:Diagnostic dilemmas in orbital inflammatory disease. 1285 23

We report a 52 year-old patient with malignant lymphoma who developed necrotizing soft tissue infection in the left lower extremity by Aeromonas veronii biotype sobria during a neutropenic period after intensive chemotherapy. We decided to amputate the involved leg when signs and symptoms of necrotizing myositis were progressing despite administration of sensitive antibiotics. He survived with subsequent intensive supportive care. It is to note that even though the patient's neutrophil count is zero, he or she should be treated aggressively by drainaging the lesion or even amputation of the involved extremities in combination with proper antibiotics.
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PMID:[A successful treatment of progressive necrotizing myositis caused by Aeromonas veronii biotype sobria]. 1467 14

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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PMID: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. 1536 98

A retrospective study was performed on 200 randomly selected cases of inflammatory myopathy in dogs from diagnostic muscle biopsies received at the Comparative Neuromuscular Laboratory, University of California, San Diego. The most common clinical signs in dogs diagnosed with an inflammatory myopathy were generalized weakness, stilted gait, dysphagia, masticatory or generalized muscle atrophy, inability to open the jaw, megaesophagus, and dysphonia. Myalgia was rarely described. Age of onset ranged from 0.25 to 14 years. Genders were equally represented. Breed distribution approximated the 2002 American Kennel Club registration statistics (r = .85) with the notable exception of Boxers and Newfoundlands. From the results of muscle biopsies, clinical signs, and presence or absence of antibodies against type 2M fibers, dogs were classified as a generalized inflammatory myopathy (gIM)--including immune-mediated polymyositis; infectious and preneoplastic myositis; and, rarely, dermatomyositislike or overlap syndromes or unclassified myositis-or a focal inflammatory myopathy (flM)--including masticatory muscle and extraocular myositis. Average creatine kinase (CK) and aspartate aminotransferase (AST) concentrations in gIMs were significantly higher than those with fIMs (P < .05). Neoplasia developed in 12 of 200 dogs within 12 months of diagnosis of polymyositis, with lymphoma diagnosed in 6 of 32 Boxers. Inflammatory myopathy was associated with antibody titers against infectious diseases in 38 dogs. Neospora caninum and Hepatozoon americanum cysts were found in tissues of 2 dogs not serologically tested. Antibodies against an unidentified sarcolemmal antigen were found in 9 of 19 Newfoundlands with polymyositis. The spectrum of canine inflammatory myopathies can be broad, with infectious etiologies relatively common, and can include preneoplastic and uncharacterized syndromes.
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PMID:Canine inflammatory myopathies: a clinicopathologic review of 200 cases. 1551 85


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