Cases reported "Hypersplenism"

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1/8. pancytopenia due to hypersplenism after allogeneic bone marrow transplantation.

    Three patients developed pancytopenia in the second month post-allogeneic bone marrow transplantation in association with progressive splenomegaly and a normocellular marrow. splenectomy resulted in a prompt and sustained improvement in all haematological parameters in all cases. None of the spleens had morphological or cytogenetic evidence of tumour. hypersplenism should be considered in patients with persistent or recurrent pancytopenia and splenomegaly post-transplantation.
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2/8. Fibrolamellar carcinoma of the liver--a case report.

    A 36-year-old woman was admitted to our hospital because of general fatigue. The physical and laboratory findings on admission revealed splenomegaly, pancytopenia, hypocoagulopathy, liver hypofunction with a hepaplastin test of 55% and ICG Rmax of 0.6 mg/kg/min. diagnostic imaging showed a hypoechoic mass 1.5 in diameter a low density area on the CT scan and a faint tumor stain on the AAG in the posterior inferior area of the liver. On a diagnosis of hepatocellular carcinoma with liver cirrhosis and hypersplenism, partial hepatectomy and splenectomy were performed. The resected hepatic specimen revealed a small liver cancer of 1.9 x 1.5 x 1.3 cm with liver cirrhosis. The specimen consisted of a firm rubbery mass. Macroscopically, the tumor appeared oval and was lobulated with a thin capsule. A fibrous scar was observed in the central area. Microscopically, malignant hepatocytes showed various shapes, ranging from polygonal to spindle form, with eosinophilic granular cytoplasm and were surrounded by abundant fibrous stroma. Orcein stain, revealed that these malignant hepatocytes contained many black granules of copper-binding protein. Immunoperoxidase staining for alpha 1-antitrypsin was also positive in the malignant hepatocytes. However, within this lamellar fibrous regions, there were many cords of tumor cells in which nucleoli were absent and abortive biliary differentiation was suggested. Consequently this tumor was diagnosed as an atypical fibrolamellar hepatocellular carcinoma. We think that this case is the 3rd case reported in japan and the 2nd case in a Japanese person.
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3/8. T-cell-rich B-cell lymphoma of the spleen presenting with severe hypersplenism.

    We report a 19-year-old woman who was presented with B-symptoms, massive splenomegaly, hepatomegaly and hypersplenism. She underwent diagnostic/therapeutic splenectomy. Microscopically, the spleen showed a vaguely micronodular and diffuse proliferation of lymphoid cells in the white pulp that also involved the red pulp. On immunohistochemical staining, this proliferation consisted predominantly of CD3( ), CD7( ) small T cells with the presence of a minor population of CD15(-),CD30(-), CD20( ) large atypical B cells. A liver biopsy also showed a similar morphology to that seen in the spleen. After splenectomy, only the pancytopenia improved. A combined immunochemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone) was utilized, which resulted in a complete remission.
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4/8. Splenic lymphoma with hypersplenism--a case report.

    A 47-year old man had hypersplenism from massive splenomegaly, the cause of which was undetermined for 2 years. He was initially asymptomatic though there was mild pancytopenia. However, 18 months after presentation he manifested both clinical and haematological deterioration, almost succumbing to sepsis. splenectomy finally provided a definite diagnosis of follicular lymphoma and also restored his blood counts to within normal range.
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5/8. Recurrent hypersplenism caused by alcoholic cardiomyopathy after distal splenorenal shunt.

    The hypersplenism associated with portal hypertension usually resolves with a successful shunting procedure. Recurrent hypersplenism has been associated with shunt thrombosis. We describe a patient with pancytopenia, jaundice, and diffuse edema after a distal splenorenal shunt. His shunt was angiographically proved patent. Extensive evaluation revealed severe alcoholic cardiomyopathy with passive splenic congestion. He died of cardiac failure. Alcohol is a systemic toxin that affects other organs, as well as the liver.
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6/8. hypersplenism in Hodgkin's disease: a report of three cases presenting with cytopenias.

    A review of the last seventy-eight consecutive cases of Hodgkin's disease seen at our hospital revealed that two presented several hematologic cytopenias. These two cases and a similar case first seen at an associated hospital revealed pancytopenia in two and leukopenia in the third. All responded to splenectomy with hematologic improvement. All met the criteria for hypersplenism. This report illustrates that Hodgkin's disease can present cytopenias due to hypersplenism, and that early splenectomy can lead to hematologic improvement and tolerance of subsequent chemotherapy.
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7/8. Leukemic reticuloendotheliosis. Loss of platelet defect after splenectomy.

    A 59-year-old woman with leukemic reticuloendotheliosis had pancytopenia and hypersplenism. Before splenectomy, she had an abnormal bleeding time and a severe defect of secondary-wave platelet aggregation. After splenectomy, the platelet count returned to normal, and the aggregation defect was no longer present. This response suggests that the spleen may contribute to the platelet dysfunction.
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8/8. Juvenile rheumatoid arthritis and common variable hypogammaglobulinemia.

    We describe a 9-year-old white boy with systemic juvenile rheumatoid arthritis (JRA) who developed pancytopenia and hypersplenism at the age of 13 years. He underwent splenectomy and 3 years later he developed Coombs' positive hemolytic anemia, alopecia, juvenile warts, and multiple bacterial infections. At that time, investigations were compatible with severe hypogammaglobulinemia associated with common variable immunodeficiency. Concomitantly with this condition he experienced complete remission of his inflammatory arthritis. Immunologic studies of B and T lymphocyte function showed that the number of circulating T and B lymphocytes were normal, while T cell function was depressed, as evidenced by markedly reduced proliferative responses to mitogens and antigens, and ability to mediate B cell help. In addition, his circulating B cells were unable to secrete IgM or IgG. He also exhibited anergy to intradermal challenge with a battery of common antigens. The literature dealing with this clinical association is reviewed, and possible immunologic mechanisms involved are discussed.
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