Cases reported "Leukemia, T-Cell"

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1/7. adult T-cell leukemia with hypercalcemia-induced metastatic calcification in the lungs due to production of parathyroid hormone-related protein.

    A 60-year-old man was diagnosed as adult T-cell leukemia with severe hypercalcemia because of production of parathyroid hormone-related protein. After admission, the patient had respiratory insufficiency with an infiltrative shadow in his lungs suggestive of pneumonia. However, neither improvement in respiratory function nor disappearance of the abnormal chest shadow was observed with administration of various antibiotics. An autopsy demonstrated the chest shadow had been caused by metastatic calcification associated with hypercalcemia due to production of parathyroid hormone-related protein. The possibility of metastatic calcification should be considered in patients with adult T-cell leukemia and hypercalcemia who have an abnormal chest shadow.
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2/7. Acute rhabdomyolysis following administration of high-dose cyclophosphamide: case report.

    rhabdomyolysis is an unusual complication of hematopoietic stem cell transplantation (HSCT). cyclophosphamide has been one of the key drugs in the most common preparative regimen for HSCT. We present here a rare case of acute rhabdomyolysis following administration of high-dose cyclophosphamide. A 47-year-old woman with adult T-cell leukemia in remission was treated with high-dose cyclophosphamide as a preparative regimen for allogeneic bone marrow transplantation. Nineteen hours later, general convulsions and acidosis suddenly occurred. Levels of serum creatine kinase (skeletal muscle type), myoglobin, and aldolase were markedly elevated to 32870 IU/l, 640 ng/ml, and 240.3 IU/l, respectively. rhabdomyolysis caused by high-dose cyclophosphamide was diagnosed, and the preparative chemotherapy was discontinued. Subsequently, her muscular signs and symptoms improved, and the results of laboratory examinations returned to normal after 2 weeks. She had previously been treated with conventional doses of cyclophosphamide, doxorubicin, vincristine, and prednisolone without evidence of rhabdomyolysis. Acute rhabdomyolysis may be an adverse effect specific to high-dose cyclophosphamide therapy.
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3/7. neutropenia and anaemia associated with T-cell large granular lymphocyte leukaemia responds to fludarabine with minimal toxicity.

    T-cell large granular lymphocyte leukaemia (T-LGL) is a clonal disorder of T cells associated with neutropenia and anaemia. The clinical consequences are recurrent infections and transfusion dependence. The optimum treatment for severely affected patients remains to be defined. Current therapies require long-term administration to maintain an effect. We report the reversal of severe neutropenia and/or anaemia in four patients treated with fludarabine which has been maintained since stopping treatment. The therapeutic side-effects were restricted to one episode of fever not associated with neutropenia. We conclude that fludarabine is effective in T-LGL, may be given safely despite severe neutropenia and induces durable treatment-free remissions.
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4/7. vancomycin-dependent antibodies associated with thrombocytopenia and refractoriness to platelet transfusion in patients with leukemia.

    Two patients with leukemia experienced profound thrombocytopenia and refractoriness to platelet transfusion during vancomycin treatment. In one patient, withdrawal of drug and administration of platelet transfusions restored platelet counts to near normal levels (approximately 100 x 10(9)/L), however, subsequent challenge with vancomycin due to recurring infection again precipitated severe thrombocytopenia (platelets less than 10 x 10(9)/L) and life-threatening hemorrhagic symptoms. Potent vancomycin-dependent antiplatelet antibodies were detected in the serum of both patients during the refractory period using staphylococcal protein a rosette formation. Employing a monoclonal antibody-antigen capture enzyme-linked immunosorbent assay (ELISA), the patients were found to have vancomycin-dependent IgG antibodies that bound specifically to platelet glycoproteins (GP) IIb and/or IIIa. One of these antibodies failed to react with platelets deficient in GPIIb/IIIa obtained from an individual with Glanzmann's thrombasthenia. These findings provide the first major evidence for drug-dependent antibodies in association with severe thrombocytopenia and refractoriness to platelet transfusion in alloimmunized leukemia patients and, further, provide the first demonstration of vancomycin-dependent antibodies reactive with platelets.
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5/7. Hyperkalaemia with renal tubular dysfunction by sulfamethoxazole-trimethoprim for pneumocystis carinii pneumonia in patients with lymphoid malignancy.

    Hyperkalaemia with renal tubular dysfunction by oral therapy of sulfamethoxazole-trimethoprim (co-trimoxazole) is described in 2 elderly Japanese patients with lymphoid malignancy, who developed pneumocystis carinii pneumonia and improved. A high dose of cotrimoxazole induced hyperkalaemia with the elevation of serum creatinine and blood urea, and increased urinary N-acetyl glucosaminase after several days of the drug administration in these patients; one patient became unconscious. Discontinuation of co-trimoxazole normalized serum potassium level and symptoms. A repeated low dose of the drug induced hyperkalaemia. Before the treatment of co-trixomazole, their serum levels of creatinine showed upper limits of normal ranges. In the present study, our cases suggested that patients receiving a high dose of co-trimoxazole should be evaluated for these potential complications during a course of treatment, particularly in elderly patients with preexisting renal dysfunction.
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6/7. Successful treatment of a patient with adult T-cell leukemia by daily oral administration of low-dose etoposide. Decrease in the amount of HTLV-I proviral dna revealed by the polymerase chain reaction method.

    BACKGROUND. Oral administration of low-dose etoposide is known to be effective against various malignancies, including malignant lymphoma. However, the effectiveness of low-dose etoposide as a treatment for adult T-cell leukemia (ATL) has not been established. methods. A 74-year-old woman with ATL in acute phase was treated by daily oral administration of low-dose etoposide (25 mg/m2). The authors assayed changes in the surface markers and the amount of human T-cell lymphotropic virus type I (HTLV-I) proviral dna in peripheral blood mononuclear cells (PBMC) by using flow cytometry and the polymerase chain reaction (PCR) method, respectively. RESULTS. Before treatment, generalized lymphadenopathy and hepatomegaly were observed. In laboratory examination, the leukocyte count was 13.7 x 10(3)/microliters, with 65% abnormal lymphocytes. The percentages of CD3-, CD4-, and CD25-positive cells in PBMC were 84.4%, 84.4%, and 76.5%, respectively. The serum lactic dehydrogenase (LDH) level was 1376 IU/l (normal range, less than 520 IU/l). After the initiation of treatment, lymph-adenopathy and hepatomegaly disappeared, and the serum LDH level was reduced to the normal level before the 20th day of the treatment. On the 55th day of the treatment, CD25-positive cells had virtually disappeared. In addition, the amount of the proviral dna in PBMC was reduced to approximately one-tenth by this treatment. Subsequently, the patient was in remission for more than 16 months. No side effects were observed. CONCLUSIONS. Daily oral administration of low-dose etoposide can be a safe and effective treatment for patients with ATL. The authors believe this to be the first report of a patient with ATL in whom complete remission (CR) was achieved by this treatment.
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7/7. Severe neutropenia in T-large granular lymphocyte leukemia corrected by intensive immunosuppression.

    Optimum treatment of severe neutropenia, a major factor for morbidity and mortality in T-large granular lymphocyte (LGL) leukemia, is undefined. We observed a rapid improvement of the neutrophil count in a patient with T-LGL leukemia and severe neutropenia after the combined administration of antilymphocyte-globulin (ALG), cyclosporin A, prednisone, and granulocyte colony-stimulating factor (G-CSF). Although G-CSF treatment was terminated after 7 days, the neutrophil count has persisted above 1.0 x 10(9)/1 for up to 6 months now. Oral methotrexate is given continuously as treatment for T-LGL leukemia. The response to this immunosuppressive regimen suggests a T-cell-mediated mechanism as the underlying cause for neutropenia in T-LGL leukemia.
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