Cases reported "Lymphatic Diseases"

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1/5. Extensive bone marrow necrosis in patients with cancer and tumor necrosis factor activity in plasma.

    Tumor necrosis factor (TNF), a macrophage secretory protein produced by peripheral blood monocytes from patients with cancer, has been shown to possess cytotoxicity toward tumor cells in vitro. TNF in the blood of individuals with cancer is usually not detectable except with extremely sensitive radioimmunoassay or enzyme-linked immunosorbent assay (ELISA) methods. We have encountered two patients with the rare syndrome of extensive bone marrow necrosis in association with cancer. The first patient presented with marrow failure secondary to necrosis and was found to have adenocarcinoma in thoracic lymph nodes, lung, and marrow lymphatics at autopsy. plasma tested at two dilutions (1:200 and 1:2,000) contained TNF at a concentration of 8.3 ng/ml, or 80 U/ml by a cytotoxicity assay using LM cells. The presence of TNF was confirmed with immunoblotting. The second patient had a poorly differentiated lymphoid tumor involving bone marrow, pancytopenia, and marrow necrosis. The plasma cytotoxicity assay indicated the presence of 0.7 ng/ml or 7 U/ml TNF. TNF was not detectable in plasma from six other patients with untreated cancer involving bone or bone marrow using either of our methods. The levels of TNF in the two patients with marrow necrosis were greater than those previously measured by others in patients with cancer but were comparable to those noted in patients with lethal sepsis. Since large doses of TNF have been shown to cause organ necrosis in animals, the data presented here are consistent with TNF involvement in mediating the observed marrow necrosis in our patients.
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2/5. Immunological studies on an unusual case of primary pulmonary amyloidosis with hilar adenopathy.

    A rare case of primary pulmonary amyloidosis with hilar lymphadenopathy is described. Immunological studies showed decreases in serum IgG and IgM levels. However, both pokeweed mitogen (PWM)-induced IgG production and proliferation of peripheral blood B cells were not disordered. The response of peripheral blood lymphocytes (PBL) to stimulation with PWM, phytohemagglutinin, or concanavalin a was found to be normal. In addition, the proportion of E and EAC rosette-forming cells in PBL from this patient did not differ from that in PBL from normal donors. The positive response of skin test to recall antigens also gave an evidence that the patient had not a depression in systemic cell-mediated immunity. These findings contrast with those previously described for systemic amyloidosis in man and in animals.
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3/5. Multiple lymphonodular cryptococcosis, cured by 5-fluorocytosine.

    A 5-year-old boy was admitted with an acute febrile illness and painful and enlarged cervical lymph nodes. A chest X-ray showed right tracheobronchial lymph nodes. A lymph node biopsy demonstrated a tuberculoid appearance, with epitheloid cells, giant cells, and also necrotic zones. cryptococcus neoformans was isolated both in culture and after animal inoculation. While amphotericin b was not tolerated by the patient, the oral administration of 5-fluorocytosine resulted in a rapid recovery.
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4/5. Polyclonal lymphoid tumor of the choroid plexus presenting as an intraventricular mass in a young gorilla.

    An unusual lymphoid lesion with reactive germinal centers, occurring in the choroid plexus of a young gorilla, is reported. It presented as a large mass in the lateral ventricle with hydrocephalus and neurological symptoms. A work-up did not reveal any underlying cause for this lesion. No similar lesion of the choroid plexus has been reported in either human or veterinary literature. Histological work-up, including flow cytometry, gene rearrangement studies and T and B cell markers, favored the lesion being a non-neoplastic lymphoid proliferation of unknown etiology. The prognosis is unknown, although, following complete removal, the animal is well and free of tumor at the time of this report.
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5/5. Massive macrophage lipid accumulation presenting as hepatosplenomegaly and lymphadenopathy associated with long-term total parenteral nutrition therapy for short bowel syndrome.

    We present a unique case of massive splenomegaly, hepatomegaly, and lymphadenopathy caused by lipid-laden macrophages in a 50 year old white female with short-bowel syndrome treated with long-term total parenteral nutrition. Using transmission electron microscopy and special stains we were able to show that the total parenteral nutrition lipid component was composed of lipid droplets and micelles morphologically identical to those found in lipid-laden macrophages which had accumulated in the patient's reticuloendothelial system leading to massive splenomegaly, hepatomegaly (without evidence of steatosis) and lymphadenopathy. While this phenomenon has been reported in animal models, no human cases have been previously reported.
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