Cases reported "Myositis"

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1/15. Nodular sarcoid myositis of skeletal muscle diagnosed by fine needle aspiration biopsy. A case report.

    BACKGROUND: Symptomatic striated muscle involvement in sarcoidosis is rare. Muscle biopsy is usually required for the diagnosis. Fine needle aspiration biopsy (FNAB) has been successfully used in diagnosing soft tissue lesions. To the best of our knowledge, FNAB of sarcoid myositis has not been reported. CASE: A 31-year-old, black female with a history of sarcoidosis presented with an enlarging, painful, left calf mass. Infected thrombi were suspected. FNAB showed numerous loosely arranged epithelioid histiocytes, multinucleated giant cells and skeletal muscle cells. The overall cytologic picture was that of granulomatous myositis. The cytologic features coupled with the patient's history and magnetic resonance imaging findings suggested sarcoid myositis. Subsequent muscle biopsy showing noncaseating granulomata and negative stains for organisms confirmed the diagnosis of nodular sarcoid myositis. CONCLUSION: Nodular sarcoid myositis can be suggested by FNAB cytology in a patient with a past history of sarcoidosis.
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2/15. The subcutaneous fascial analogue of myositis proliferans: electron microscopic examination of two cases and comparison with myositis ossificans localisata.

    Two cases of the so-called fascial analogue of myositis proliferans were investigated by histological and electron microscopic methods. It was found that the structure of the fascial variant corresponds almost completely to the true myositis proliferans localized within the musculature. The electron microscopic observations show a preponderantly histiocytic differentiation of the cells and strongly activated proliferating capillaries, and exclude a myogenic origin of the characteristic ganglion-like giant cells. Ultrastructurally a traumatic genesis appears possibly, the cells of the lesion could derive from multipotent cells of the microvasculature. The relations to myositis ossificans and fascitis nodularis are discussed.
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3/15. A case report of giant cell myocarditis and myositis observed during the clinical course of invasive thymoma associated with myasthenia gravis.

    The patient is a 62-year-old man who was diagnosed with myasthenia gravis and invasive thymoma at the age of 45 years, and had received treatment by extended thymectomy and radiotherapy. At the age of 61, he had suffered from a myasthenic crisis, and been administered immunoadsorption therapy under managed ventilatory care. Treatment had then been continued with steroids; however, due to subsequent deterioration of his diabetic state, treatment was switched to the immunosuppressant drug tacrolimus. Three months after the commencement of tacrolimus administration, the patient developed generalized malaise and dyspnea. The serum creatine phosphokinase (CPK) level was abnormally elevated, and abnormal electrocardiographic findings were noted, including atrioventricular dissociation and ventricular escape contraction. Steroid pulse therapy was therefore initiated, however, 4 days later, the patient suddenly died. autopsy examination revealed inflammatory cell infiltration with giant cells in the myocardium, diffuse myocardial degeneration, and polymyositis. The case was therefore considered as one with the syndrome of myasthenia gravis, polymyositis, giant cell myocarditis, and thymoma.
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4/15. Diabetic (lymphocytic) mastopathy with exuberant lymphohistiocytic and granulomatous response: a case report with review of the literature.

    We report a case of a 66-year-old woman who presented with multiple painless masses in both breasts. Prior bilateral biopsies were diagnosed as Rosai-Dorfman disease (Sinus histiocytosis with Massive Lymphadenopathy). A recent lumpectomy specimen revealed a gray-white smooth cut surface with a discrete masslike lesion. The histopathology demonstrated a fibrotic breast parenchyma with foci of dense fibrosis and scattered inconspicuous breast epithelium surrounded by lymphocytes that formed aggregates and follicles with germinal centers. The inflammation was in a periductal, perilobular, and perivascular distribution. In addition, an exuberant inflammatory response with histiocytes and fibroblasts was present. This inflammatory response focally surrounded areas of fat necrosis and formed noncaseating granulomas with rare multinucleated giant cells. This process had infiltrative, ill-defined edges and involved the subcutaneous tissues. The overlying epidermis was normal. The final diagnosis was diabetic mastopathy with an exuberant lymphohistiocytic response. The differential diagnosis included Rosai-Dorfman disease, inflammatory myofibroblastic tumor, granulomatous mastitis, sclerosing lipogranulomatous response/sclerosing lipogranuloma, lupus panniculitis, and rheumatoid nodules. Immunohistochemical studies and flow cytometry confirmed the polyclonal nature of the lymphoid infiltrate. After the histologic evaluation, we inquired if the patient had a history of diabetes mellitus, and learned that she did have type 2 noninsulin-dependent diabetes mellitus. In conclusion, we report a case of diabetic mastopathy that presents with bilateral tumorlike masses and an unusual exuberant lymphohistiocytic response with granuloma formation. The pathologist may not be provided with a history of diabetes mellitus, but the characteristic fibrosis, lymphocytic ductitis/lobulitis, and sclerosing lobulitis with perilobular and perivascular lymphocytic infiltrates should provide clues for an accurate diagnosis, even when an exuberant and an unusual lymphohistiocytic response is present. A timely accurate diagnosis can help limit repeat surgeries in this vulnerable group of patients.
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5/15. Giant cell myocarditis and myositis associated with thymoma and leprosy.

    myocarditis is an inflammatory form of heart disease which is usually preceded by a viral infection. Giant cell myocarditis is an uncommon and nonspecific form of this disease. Sporadic reports have linked giant cell myocarditis with thymoma and concomitant myositis. The authors report a patient with leprosy who, six months after initiation of treatment, developed sudden onset of congestive heart failure and cardiac arrhythmias unresponsive to aggressive medical therapy. In addition to confirming leprosy, autopsy showed a mixed cell type thymoma, severe giant cell myocarditis and extensive myositis.
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6/15. Bilateral orbital involvement in fatal giant cell polymyositis.

    The case of a young woman with giant cell polymyositis is described. She had bilateral, severe, midly painful proptosis and ophthalmoplegia. Extensive pharyngeal, laryngeal, and cardiac muscle involvement occurred 18 months later coincident with fatal cardiac arrhythmia. At autopsy, extensive muscle necrosis and giant cells were noted in extraocular, pharyngeal, laryngeal, and cardiac muscle with only minimal involvement of other striated muscles.
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7/15. orbital myositis and giant cell myocarditis.

    A 65-year-old woman developed progressive, bilateral ophthalmoplegia, with thickened extraocular muscles on CT. One month later, a cardiac arrhythmia led to her death. Pathologically, the extraocular and skeletal muscles showed diffuse mononuclear cell inflammation, while the heart contained granulomatous myositis. This patient's syndrome of idiopathic, orbital myositis and giant cell myocarditis may be a distinct nosologic entity.
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8/15. Proliferative myositis and fasciitis. Report of five cases with an ultrastructural and immunohistochemical study.

    Cases of proliferative myositis and fasciitis were studied immunohistochemically and ultrastructurally for further understanding of the nature of ganglion cell-like giant cells. blood coagulation factor xiiia, fibronectin, myoglobin, myosin, CPK MM, and alpha-1-antichymotrypsin were detected in three cases of proliferative myositis and two cases of proliferative fasciitis by the avidin-biotin-peroxidase complex method. factor xiiia (a fibrin-stabilizing factor) and fibronectin were strongly positive in the giant cells, but not in striated muscle fibers. A small quantity of myosin was demonstrated in the giant cells, but myoglobin and CPK MM were never demonstrated in these cells. No alpha-1-antichymotrypsin was demonstrated in the giant cells. One case of proliferative myositis showed ultrastructural features suggestive of fibroblast rather than muscle cell or histiocytic origin. Strongly positive factor xiiia in the giant cells is suggestive of the fact that they are active fibroblasts.
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9/15. Giant cell myocarditis in association with drug-induced skin eruption.

    A case of giant cell myocarditis in a 19-year-old woman is presented. She had high fever, vomiting, epigastralgia, cardiomegaly, and disseminated papular erythema probably due to anti-epileptic agents. At autopsy, giant cell myocarditis and the myositis of the systemic skeletal muscles were found. To our knowledge, no case of giant cell myocarditis in association with drug-induced skin eruption was reported. This is a rare case of giant cell myocarditis.
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10/15. Proliferative myositis in an infant: report of a case with electron microscopic observations.

    Proliferative myositis presented in a 7-month-old female infant as a poorly circumscribed mass growing rapidly within the interscapular skeletal muscle. Muscle fascicles and individual fibers were dissected by an inflammatory infiltrate of lymphocytes, plasma cells, and histiocytes immersed in a basophilic intercellular substance. Numerous ganglionlike giant cells were present and had ultrastructural features suggestive of histiocytic origin. The possible relation to other rapidly growing lesions that appear in soft tissues is discussed. This probably represents the first reported case of proliferative myositis in a pediatric patient.
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