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)

A 40-year-old man was admitted with high fever and cough. Pneumonic shadows of the left middle and lower lung fields increased rapidly, and his blood gases worsened. Initial treatment with cefmenoxime, piperacillin, and minocycline was ineffective. Administration of rifampicin was started for suspected legionella pneumonia, but it did not control the spread of the pneumonia shadows. After addition of an antifungal agent and trimethoprim-sulfamethoxazole, his symptoms gradually improved. Isolation of Legionella pneumophila from sputum specimens collected on the 4th day of admission confirmed the diagnosis on day 10. The patient was then given oral rifampicin plus cefmenoxime to prevent mixed infection, and showed a satisfactory improvement. Legionella pneumonia developed secondary to compromise of the patient's immunity due to steroid therapy for MDS. After recovering from Legionella pneumonia, the patient subsequently developed tuberculous pleurisy and Pneumocystis carinii pneumonia, which were cured by antituberculous therapy and trimethoprim-sulfamethoxazole. However, acute hepatitis followed by hepatic failure developed, and he died on day 121 after admission.
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PMID:[A case of Legionella pneumonia with myelodysplastic syndrome]. 128 32

A 17 year old male was admitted because of pancytopenia. Bone marrow aspiration revealed myelodysplasia, no increase of blast cells and excessive expansion of megakaryocytic lineage. Although mild increase of bone marrow reticulin fiber was observed, no hepatosplenomegaly was recognized. Therefore he was diagnosed as refractory anemia (RA) or MDS with myelofibrosis and treated with low dose Ara-C regimen. Remission was achieved in June 1987, but the relapse occurred in Oct. 1987. His bone marrow at the relapse showed more remarkable dysplastic change than before. Sequential bone marrow examinations thereafter, revealed an increase of megakaryocytic lineage, especially immature dysplastic megakaryocytes, leading to the appearance of the abnormal megakaryoblasts (detected with anti GP IIb/IIIa antibody) as well as uncharacterized blast cells in his terminal stage. Transformation from MDS to megakaryocytic leukemia was strongly suggested. He died of severe pneumonia in March 1989. The invasion of abnormal immature megakaryocytic cells including megakaryoblasts was observed in liver, spleen and lymph nodes at autopsy. There are several reports on cases having a common hematological features such as 1) pancytopenia in peripheral blood, 2) myelodysplasia, 3) excessive growth of megakaryocytic lineage, 4) myelofibrosis without hepatosplenomegaly, although other clinical features were different. We propose all these cases should be reviewed at the point of MDS mainly involved in megakaryocytic lineage.
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PMID:[Myelodysplasia predominantly involving in megakaryocytic lineage successfully treated with low-dose Ara-C]. 194 32

Seven cases of miliary tuberculosis in patients with hematologic disease were analyzed clinicopathologically. Mean age of the patients was 65 years, and the hematologic diseases were CML, AML, ALL, MDS and malignant lymphoma. Diabetes mellitus was present as a complication in three patients. Miliary tuberculosis was found in 5 cases during the first admission to our hospital owing to hematologic problems. In 4 of 6 cases, fever had started more than two months before admission, consequently, the tuberculosis probably began about that time. After admission, chemotherapy was administered in 5 cases, and steroid in 6 cases for hematologic disease. The mean total quantity of steroid administered was 2,134 mg of prednisolone and average treatment duration was 69 days. The chest roentgenographic shadow was so atypical that miliary tuberculosis was suspected in only one case. The initial chest roentgenogram showed hilar and mediastinal lymph node swelling as well as the shadow of pulmonary tuberculosis in two cases. It was thought that the hilar and mediastinal lymph node swelling could be explained by primary complex, although the patients were of advanced age, or by "secondary complex" reported by Terplan, K in 1940. The diagnosis of tuberculosis was made in two patients before their death by smear of aspirated fluid of cervical lymph node and by bone marrow cell block in one patients, and by pathological examination of mediastinal lymph node biopsy in the other patients. Tubercles were found from bone marrow cell block in 2 out of 5 patients and from bone marrow biopsy in 1 out of 3 patients, but the positive results were reported in 2 patients following death. Smears of sputum, gastric juice, urine, spinal fluid and pleural effusion were negative in all cases. One patient diagnosed as miliary tuberculosis also had pneumocystis carinii pneumonia. This case was treated with antituberculosis drugs for 20 days without improvement. Another patient diagnosed as miliary tuberculosis improved under treatment with antituberculosis drugs, but died of cytomegalovirus pneumonia. Autopsy in 5 cases revealed non-reactive miliary tuberculosis, and pulmonary hemorrhage probably due to DIC was present as a complication in two cases. In these cases, severe immunosuppression, which is a major precipitating factor of miliary tuberculosis, is thought to be induced by hematologic disease itself, chemotherapy, steroid or other underlying disease such as diabetes mellitus. Miliary tuberculosis in such compromised host is cryptic and progresses rapidly. Consequently, early diagnosis is very important. Retrospectively, the unexplained pyrexia was most important to suspect tuberculosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinicopathological study of miliary tuberculosis in patients with hematologic disease]. 237 32

We report a patient with refractory anemia with excess blasts who showed a lineage-unrestricted hematologic response to granulocyte colony-stimulating factor (G-CSF). After 17 months of a stable disease state, the patient developed pneumonia, progression of cytopenia, and reduced cellularity and blast mass in the bone marrow. He was given G-CSF to overcome the pneumonia. Not only the neutrophil count, but also the platelet count increased soon after initiation of the G-CSF therapy; both counts became normal on the fifth day of the G-CSF therapy. Additionally, the anemia improved gradually. The neutrophil and platelet counts were maintained in the normal range for 3 months after cessation of the G-CSF. In vitro studies showed that G-CSF alone stimulated megakaryocyte colony formation from bone marrow mononuclear cells (BMMNC), and accessory cells in the BMMNC were necessary for expression of this G-CSF-induced in vitro megakaryocytopoiesis. These results suggest that, in coordination with accessory cells, G-CSF stimulated megakaryocytopoiesis in the patient. This case provides valuable information for understanding the mechanisms of a lineage-unrestricted hematologic response to G-CSF, which is very rarely observed in MDS.
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PMID:Lineage-unrestricted hematologic response to granulocyte colony-stimulating factor in a patient with refractory anemia with excess blasts. 753 78

A 78 year old female was found to have pancytopenia in February 1991. Bone marrow was normocellular with 11.7% blasts and showed dysmegakaryopoietic changes. A diagnosis of MDS (RAEB) was made and she was treated with transfusions and ubenimex. Leukemic transformation was noted in July. On Admission in October 1991, her laboratory examinations revealed the following: WBC 38,900/microliters with 93% blast, Hb 8.0 g/dl, Plt 2.1 x 10(4)/microliters, a hypercellular bone marrow with 74% blasts which were negative for myeloperoxidase (MPO) by light microscopy, but were positive by electron microscopy. Surface marker for CD13 was positive. These findings corresponded to M0 of the FAB subtype. Chromosome analysis revealed Ph1 chromosome with 46XX, t (9;22) (q34;q11) in 3 of 3 cells examined, Southern analysis showed the rearrangement of the break point cluster region (bcr). Reverse transcriptase polymerase chain reaction technique demonstrated the presence of major bcr/abl mRNA. She was treated with transfusions and methyl-prednisolone. Her blast counts declined and Ph1 chromosome was only positive in 1 of 12 metaphases examined. She died of pneumonia in December 1991. Eleven cases with MDS showing Ph1 chromosome have previously been reported. The observations indicate that Ph1 chromosome positive acute leukemias were heterogenous in nature.
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PMID:[RAEB transformed into AML (M0) showing Ph1 chromosome and rearrangement of major cluster region]. 825 8

We analyzed the 67 of 278 patients with newly-diagnosed AML or 'high-risk' MDS, treated in 1994 and 1995, who developed pneumonia during course 1 of their induction therapy. Pneumonia responded to treatment in 66%, but outcome depended on when pneumonia was diagnosed. Patients with pneumonia diagnosed during week 1 or 2 (group 2 patients) had the lowest response rate (43%). Patients who developed pneumonia in the 3rd week after treatment initiation had the best outcome with all 16 patients recovering. Patients presenting with pneumonia had an intermediate response rate (75%). The different patient groups were comparable with regard to age, underlying disease, prophylactic therapy, and G-CSF application. Although a lower CR rate was not entirely responsible for the lower response rate in group 2, failure to achieve CR predicted unsuccessful treatment of pneumonia in all groups. Fungal pathogens appeared more common in group 2 patients. However, in these patients, administration of amphotericin B was associated with a significantly higher failure rate (15/21 failures vs 2/9 who received no amphotericin B). We conclude that patients who develop pneumonia during week 1 or 2 are a high-risk group, and that use of amphotericin B indicates a particularly poor prognosis, although we present data suggesting that earlier use of amphotericin might be beneficial. Furthermore, since achievement of CR was an important prognostic factor in all groups, WBC transfusions particularly from donors given G-CSF should be considered as a therapeutic option. Finally, since time to failure of induction therapy and time to CR were similar in high-risk patients, new chemotherapy regimens could potentially improve both the CR rate and the outcome of pneumonia.
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PMID:Pneumonia during remission induction chemotherapy in patients with AML or MDS. 894 24

A 37-year-old female highly alloimmunized by multiple transfusions received a sex matched HLA-identical unrelated bone marrow transplant for hypoplastic MDS-RA with moderate myelofibrosis. Conditioning consisted of total body irradiation, cyclophosphamide and ATG, GVHD prophylaxis consisted of CsA, MTX and prednisolone. The CD34+ stem cell content of the first graft was relatively low due to an inadequate harvest. The patient appeared not to have engrafted by day 23 post-BMT. She therefore received a second sex mismatched HLA-identical unrelated bone marrow graft on day 25 after two days of 3.5 mg/kg methylprednisolone from a different donor. Over the ensuing days, the first marrow showed slow engraftment followed by engraftment of the second graft. The first graft was then rejected, as monitored by peripheral blood studies of chimerism. No signs of acute GVHD were observed. Despite successful trilineage engraftment and complete second donor chimerism, the patient died from disseminated toxoplasmosis encephalitis and pneumonia on day +104.
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PMID:Second unrelated bone marrow transplantation without additional conditioning therapy after engraftment failure. 948 60

We diagnosed a probable fludarabine-induced secondary MDS approximately 18 months after treatment of a low grade non-Hodgkin's lymphoma. After diagnosis of a B-cell lymphoma composed of relatively small cells, fludarabine was administered between May and October, 1997, to a 64-year-old female patient. In December 1998, a mild bicytopenia was present with a leukocyte count of 3800/microl and platelets of 142000/microl. The white cell differential count was normal. The hemoglobin level was normal, but MCV was elevated. Bone marrow cytology revealed normal cellularity with dyserythropoiesis and dysmegakaryocytopoiesis. PAS staining showed scattered positivity in early erythroid cells. In 12 of 20 mitoses, the karyotype showed complex rearrangements, described as 46,XX,t(4;11)(q23?24;q13),del(5q),del(7)(q22),+mar[8]/45,-3. A diagnosis of treatment-related MDS was made. While there was no evidence of bone marrow infiltration by the lymphoma, CT scans demonstrated paraaortic lymph nodes up to 10 cm in diameter. After one course of CHOP chemotherapy, prolonged bone marrow aplasia and septic complications occurred. Chemotherapy was abandoned and Rituximab was administered. In July and November, 1999, bilateral pneumonia and urinary tract infection, respectively, were treated with antibiotics. NHL was in complete remission, but peripheral blood counts deteriorated markedly, and transfusions of packed red cells had to be started in November, 1999. The suspicion of leukemic transformation could not be confirmed because the patient declined further bone marrow biopsies. In December, 1999, the patient died from pneumonia.
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PMID:Secondary myelodysplastic syndrome after fludarabine therapy of a low-grade non-Hodgkin's lymphoma. 1113 66

We report a case of therapy-related myelodysplastic syndrome (t-MDS) in adult T-cell lymphoma. A 69-year-old man suffered from cutaneous adult T-cell lymphoma, which was treated with radiation to the skin and combination chemotherapy of CHOP-V-MMV and VEPA-B. After 14 months of these therapies, anemia and thrombocytopenia appeared, and bone marrow aspiration smears showed immature myeloblasts, dysplastic erythroblasts, and micromegakaryocytes. Therapy-related MDS of refractory anemia with an excess of blasts was diagnosed. Cytogenetic study of the bone marrow cells showed 5q- and additional abnormalities. Rearrangement of the MLL gene was observed in the bone marrow cells. Mutations of N-ras codons at 12,13, and 61, p53 tumor suppressor gene, and monoclonal integration of human T-lymphotrophic virus -1 provirus DNA were not observed in the bone marrow cells. The patient died of pneumonia 21 months after diagnosis of cutaneous adult T-cell lymphoma.
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PMID:Therapy-related myelodysplastic syndrome in a case of cutaneous adult T-cell lymphoma. 1184 94

A 62-year-old woman was diagnosed as having malignant lymphoma, diffuse large B-cell type. She underwent chemotherapy with the standard dose of CHOP and MINE regimens, resulting in complete remission. Four months later, the myelodysplastic syndrome of RA (refractory anemia) with pancytopenia developed and rapidly progressed to acute myelogenous leukemia (AML-M6) in 4 months. Cytogenetic analysis for the bone marrow specimens of both periods of MDS and AML-M6 revealed complex karyotypic abnormalities involving chromosome 5, 7, 11q23 and 20q11.2. Neither rearrangement of the MLL gene by Southern blot analysis nor tandem duplication of MLL gene by RT-PCR technique was detected. The patient was died from progression of leukemia and pneumonia. The autopsy showed no residual disease of lymphoma-related disease.
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PMID:[Therapy-related acute myelogenous leukemia (AML-M6) with add(11) (q23) and del(20) (q11.2) developing via myelodysplastic syndrome after chemotherapy for malignant lymphoma]. 1272 43


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