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At least 289 records · Page 16Linked to original sources
PubMed2001

[Skeletal muscle pathology of chronic graft versus host disease accompanied with myositis, affecting predominantly respiratory and distal muscles, and hemosiderosis].

We report the muscle pathology in a 43-year-old woman who died of chronic graft versus host disease (GVHD) complicated by myositis and systemic transfusional hemosiderosis, after an allogeneic bone marrow transplantation and a donor leukocyte transfusion for acute myelogenous leukemia. Despite cyclosporin A treatment, fatal ventilatory failure progressed while she was still ambulant. Autopsy revealed the presence of chronic GVHD mildly involving the liver, skin, pericardium, pancreas, and salivary glands, in addition to skeletal muscles. Myopathic changes with mild inflammation and prominent iron deposition were found in the tibialis anterior muscle and, to a lesser degree, in the diaphragm and the intercostal muscle. There were iron deposits in both macrophages and sarcoplasm in the tibialis anterior. The iliopsoas and pectoralis major muscles showed prominent type 2 fiber atrophy; inflammation and iron deposition were minimal in the iliopsoas, but none in the pectoralis. Although we ascribed respiratory failure largely to GVHD myositis, weakness of the lower leg appeared to be aggravated by iron deposition superimposing the underlying GVHD myositis.

Adult↗
PubMed1976

Acute myositis associated with influenza B infection.

An epidemic of acute myositis affecting children occurred in association with influenza B infections. The myositis followed the initial influenza-like episode, and almost exclusively involved the gastrocnemius and soleus muscles. Patients improved without specific treatment and made a complete recovery in four to five days. Laboratory studies characteristically showed elevated CPK, SGOT values, and a low peripheral white blood cell count. Influenza B virus was isolated from 11 of the 17 patients studied. This influenza-associated acute myositis of childhood is a recognized syndrome that should not be confused with dermatomyositis.

Acute Disease↗
PubMed2003

[A case with myositis as a manifestation of chronic graft-versus-host-disease (GVHD) with severe muscle swelling developed after aggressive muscular exercise].

We report a 21-year-old-man, with myositis as a manifestation of chronic graft-versus-host-disease (GVHD). He was diagnosed as having acute myelogenous leukemia at the age of 18 years, and had bone marrow transplantation (BMT) two years after the onset of the disease. Cutaneous manifestation of acute GVHD appeared on the twelfth day following BMT, which responded to prednisolone. Thereafter, GVHD has been well-controlled except for mild liver dysfunction which was thought to be a sign of chronic GVHD. Eleven months after BMT, he enjoyed snowboarding for two days from morning till night. Two days later, he experienced muscle swelling with pain and fever, which gradually worsened for which he was admitted to our hospital. Neurological examination revealed severe proximal and distal muscle swelling with fever and tenderness in all extremities. Mild, symmetrical, proximal weakness was observed in all four limbs. Severity of muscle swelling and its generalized nature restricted the movements of shoulder-, elbow- and ankle-joints and he was unable to walk. Laboratory investigations revealed creatine kinase (CK) of 7,860 IU/L, C-reactive protein (CRP) of 21.5 mg/dL and raised biliary enzymes. MRI generated high intensity signals from the swollen muscles. Muscle biopsy examination of involved areas showed severe interstitial edema and mononuclear cells infiltration. Macrophages were scattered through out the perimysium and endomysium. On the other hand, T cells and B cells were localized to the endomysium. Although a lot of CD8 positive T cells were seen adjacent to non-necrotic fibers, none of them was obviously invading the non-necrotic fibers. Perifascicular atrophy was not seen. Symptoms gradually worsened over two weeks or so when prednisolone was started to which he responded rapidly. While tapering steroids, the symptoms relapsed on resuming aggressive exercise. Resumption of the treatment regime promptly controlled the symptoms. The cause of myositis as a manifestation of chronic GVHD is unclear. T-cell or B-cell dysfunction, collagen-vascular-like processes, viral infection and direct damage by radiation or chemotherapy have been supposed to involve in the disease process. Our case suggests that aggressive muscular exercise could play as a initiator of myositis as a manifestation of chronic GVHD.

Adult↗
PubMedDate not supplied

Chemotherapy-induced radiation recall myositis.

Myofasciitis syndrome encompasses a group of disorders characterized by chronic inflammation and/or fibrosis of the subcutaneous septa and muscular fascia. We report on a patient in whom myositis was diagnosed in the areas previously irradiated for papillary thyroid carcinoma and anal canal carcinoma respectively 21 and 3 years after radiotherapy. We are not able to explain why myopathy developed at the same time in two different sites at a different interval from the two radiotherapic schemes. We can suppose that the patient developed a subclinical regional myopathy after the first radiotherapic scheme. Radiation induced heritable mutations within surviving cells that were unable to tolerate the second damage by systemic chemotherapy. It is unclear how radiosensitization correlates with an ability to reactivate latent effects in normal tissue. Physicians using chemotherapic radiosensitizers should be aware of their potential to induce a delayed form of radiosensitization. We report this case to encourage physicians to be alert to the knowledge of the clinical, histologic and morphologic characteristics of radiation myositis in order to distinguish it from an infectious or immune fasciitis or myositis.

Carcinoma, Papillary↗
PubMed2003

[Two cases of radiation myositis probably induced by recall phenomenon].

Two cases of radiation myositis following gemcitabine-based chemotherapy for advanced non-small cell lung cancer are presented. In the two cases, myositis appeared 3 and 5.5 months after the completion of radiation therapy and 2 and 2.5 months after the beginning of chemotherapy, respectively. The affected areas, the upper back and right thigh, appeared as areas of increased signal intensity on T2-weighted MR imaging and were enhanced by the administration of Gd-DTPA in the skeletal muscles. These coincided with the previously irradiated area. Although radiation myositis is a rare complication, it is important to be careful of radiation recall induced by chemotherapeutic agents.

Aged↗
PubMed2003

[A patient with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis].

We report a 62-year-old man with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis (MG). He was diagnosed as having MG and invasive thymoma at the age of 45. After he had a myasthenic crisis at the age of 61, tacrolimus was indicated in order to improve his neurological symptoms, in addition to glucocorticoid. Three months later, he was readmitted to our hospital complaining of general fatigue and dyspnea. Serum level of creatine phosphokinase (9,835IU/L) and myocardium-derived troponin T (3.24 ng/mL) were elevated, and the ECG showed atrioventricular dissociation and accelerated idioventricular rhythm. In spite of glucocorticoid pulse therapies and high-dose immunoglobulin therapies, he died of cardiac failure within a few days. Autopsy was done, and histological examination of the myocardium and the skeletal muscle showed massive necrosis with infiltration of inflammatory cells including giant cells. These findings constituted giant cell myocarditis and myositis. Although it has been suggested that myocardial disorders can often occur in patients with thymoma and/or MG, the mechanism involved is still unknown. This report may provide new knowledge about the pathophysiology of giant cell myocarditis and myositis associated with thymoma and MG.

Giant Cells↗
PubMed1992

Proliferative myositis and fasciitis. A light and electron microscopic, cytologic, DNA-cytometric and immunohistochemical study.

Two cases of proliferative myositis, four cases of proliferative fasciitis and one mixed form of proliferative myositis and fasciitis have been analyzed in terms of cell differentiation and DNA content. Light microscopically, the lesions were characterized by a mixture of proliferating spindle-shaped cells and uni-, bi- or occasionally multinucleated ganglion cell-like cells. The spindle cells showed ultrastructural features and immunohistochemical properties, including an immunoreactivity for smooth muscle-specific actin, indicative of a myofibroblastic differentiation. The ganglion cell-like cells displayed some resemblance to active osteoblasts ultrastructurally and differed immunohistochemically from the spindle cells by being non-immunoreactive for smooth muscle-specific actin. None of the two cell types showed immunoreactivity for desmin, myoglobin or factor VIII RAG. It is suggested that the two cell types represent different lines of cell differentiation. The cytologic features in smears, as seen in two cases of proliferative fasciitis and one case of proliferative myositis, are considered to be characteristic of these lesions and to permit the diagnosis to be made by fine-needle aspiration. In two of the cases, the lesion was diagnosed only cytologically and thereafter disappeared spontaneously within a month. Cytometric DNA measurements, using two different image analysis systems on Feulgen-stained sections and smears, revealed a "diploid" spindle-shaped cell population with a variable proportion of cells with scattered DNA values. The ganglion cell-like cells differed from the spindle cells by having a broad DNA peak in the diploid region and additional peaks in the tetraploid region, as well as a higher proportion of cells with scattered DNA values compared with those of the spindle-shaped cells. The results of the quantitative DNA analysis are well in keeping with the benign and proliferative nature of these lesions. However, with the technique used here, quantitative DNA analysis, does not distinguish these pseudosarcomatous fibrous lesions from diploid and tetraploid soft tissue sarcomas.

Actins↗
PubMed1992

The NIH-3 immunodeficient mouse is a model for Lyme borreliosis myositis and carditis.

Experimental infection of immunodeficient NIH-3 (N:NIH-bg-nu-xid) mice with Borrelia burgdorferi was found to result in multisystem histopathologic lesions. In addition to T-cell deficiency due to the nude mutation, these mice have an x-linked defect affecting the B-cell maturation and the beige mutation resulting in the absence of NK cells. NIH-3 mice were susceptible to progressive infection with B. burgdorferi resulting in pancarditis, synovitis, and skeletal interstitial myositis whereas controls remained normal. Cardiomyopathy was characterized by inflammatory mononuclear infiltration and fibrillar necrosis. Synovial hyperplasia and inflammation were seen in the tibiotarsal and ulna-carpal joints. Advanced myositis was observed in peripheral skeletal muscle. Gastrointestinal submucosa, heart, and skeletal muscle were heavily colonized with B. burgdorferi. This mouse is proposed as a model for Lyme borreliosis carditis, synovitis, and myositis.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Eosinophilic myositis in Canadian cattle.

Musculature from 198 Canadian cattle with suspected lesions of eosinophilic myositis were examined histologically and by pepsin digestion. Sera from 51 of the 198 animals were also examined by enzyme-linked immunosorbent assay (ELISA) for anti-Trichinella antibodies. Viable larvae of Trichinella were not recovered from any of the cattle but one animal from Ontario tested positive for anti-Trichinella antibodies. Histologically, focal and/or diffuse eosinophilic myositis lesions were observed in 149 (75.2%) of the animals studied. Other conditions identified were sarcocystiosis, abscesses, cysticercosis, steatosis, fibrosis, granuloma, lymphosarcoma and necrosis. Sarcocystiosis was identified in 105 of the 198 animals in both normal and affected musculature. The study indicates that trichinosis is not a primary cause of eosinophilic myositis in cattle.

Animals↗
PubMedDate not supplied

Myositis ossificans.

Myositis ossificans is a fairly common disorder that typically involves progressive heterotropic bone formation. A typical case is discussed in this paper. The radiographic findings in myositis ossificans are relevant in differentiating it from a malignant bone tumor and a benign process. Myositis ossificans can cause impairment to a joint with poor rehabilitative results. Limitation of joint function and little reabsorption of the heterotopic bone formation is common. Most cases are posttraumatically related with the brachialis and the quadricep femoris muscles frequently involved. This is especially true for sport injuries.

Hematoma↗
PubMed1989

[Clinico-biological aspects of myositis due to Trichinella T3 with special regard to a rheumatologic study].

One hundred and fifty patients living in Salsomaggiore Terme developed signs and symptoms of trichinellosis after eating infected horse meat. The etiological agent was identified as Trichinella T3. This large outbreak gave us the opportunity of studying the rheumatic manifestations during this kind of parasitic disease. Myositis was observed in 62% of the entire series whereas arthralgias were recorded in only 20% of the patients. The muscle pain was described in several ways, but in the majority it appeared during isokinetic movements. The scapular girdle was involved much more than the pelvic girdle. Arthralgias correlated with the degree of myositis, thus allowing us to conclude that the involvement of the muscle groups proximal to the joint clearly determined a painful sensation in the joint itself. Our histopathologic data suggest that the eosinophils may play an important role in the myositis process.

Adolescent↗
PubMed1989

Tropical myositis. A clinical immunological and histopathological study.

Thirty cases of tropical myositis, (22 suppurative, 8 non-suppurative) aged 11 to 65 years were seen in a period of one year. There were 22 males and 8 females. There was a total of 78 muscular lesions in 22 suppurative cases and 19 muscular lesions in 8 non-suppurative cases. The most common presentation was localised myalgia (100%), fever (96.7%) generalized myalgia (56.7%), arthralgia (40%), pain in abdomen (33.3%) and breathlessness (30%). Extramuscular complications were present in 50% cases. Twenty four muscle biopsies were taken. Sixteen showed changes of suppurative myositis i.e. non-specific acute inflammatory reaction, muscle necrosis with myocytolysis, vacuolation of cytoplasm and loss of striations. Cell mediated immunity was found to be suppressed in patients of non-suppurative myositis in comparison with the suppurative group. IgG, IgA and IgM were significantly raised in patients in comparison to controls (p less than 0.05). The intact humoral immunity indicates good response to acute phase reaction and increased levels of IgG, IgA and IgM (specially IgG) can be taken as good prognostic parameter.

Abscess↗
PubMed1986

Myositis associated with Crohn's colitis.

A patient with myositis associated with Crohn's colitis is reported. Myositis preceded the clinical manifestations of colitis. Both symptoms responded promptly and rapidly to sulfasalazine. Serum creatine phosphokinase was markedly elevated and returned to normal after treatment. Muscle biopsy and electromyography were nondiagnostic. Myositis may be more common than reported in patients with inflammatory bowel disease. Careful attention to muscle pain and serum level of creatine phosphokinase in patients with inflammatory bowel disease is suggested.

Adult↗
PubMed1985

[Localized myositis with eosinophilia].

A 49-year old man developed myositis of the left masticatory muscles followed by myositis of the right supinator longus; these two lesions were histologically confirmed. Blood and bone marrow eosinophilia was present. Cure was obtained with systemic corticosteroids. Only one similar case was found in the literature. These cases differ from the various localized or focal forms of myositis as well as from eosinophilic polymyositis. Despite some similarities with masseteric myopathies in animals, no hypothesis can be formulated concerning the cause of the disease.

Eosinophilia↗
PubMed1984

Immunolocalization of complement component C9 on necrotic and non-necrotic muscle fibres in myositis using monoclonal antibodies: a primary role of complement in autoimmune cell damage.

Monoclonal antibodies to human complement component C9 were used to localise the membrane attack complex (MAC) of human complement on muscle fibres from patients with autoimmune myositis. A pigeon erythrocyte 'model' system was used to screen the available monoclonal antibodies for their ability to bind C9 after its insertion into the MAC. Three of the five antibodies tested were demonstrated, using radioiodine- or rhodamine-labelled second antibody, to bind. The antibody giving maximum binding in this system was used to demonstrate that MACs were present on histologically normal as well as on necrotic fibres in myositis. No binding was seen in muscle from control subjects. These results suggest a primary role of complement in the pathogenesis of muscle fibre necrosis in myositis.

Adult↗
PubMedDate not supplied

The Jo-1 antibody system in myositis: relationships to clinical features and HLA.

Antibodies to Jo-1, a saline extractable nuclear antigen, were found in 11/47 (23%) patients with myositis and in 0/35 controls with systemic lupus erythematosus or progressive systemic sclerosis (p less than or equal to 0.01). Within myositis subgroups, anti-Jo-1 occurred in 6/20 (30%) with polymyositis, 2/16 (13%) with dermatomyositis and 3/7 (43%) with overlap. There was an association between Jo-1 antibodies and HLA-DR3, irrespective of race or clinical subgroups (p less than or equal to 0.05). All anti-Jo-1 positive patients had either HLA-DR3, HLA-DRW6 or both (p less than or equal to 0.01). Thus, this antibody system might arise as a result of an aberrant immune response mediated at or near HLA-D in patients with myositis.

Antibodies, Antinuclear↗
PubMed1980

Denervating changes in focal myositis, a benign inflammatory pseudotumor.

Focal myositis is a benign pseudotumor of skeletal muscle, the cause of which is obscure. It usually appears as a steadily enlarging mass within the muscle of an extremity. The pathologic features are those of an inflammatory myopathy in which lymphocytic infiltrates, muscle cell necrosis, and regeneration are seen. Four cases of focal myositis were studied using enzyme histochemistry and electron microscopy. The changes of denervation atrophy, reinnervation, and fiber hypertrophy were found. Intramuscular nerve damage manifested by axonal swelling, demyelination, and endoneurial fibrosis was evident. The findings suggest that a denervating process plays an important role in the pathogenesis of focal myositis.

Adult↗
PubMed1978

[Proliferating myositis].

A clinico-morphological analysis of 6 cases of proliferating myositis is presented. The patients varied in ages from 31 to 59 years. All the patients reported an extremely rapid growth of swellings: the period from the moment of the "tumour" detection to the operation was within 1 month, and in 4 cases 2 weeks. The main features of the microscopic structure of proliferating myositis included marked proliferation of fibroblasts and random arrangement of large cells with basophilic cytoplasm resembling rhabdomyoblasts and ganglionic cells. A detailed clinico-morphological analysis of the disease permits to differentiate proliferating myositis from similar soft tissue neoplasms (embryonal rhabdomyosarcoma, ganglioneuroblastoma, fibrosarcoma, extraabdominal desmoid, nodular fascitis).

Adult↗