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 48-year-old woman was referred to Tohoku University Hospital in November 1981 because of leukocytosis pointed out in a group examination. At that time white blood cell count was 26.8 x 10(3)/microliters with no blasts, platelet count 268.0 x 10(4)/microliters and hemoglobin 11.4 g/dl. Bone marrow aspirates showed marked increase of megakaryocytes (15,900/microliters). Bone marrow chromosome analysis revealed 46, XX, -18, +mar without Ph1 chromosome, and DNA analysis showed no bcr rearrangement. She was diagnosed as having essential thrombocythemia and was treated with busulfan. On November 1986, she developed remarkable leukocytosis with leukemic blasts. White blood cells reached 153 x 10(3)/microliters with 33% blasts. Her blasts were positive for peroxidase staining, but negative for platelet peroxidase on electron microscopic study and platelet specific glycoproteins. A diagnosis of acute myeloblastic leukemia (M2) was made. The patient received various combination chemotherapy, which was ineffective, and she died due to pneumonia on June, 1989. In Japan, there has been reported only 8 cases of essential thrombocythemia transformed to acute leukemia. The clinical pictures of these 9 cases were discussed.
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PMID:[Essential thrombocythemia transformed to acute myeloblastic leukemia]. 225 58

A fifty-six-year old man complained of arthralgia and swelling of both feet, morning stiffness in both hands and finger joints in March 1987, and was treated with non-steroidal anti-inflammatory agents at another hospital. He has been treated for chronic myelogenous leukemia (CML) since May 1990. He was admitted to our hospital in March 1991 because of worsening of his multiple arthralgias, and a diagnosis of rheumatoid arthritis (RA) (Stage I, Class 2) was made on the basis of gait disturbance, arthralgia persisting for more than 6 weeks, the presence of subcutaneous nodules and X-ray findings. CML was confirmed by peripheral blood and bone marrow findings and the presence of the Philadelphia chromosome and bcr gene rearrangement. High fever and dyspnea developed suddenly 3 days after administration of interferon in May 1991. In addition to pneumonia, a leucostasis was suspected and he was treated with high dose steroids and antibiotics. After improvement, the steroids were tapered and he was discharged from hospital in July 1991.
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PMID:[Case report: rheumatoid arthritis complicated by chronic myelogenous leukemia treated with interferon]. 755 41

A 57 year-old-female was incidentally found to have leukocytosis in September 1988. Physical examination revealed anemia and marked hepatosplenomegaly. Her WBC count was 33,400/microliters with 95% mature neutrophils showing toxic granules. Her neutrophil alkaline phosphatase score was 482, and serum VB12 14,600 pg/ml. Serum immunoglobulin concentrations were 582 mg/dl for IgG, 3,628 mg/dl for IgA and 48 mg/dl for IgM. IgA was determined as monoclonal origin of lambda type. Bone marrow aspiration revealed a hypercellular marrow with active granulocytopoiesis and increased plasma cells. Cytogenetic study revealed normal karyotype. The bcr rearrangement was negative for bone marrow cells. An electronmicroscopy demonstrated fibrillar inclusions in granulocytes. We diagnosed this case as a chronic neutrophilic leukemia (CNL) associated with multiple myeloma. She was treated with a course of low dose busulfan without beneficial response. She was admitted for development of huge subcutaneous hematoma of left waist in October 1990. Laboratory findings were: Hb 7.0 g/dl, WBC 55, 300/microliters, Platelets 3.3 x 10(4)/microliters, and IgA 6,607 mg/dl. She required frequent transfusions. She died of pneumonia in July 1991. The peculiar fibrillar inclusions with CNL has not been reported so far. The origin and significance of such structure remains uncertain.
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PMID:[Association of chronic neutrophilic leukemia and myeloma with fibrillar inclusions in granulocytes]. 771 83

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 65-year-old man visited our department for further leukocytosis examination. Hematological examinations disclosed elevation of the leukocyte count with left deviation. The neutrophilic alkaline phosphatase score was reduced. Bone marrow was hypercellular and consisted almost entirely of granulocytic cells in all stages of maturation. However, cytogenetic analysis revealed no Philadelphia chromosome, and genotypic analysis disclosed no bcr rearrangement. He was ultimately diagnosed as having unclassified chronic myeloproliferative disorder. He had been followed without chemotherapy, and he developed blastic crises (CD10+, CD13+, CD24+). Chemotherapy was effective, and then he was followed with carboquone. However, myeloid crisis (CD13+, CD33+) developed again. Standard chemotherapies had no effect, he developed pneumonia, and he was in poor general condition. Therefore, low-dose combination with cytarabine and etoposide was performed. The result was that the blasts disappeared, his general condition improved and infection was reduced. Major side effects were absent; however, the blasts proliferated again after the treatment was discontinued. In conclusion, this combination may be useful treatment for myeloid blastic crises even if the patient is in poor condition. But the modification of the administration schedule requires some consideration.
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PMID:[Low-dose combination cytarabine and etoposide for myeloid crisis transformed from unclassified chronic myeloproliferative disorder]. 868 21

A 78-year-old man was diagnosed as leukocytosis in February 1994. Physical examination revealed marked hepatosplenomegaly. A peripheral blood examination disclosed 95,090/microliter leukocytes without hiatus leukemicus, 6.5 g/dl Hb, and 15.0 x 10(4)/microliter platelets. The neutrophil alkaline phosphatase score was 27, and serum VB12 was above 1,600pg/ml. IgG was identified as monoclonal immunoglobulin of type lambda. Bone marrow specimens demonstrated marked granulocytic hyperplasia. Neither the Philadelphia chromosome (Ph1) nor BCR gene rearrangement was detected; hence, the diagnosis of Ph1 (-) chronic myeloid leukemia (CML) was made. The patient was treated with hydroxyurea and low-dose VP-16 with no improvement, and died of pneumonia and sepsis in June 1995. This case was considered to be consistent with atypical CML (aCML) according to the FAB classification because monocytosis was not observed. It seems likely and interesting that the coexistent monoclonal gammopathy and aCML might have arisen from common abnormal hematopoietic stem cells.
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PMID:[Atypical chronic myeloid leukemia presenting with trilineage dysplasia and IgG (lambda) type monoclonal gammopathy]. 1019 7

The authors report an unusual presentation of a Philadelphia chromosome-positive acute lymphoblastic leukemia with two unusual features: a bcr-abl fusion mRNA coding for p210 protein and a T-cell immunophenotype. The patient was a 16-year-old boy who presented with septic shock and pancytopenia, likely precipitated by an acute parvovirus B19 infection. Management consisted of supportive therapy, followed by chemotherapy for T-cell acute lymphoblastic leukemia and stem cell transplantation. He died 8 months after transplant due to idiopathic pneumonia syndrome, but without evidence of relapsed disease.
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PMID:bcr-abl-positive T-cell acute lymphoblastic leukemia associated with parvovirus B19 infection. 1646 83

Imatinib mesylate is a targeted therapy that acts by inhibiting tyrosine kinase of the bcr-abl fusion oncoprotein, which is specific to chronic myeloid leukemia (CML), and the c-transmembrane receptor, which is specific to gastrointestinal stromal tumors. Interstitial pneumonitis is a rare adverse event of imatinib therapy. It is clinically difficult to distinguish from infectious pneumonia, which can frequently occur due to the underlying disease. The standard treatment for imatinib-induced pneumonitis is to discontinue the medication and optionally administer corticosteroids. However, there are a few cases of successful retrial with imatinib. We describe a case of successful rechallenge of imatinib in a patient with imatinib-induced interstitial pneumonitis and CML without a recurrence of the underlying disease after 3 months of follow-up.
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PMID:Successful rechallenge with imatinib in a patient with chronic myeloid leukemia who previously experienced imatinib mesylate induced pneumonitis. 2441 57