Cases reported "Osteolysis"

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1/8. Fine-needle aspiration cytology of a case of hiv-associated anaplastic myeloma.

    Plasma cell neoplasia occurs much less frequently than high-grade B-cell non-Hodgkins lymphoma in hiv-infected patients, but is nevertheless an AIDS-associated malignancy. In this report, we describe the fine-needle aspiration (FNA) findings of a mass in the left parotid region with plasmablastic features that occurred in a 41-yr-old hiv-infected homosexual man whom we diagnosed as having anaplastic myeloma. The patient had normochromic, normocytic anemia with a hematocrit of 21%, a white blood count of 2.2 x 10(9)/l with 76% neutrophils, and a CD4 count of 31%. He also had elevated levels of calcium (13.2 mg/dl), alkaline phosphatase (25,400 IU/l), blood urea nitrogen (2,600 mg/dl), and creatinine (2.5 mg/dl). serum protein electrophoresis showed polyclonal hypergammaglobulinemia without any monoclonal component. A bone survey revealed multiple punched-out lytic lesions. FNA smears showed large plasmacytoid cells with eccentrically placed nuclei, prominent nucleoli, and moderate amounts of basophilic cytoplasm. By immunocytochemical staining, tumor cells were negative for CD19, CD20, and leukocyte-common antigen (LCA), but strongly positive for CD38 and kappa light chain. Anaplastic myeloma and plasmablastic lymphoma were considered in the differential diagnosis. Although the cytomorphologic and immunophenotypic findings of our case overlapped with those of plasmablastic lymphoma, the pattern of bone involvement with punched-out lytic lesions and absence of localization of the tumor to the mucosa of the oral cavity led us to a diagnosis of anaplastic myeloma. The patient initially received antiretroviral therapy followed by thalidomide and pulse dexamethasome therapy, but his response was poor. His hiv load increased, and his malignancy rapidly progressed with the development of multiple vertebral lesions, extraosseous extension, and eventually cord compression. He died of the disease less than 2 mo after presentation.
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2/8. Ki-1 positive large cell anaplastic lymphoma: multiple bone lytic lesions and interleukin-6.

    Ki-1-positive large cell anaplastic lymphoma (Ki-1 LCAL) is recognized as a clinicopathologic syndrome with fever, peripheral lymphadenopathy and cutaneous nodules; the neoplastic cells express Hodgkin's disease-associated antigen, Ki-1 (CD30). We review here a recent case of Ki-1 LCAL with multiple bone lesions with destruction and present additional information. Although bone absorption is reported in some cases of Ki-1 LCAL, the genesis of bone absorption is unclear. interleukin-6 (IL-6) is an important regulator of osteoclast formation and activation and can induce bone absorption. In our case, the surgically removed tumor tissue was studied for IL-6 mRNA expression and IL-6 secretion without any stimulation. Northern blot analysis showed strong IL-6 mRNA expression in the tumor tissue and ELISA assay showed a large amount of IL-6 in culture supernatants of the tumor tissue. Based on these results, coupled with the reported evidence, we discuss the close relationship between the presence of osteolytic lesions and IL-6 production in Ki-1 LCAL.
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3/8. rhabdomyosarcoma with primary osteolytic lesions simulating non-Hodgkin's lymphoma.

    We report the case of an 8-year-old child presenting with the pathological fracture of two vertebral bodies due to bone lytic lesions. Physical and instrumental examinations did not show any further evidence of disease. However, bone marrow aspirate showed an infiltrate of poorly differentiated cells. When the child was transferred to the Department of pediatrics, lymphoblastic leukemia was suspected. Although the morphology of the bone marrow biopsy could have suggested a lymphoblastic lymphoma, further immunochemical and immunological studies together with the study of tissue surface antigens resulted in a diagnosis of embryonal rhabdomyosarcoma with an unusual presentation.
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4/8. carcinoembryonic antigen production associated with an osteolytic meningioma. Case report.

    An elevated serum carcinoembryonic antigen (CEA) without evidence of neoplasia was noted in an 84-year-old woman. She subsequently developed a lytic skull lesion, which at surgery proved to be an atypical meningioma. Immunohistochemical analysis demonstrated that this tumor was producing CEA. This aggressive meningioma required two further resections and adjuvant radiotherapy in the following 18 months. serum elevation of CEA has been reported only twice in association with meningiomas; both of those tumors were of the secretory subtype.
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5/8. An adult case of histiocytosis X with a vulvar ulcer and multiple bone lesions.

    A 62-year-old female with histiocytosis X presented with a vulvar ulcer. Multiple osteolytic lesions were later detected. Histological examination of the ulcerated skin showed diffuse proliferation of histiocytic cells with folded nuclei and pale eosinophilic cytoplasm. immunohistochemistry revealed S100 protein and vimentin as well as CD1a, CD4, and hla-dr antigens in the proliferating cells. Electron microscopy demonstrated Birbeck granules in the cytoplasm of the cells. The patient was successfully treated by complete surgical excision of the ulcer followed by radiotherapy for recurrent vulvar erythema.
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6/8. Integrin VLA-5 negative primary plasma cell leukemia.

    We present a case of primary plasma cell leukemia with Bence Jones proteinuria. After combination chemotherapy, leukemic cells and the urinary levels bence jones protein were decreased. Small lytic bone lesions were detected only in the skull. Typical plasma cells were rarely seen in peripheral blood on the hyperleukocytic phase, however they were increased in the advanced stages. The most important diagnostic sign was persistent expression of CD38 antigen on leukemic cells throughout the entire course of the illness and these leukemic cells expressed very late antigen-4 (VLA-4) but not VLA-5.
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7/8. multiple myeloma with monoclonal surface immunoglobulin expression: a case report.

    BACKGROUND: plasma cells from patients with multiple myeloma have been found to express the immunophenotype of normal plasma cells without surface immunoglobulin expression. CASE: A case occurred of multiple myeloma with monoclonal surface immunoglobulin expression, defined by morphology and flow cytometric immunophenotyping of a fine needle aspiration biopsy of an osteolytic rib lesion and a bone marrow aspirate as well as urine and serum protein electrophoresis with immunofixation. CONCLUSION: The clinical significance of monoclonal surface immunoglobulin expression in rare cases of multiple myeloma is uncertain, and other parameters with clinical significance (CD10 positivity, multiple myeloid antigen expression) will continue to be more useful until additional cases accrue.
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8/8. multiple myeloma (light chain disease) with rheumatoid-like amyloid arthropathy and mu-heavy chain fragment in the serum.

    A 52 year old man presented with multiple myeloma and widespread amyloidosis involving joints, bursae- carpal tunnels, lymph nodes and subcutaneous tissue. Osteolytic bone lesions and pathologic fracture of the neck of the left femur were found. bone marrow was infiltrated with both plasmacytes and lymphocytes. The majority of plasma cells contained large cytoplasmic vacuoles. Free kappa II type light chains and mu-heavy chain fragment were detected in the serum, and kappa II type bence jones protein was found in the urine. The molecular weight of the mu-heavy chain fragment was found to be approximately 50,000 daltons. An immunofluorescence study, using the double labelling technic, showed that the majority of plasmacytes in bone marrow contained both mu and kappa antigenic determinants in the cytoplasm. A review of the 12 previously described patients with mu-heavy chain fragment in the serum showed a variable clinical picture, thus their natural history and therapeutic response are difficult to evaluate at the present time. It seems that mu-heavy chain fragment can be found in a variety of clinical conditions and that mu-heavy chain disease cannot yet be accepted as a separate clinical entity.
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