Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here a case of hypoplastic leukemia with T cell markers in whom complete remission was obtained with granulocyte-colony-stimulating factor (G-CSF) alone. A 23-year-old male was diagnosed with hypoplastic leukemia: Hb 2.6 g/dl, platelet count 29.0 x 10(9)/l after transfusion, WBC 2.9 x 10(9)/l, hypocellular bone marrow with 70.7% blasts. He was given G-CSF 300 micrograms/day by intravenous drip infusion without antileukemic agents for severe pneumonia. After the administration of G-CSF for 15 days, hematological examination and bone marrow findings had improved to normal, and complete remission was obtained. However, the patient relapsed 45 days after discontinuation of G-CSF. The characteristics of the relapsed leukemia cells were similar to those on admission: negative for myeloperoxidase and positive for T cell markers (CD2 and CD7). The possibilities for the differentiation of leukemic cells and the recovery of normal hematopoiesis with G-CSF are discussed.
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PMID:Complete remission in a patient with hypoplastic acute lymphoblastic leukemia induced by granulocyte-colony-stimulating factor. 754 23

A 47-year-old man presented with fever, cough and chest pain in January, 1989. He was found to have mediastinal tumor and generalized lymphadenopathy. Peripheral blood and bone marrow findings were typical for the chronic phase of chronic myelogenous leukemia (CML). Although the histological findings of a cervical lymph node were indistinguishable from those of malignant lymphoma, cytogenetic studies of the lymph node cells showed positive Ph1 chromosome and rearrangement of the bcr gene as well as bone marrow cells. Double fluorescence analysis of lymph node cells demonstrated co-existence of CD5, CD7 and CD33 positive cells and of cells sharing both CD5 or CD7 and CD33 antigens. These findings suggest that tumor cells originate from the stage at which the differentiation pathways of hematopoietic stem cells branch into precursor T and myeloid cells. Various combination chemotherapies had only partial effects on lymph node swelling. Chronic daily administration of low dose etoposide was very effective to control both lymphadenopathy and leukocytosis and the patient remained well for over 2 years until July, 1991 when hematological myeloid blast crisis developed. He died of pneumonia in October, 1991. This is a rare case of CML with extramedullary mixed crisis which survived for a long time.
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PMID:[Extramedullary blast crisis of mixed precursor T lymphoblastic and myeloblastic features in a patient with chronic myelogenous leukemia successfully treated with low-dose oral etoposide]. 829 29

A 63-year-old male was admitted because of pneumonia. Peripheral blood findings showed pancytopenia with increase of blasts. A bone marrow specimen showed hypocellular marrow with increase of blasts. The blasts were positive for CD7, CD34, and HLA-DR and negative for other lymphoid antigens and myeloid antigens involving myeloperoxidase. Rearrangement of immunoglobulin heavy chain was demonstrated by Southern blotting analysis. T cell receptor beta, T cell receptor gamma and immunoglobulin light chain rearrangement were negative. A diagnosis of stem cell leukemia was made. In vitro, the blasts did not respond to recombinant human granulocyte colony-stimulating factor (rhG-CSF), cytarabine (Ara-C) and all-trans retinoic acid (ATRA). However, in the blasts of culture without cytokeins, CD33 expression was newly induced. Remission was not obtained by chemotherapies with cyclophosphamide, etoposide, prednisolone and Ara-C. Four months later, marrow specimens showed hypoplasty with myelofibrosis. One year later, the blasts showed CD33 expression with negative myeloperoxidase. The leukemia was transformed to minimally differentiated myeloid leukemia from stem cell leukemia. This condition was thought to be "smoldering leukemia" because of the slow development and refractoriness to chemotherapy. Nineteen months later the patient died due to respiratory failure by pneumonia and pulmonary bleeding despite therapy.
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PMID:[Smoldering leukemia with CD7.CD34(+), immunoglobulin heavy chain rearrangement (+) and hypoplastic marrow with myelofibrosis]. 902 57

Anewborn with a transient myeloproliferative disorder and a myeloid/natural killer cell leukemia phenotype is described. The blasts expressed CD7, CD33, CD34, CD56, and CD117 but did not react with cytoplasmic myeloperoxidase and were negative for cy CD22, HLA-DR, and CD90 expression. No megakaryoblastic surface markers were identified. The blast population disappeared from the peripheral blood and bone marrow within 2 months, but hepatomegaly and recurrent respiratory insufficiency persisted. The patient died of unilateral pneumonia in the third month of life. Neither extramedullary infiltration nor other hematologic signs of disease progression were found.
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PMID:Transient myeloproliferative disorder with a CD7+ and CD56+ myeloid/natural killer cell precursor phenotype in a newborn. 1214 90

This article describes a rare case of bone marrow transplantation (BMT) from an unrelated donor (URD) in an adult Japanese male with Down syndrome (DS) diagnosed as having acute mixed lineage leukemia. Examination of peripheral blood demonstrated WBC 6.2 x 10(9)/l with 45.5% blasts at admission. Leukemic blasts with positive peroxidase stain, but negative periodic acid-Schiff stain comprised 91.6% on bone marrow specimen. Surface marker analysis of these blasts showed the following: CD3(-), CD5(-), CD7(-), CD10(+), CD19(+), CD13(+), CD14(-), CD33(+), CD34(+), CD41a(-), and CD56(-). Based on these data, he was diagnosed as having acute mixed lineage (myeloid and B-lymphoid lineage) leukemia. He achieved complete remission (CR) by lymphoid-oriented chemotherapy performed after ineffective myeloid-oriented therapy. After four courses of consolidation chemotherapy for lymphoid lineage blasts, recurrence due to proliferation of myeloblasts had occurred. Thereafter, a second CR was obtained by low dose cytosine arabinoside (AraC) therapy. As this patient was considered to have a high risk of relapse, we selected allogeneic BMT from URD. Severe stomatitis due to methotrexate (MTX) occurred probably due to altered pharmacokinetics usually observed in DS patients. Though acute graft-versus-host disease (GVHD) of systemic skin (grade II) and pneumonia were observed during neutropenia due to the post-conditioning regimen, he could be discharged from our hospital on the 135th day after BMT. On day 205 post-BMT, however, bronchiolitis obliterans (BO) occurred as a chronic GVHD disorder. Despite therapy with prednisolone and FK506, he died on day 400 post-BMT because of respiratory failure due to BO. In DS patients, superfluous toxicities due to MTX and AraC treatment have been reported, and these toxicities have been considered due to altered pharmacokinetics in patients with DS. This patient could tolerate the transplant conditioning regimen commonly used in patients without DS.
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PMID:Unrelated donor bone marrow transplantation for acute mixed lineage (myeloid and B-lymphoid lineage) leukemia in an adult with Down syndrome. 1270 27

Leukemias arising from immature nature killer (NK) cells have been proposed as distinct entities and are rare. Treatment and prognosis of these diseases are controversial, and data on children are limited. According to the literature, one of these distinct leukemias may be myeloid/NK cell precursor acute leukemia (MNKPL), with the blasts being cytochemically myeloperoxidase negative (MPO(-)) and phenotypically CD56(+)CD3(-)CD7(+)CD34(+) and myeloid antigens(+). The other may be myeloid/NK cell acute leukemia (MNKL), in which the blasts were cytochemically MPO(dim) and phenotypically CD56(+)CD16(-)CD3(-)CD33(+)HLA-DR(-). Between 2005 and 2008, 4 MNKPL and 1 MNKL children aged 1.3 to 12.5 years were encountered in the First Affiliated Hospital of Sun Yat-Sen University. In those with MNKPL, remarkable extramedullary involvement usually occurring in adults was not observed; however, myelofibrosis was found in 2 children. The child with MNKL abandoned treatment. Those with MNKPL were treated with a protocol designed for childhood high-risk acute lymphoblastic leukemia (ALL) containing cytarabine, mitoxantrone, etoposide, l-asparaginase, and methotrexate according to the myeloid and lymphoid characteristics of MNKPL. They responded slowly to chemotherapy and were in complete remission (CR) for 26 to 63 months, except 1 who died in CR from pneumonia. They had longer survival and seemed to have a better outcome than those reported previously. In conclusion, childhood leukemias with immature NK cell markers may have different characteristics from their adult counterparts. A protocol including agents used for acute myeloid leukemia combined with those for ALL is seemingly effective for treatment of MNKPL. However, a modified treatment strategy designed more specifically for MNKPL and longer observations are needed.
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PMID:Five Chinese pediatric patients with leukemias possibly arising from immature natural killer cells: clinical features and courses. 2127 77

Inflammatory pseudotumour is a rare condition that can affect various organs. The clinical and histologic appearance of the pseudotumour may mimic haematological, lymphoproliferative, paraneoplastic or malignant processes. A previously healthy 39-year-old man presented with nephrotic syndrome. He had a history of headaches, nausea and swollen ankles. Computed tomography of the abdomen revealed a 6-cm mass in the spleen. Following a renal biopsy, a diagnosis of membranoproliferative glomerulonephritis (MPGN) type I was made. Splenectomy was performed and the examination revealed a mixed population of lymphocytes with predominantly T-cells, B-cells and lymphoplasmacytoid cells. Immunostaining confirmed that the small cells were mostly T-cells positive for all T-cell markers including CD2, CD3, CD4, CD5, CD7 and CD8. A diagnosis of inflammatory pseudotumour was established. The removal of the spleen was followed by remission of glomerulonephritis, but it was complicated by a subphrenic abscess and pneumonia. This association between an inflammatory pseudotumour of the spleen and MPGN has not been previously described. Abnormal immune response due to the inflammation leading to secondary glomerulonephritis might be the main pathogenic mechanism.
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PMID:Membranoproliferative glomerulonephritis and inflammatory pseudotumour of the spleen. 2356 42