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)

The functional status of immune cells within human transplanted lungs was analyzed during cytomegalovirus (CMV) pneumonia complicating lung and heart-lung transplantations. The expression of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) genes is a marker for the activation of macrophages as is that of serine esterase B (SE-B) gene for cytotoxic cells. The levels of expression of these genes by bronchoalveolar lavage (BAL) cells were determined by in situ hybridization. Eight cases of CMV pneumonia were included in this study. BAL cells from either rejection episodes (eight cases) or control transplanted patients experiencing neither infection nor allograft rejection (eight cases) were analyzed in parallel. In the control patients, virtually no cells expressed the IL-1 beta, the IL-6, or the SE-B genes. In contrast, these three genes were all expressed in samples from patients with CMV pneumonia. IL-1 beta gene-expressing cells were abundant in all infected patients (mean +/- SEM: 898 +/- 449 positive cells per 10(4) cells, p less than 0.001, compared with those in control patients). IL-6 gene-expressing cells were less numerous (92 +/- 74 positive cells per 10(4) cells) and present in five of the eight cases of CMV pneumonia. Activated cytotoxic cells were detected in seven of the eight cases of CMV pneumonia (36.5 +/- 19 SE-B gene-expressing cells per 10(4) cells, p less than 0.001). During allograft rejections (eight cases) IL-1 beta gene-expressing cells were present in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of macrophages and cytotoxic cells during cytomegalovirus pneumonia complicating lung transplantations. 131 30

We report a case of infantile acute leukemia with t(16; 21) (p11; q22). The patient was a phenotypically normal one-year-old girl without lymphadenopathy or hepatosplenomegaly. Her peripheral blood at diagnosis showed anemia, thrombocytopenia, and many circulating blasts. Bone marrow blasts were monocytoid with fine reticular nuclear chromatin, abundant grayish-blue cytoplasm with occasional pseudopods or cytoplasmic projections and active hemophagocytosis. Serum levels of lysozyme and ferritin were normal. These blasts were not stained with butyrate esterase and immunologic study showed KOR-P77+ (anti-megakaryocyte monoclonal antibody), MY9+, Ia-. Electron microscopic examination failed to show platelet peroxidase activity. Remission was not induced by mini-COAP or VP-16 and the patient died of measles pneumonitis. The patient's blasts took typical appearance of megakaryoblasts later in the course, although some of them retained the ability of hemophagocytosis observed in the original blasts. This case is considered to be quite atypical since leukemic cells with active hemophagocytosis, megakaryoblastic appearance and t(16; 21) (p11; q22) have not been reported in the literature.
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PMID:[Acute leukemia with active hemophagocytosis, positive immunologic markers for the megakaryocyte-platelet lineage, and translocation (16; 21) (p11; q22]. 231 8

A 34 year-old female was admitted because of anemia and leukopenia. Her bone marrow contained abundant blastic cells, which were histochemically positive for peroxidase and alpha-naphthyl butyrate esterase, but negative for ASD chloroacetate esterase. She was diagnosed as acute monocytic leukemia (FAB, M5a). Complete remission was achieved after the administration of BHAC, daunorubicin, 6MP and prednisolone, and she was discharged after consolidation therapies. But shortly later, she noticed hoarseness and erythematous nodules on her breast and abdomen. Though the examinations of peripheral blood and bone marrow did not show any abnormality, hoarseness rapidly worsened and she complained of dyspnea. X-ray and CT scan demonstrated narrowing of the trachea under the cricoid cartilage, and trans-tracheal biopsy revealed leukemic involvement. In addition, erythematous skin lesion showed the infiltration of leukemic cells by biopsy. Although radiation and chemotherapy was initiated, she died of pneumonia. We tried to discuss the laryngo-tracheal and skin involvement of acute monocytic leukemia as early symptoms of relapse.
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PMID:[Relapse of acute monocytic leukemia present with skin and tracheal involvement]. 262 95

We report 2 cases of agranular CD2- CD4+ CD56+ non-Hodgkin lymphoma in which skin seemed to be the primary site. A 21-year-old woman's initial symptom was a skin nodule on the right cheek. She also had tumors in the nasopharynx, and the bone marrow subsequently became involved. No lymphadenopathy was present. She experienced complete remission after dose-intensified therapy with cyclophosphamide, hydroxydaunomycin, vincristine [Oncovin], and prednisone (CHOP), but the disease relapsed in the central nervous system 6 months later. An 81-year-old man experienced an 11-month history of skin nodules in the left forearm. On admission, he had a bone marrow infiltration of lymphoma cells. He died of pneumonia during chemotherapy. The malignant cells of the 2 patients had similar morphologic features, with a monocytoid nucleus and no cytoplasmic granules. The cells in both cases showed a unique phenotype: CD2-, CD3-, CD4+, CD8-, CD13-, CD14-, CD34-, CD16-, CD56+, CD57-, HLA-DR-positive. Staining for peroxidase and alpha-naphthyl butyrate esterase was negative. The T-cell receptor beta, gamma, delta, IgH, kappa, lambda genes were of germ line configurations. The DNA of Epstein-Barr virus was not detected from the bone marrow cells by polymerase chain reaction. Only 3 other cases with similar phenotypes have been reported; all had skin lesions. Although the origin of these cells remains unknown, we propose that this is a distinct clinicopathologic entity.
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PMID:A cutaneous agranular CD2- CD4+ CD56+ "lymphoma": report of two cases and review of the literature. 1043 11

Phenotypic switch in acute leukemia is a rare phenomenon. We report on a female infant with minimally differentiated acute leukemia (M 0) which underwent a lineage switch on relapse. In March 1997, a 1-year-8-month old girl was admitted to our hospital with a high-grade fever and generalized purpura. Bone marrow showed 84% blasts. The blasts were negative for peroxidase, periodic acid-Schiff and alpha-naphthyl butyrate esterase. Immunophenotypic analyses of the blast cells were positive for CD 13, CD 33 antigens, as well as CD 34. Lymphoid markers all were negative. Though some blasts morphologically demonstrated cytoplasmic blebs, CD 41 was negative and ultrastructural platelet peroxidase was absent. Based on these hematological features, the patient was diagnosed as having AML-M 0. She was treated according to the Children's Cancer and Leukemia Study Group schedule and a complete remission was achieved 1.5 months after starting induction therapy. However, she relapsed in spite of continued chemotherapy in July 1997, when the cytomorphological pattern changed and the patient was diagnosed both morphologically and immunologically as having M 7. Electron microscopy revealed platelet peroxidase (+) and CD 41 (+). Cytogenetic studies on relapse demonstrated inv(3) (q 21 p 25). We attempted aggressive reinduction therapy, but without effect. The patient simultaneously developed severe pneumonia and died in February, 1998. A lineage switch on relapse and resistance to chemotherapy may be associated with the occurrence of genetic aberration.
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PMID:[Lineage switch on recurrence from minimally differentiated acute leukemia (M0) to acute megakaryocytic leukemia (M7)]. 1222 23

The effects of loading doses and probenecid coadministration on oseltamivir pharmacokinetics at four increasing dose levels in groups of eight healthy adult Thai volunteers (125 individual series) were evaluated. Doses of up to 675 mg were well-tolerated. The pharmacokinetics were dose linear. Oseltamivir phosphate (OS) was rapidly and completely absorbed and converted (median conversion level, 93%) to the active carboxylate metabolite. Median elimination half-lives (and 95% confidence intervals [CI]) were 1.0 h (0.9 to 1.1 h) for OS and 5.1 h (4.7 to 5.7 h) for oseltamivir carboxylate (OC). One subject repeatedly showed markedly reduced OS-to-OC conversion, indicating constitutionally impaired carboxylesterase activity. The coadministration of probenecid resulted in a mean contraction in the apparent volume of distribution of OC of 40% (95% CI, 37 to 44%) and a reduction in the renal elimination of OC of 61% (95% CI, 58 to 62%), thereby increasing the median area under the concentration-time curve (AUC) for OC by 154% (range, 71 to 278%). The AUC increase for OC in saliva was approximately three times less than the AUC increase for OC in plasma. A loading dose 1.25 times the maintenance dose should be given for severe influenza pneumonia. Probenecid coadministration may allow considerable dose saving for oseltamivir, but more information on OC penetration into respiratory secretions is needed to devise appropriate dose regimens.
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PMID:Pharmacokinetics of high-dose oseltamivir in healthy volunteers. 1910 28