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 oxidative response of activated phagocytes is a primary host defense mechanism in pneumonia, but is in addition capable of causing tissue damage. We evaluated amount and significance of the local oxidant production in immunocompetent and immunocompromised pneumonia patients; the relative contribution of neutrophils and alveolar macrophages to the total oxidant load was differentiated using chemiluminescence (CL) with different amplifiers. Luminol-enhanced CL correlated to neutrophil percentage and myeloperoxidase levels in the bronchoalveolar lavage and was markedly increased in both pneumonia groups. Lucigenin-enhanced CL was produced by both phagocyte types and not significantly increased. In both pneumonia groups elevated levels of serum proteins indicated severe alveolocapillary leakage. In conclusion the oxidative response in acute pneumonia was mainly due to neutrophil recruitment and activation; this defense mechanism was preserved even in severely immunocompromised patients.
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PMID:Oxidative metabolism of pulmonary phagocytes in acute pneumonia. 804 17

In order to clarify the mode of inactivation of alpha1-proteinase inhibitor (alpha 1-PI) in pneumonia, 21 immunocompetent patients and 19 immunocompromised patients with acute pneumonia (Groups I and II) were studied. Nine patients successfully treated for pneumonia and 10 healthy volunteers served as controls (Groups III and IV, respectively). The concentrations of alpha 1-PI, elastase and myeloperoxidase (MPO) in bronchoalveolar lavage fluid (BALF) were determined using a luminometric assay. Elastase inhibition capacity was determined using a colorimetric assay. Thus, the functional activity of alpha 1-PI was calculated. Both elastase and MPO were significantly higher in group I, when compared with the other groups. The mean concentration of alpha 1-PI was significantly higher in patients with acute pneumonia (Group I 13 mg.l-1, Group II 4.22 mg.l-1) than in Groups III and IV (2.65 and 0.33 mg.l-1, respectively), whereas, the proportion of active alpha 1-PI was significantly lower in Group I than in the other groups. Only a small proportion was present as a complex with elastase (ca. 5.9%) or in oxidised form (ca. 4.8%), 85% of alpha 1-PI was irreversibly proteolyzed. This resulted in free elastase activity in 7 of the 40 patients (18%) with acute pneumonia. We conclude that functional activity of alpha 1-PI is markedly impaired due to irreversible proteolysis in acute pneumonia, despite high immunological concentrations.
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PMID:Characterization of protein-antiproteinase imbalance in bronchoalveolar lavage from patients with pneumonia. 814 11

For the differential diagnosis of pulmonary infiltrates after bone marrow transplantation, cytomegalovirus (CMV) antigenemia was evaluated in 9 episodes of pneumonia which developed in 7 allogeneic marrow transplant patients between 9 and 495 days after transplant. The diagnosis of lung infiltration was made based on clinical findings including histological, cytological or microbiological examinations using bronchoalveolar lavage fluid specimens, sputum or lung tissue. The CMV antigen-positive leukocytes were detected with a direct immunoperoxidase technique using a peroxidase-labeled monoclonal antibody (HRP-C7) against CMV immediate early antigen. The episodes included 2 CMV pneumonias, 1 pneumocystis carinii pneumonia, 1 adenovirus pneumonia, 1 bacterial pneumonia, 1 bacterial and fungal pneumonia, 2 idiopathic pneumonias and 1 capillary leak syndrome associated with hyper acute GVHD. The CMV antigenemia became positive only in two patients with CMV pneumonia and the number of CMV antigen-positive leukocytes exceeded 10 per 50000 WBCs. The CMV antigenemia test required only 24 hours to obtain results. These observations suggest that the detection of CMV antigenemia is of great value in the differential diagnosis of pulmonary infiltrates in marrow transplant patients.
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PMID:[Cytomegalovirus antigenemia in the differential diagnosis of pulmonary infiltrates after allogeneic bone marrow transplantation]. 825 5

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

Idiopathic pulmonary fibrosis (IPF) is characterized by a chronic inflammatory process in the lower respiratory tract of unknown etiology and poor prognosis. There is evidence that cytotoxic mediators released by neutrophils and eosinophils, such as myeloperoxidase (MPO) and eosinophil cationic protein (ECP) play a central role in the pathogenesis of this disease. The aim of this study was to assess disease activity in patients with IPF by measuring MPO and ECP concentrations in bronchoalveolar lavage (BAL). 14 patients with IPF had significantly higher concentrations of BAL-MPO and ECP (median = 117.2 micrograms/l, range: 4-217 micrograms/l and median = 16 micrograms/l, range: 4-34 micrograms/l, respectively) than patients with sarcoidosis (n = 9) (median = 6.5 micrograms/l, range: 4-12 micrograms/l and median = 7.1 micrograms/l, range: 2-13 micrograms/l, respectively) or pneumonia (n = 13) (median = 10.8 micrograms/l, range: 5-14 micrograms/l and median = 7.6 micrograms/l, range: 3-10 micrograms/l, respectively) (p < 0.01). Follow-up of MPO and ECP concentrations in BAL was performed in 8 patients with IPF before and after 4 weeks high-dose and 12 months low-dose corticosteroid therapy. Changes in MPO and ECP levels paralleled the clinical course and successful treatment resulted in a significant decrease of both MPO and ECP concentrations (p < 0.05), while clinical deterioration or treatment failure was associated with an increase of BAL-MPO and ECP levels. Increased MPO and ECP concentrations in BAL seem to reflect ongoing disease activity and may be useful prognostic markers in the management of patients with IPF.
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PMID:[Diagnostic value of secretory products of eosinophils and neutrophils in bronchoalveolar lavage in patients with idiopathic lung fibrosis]. 839 88

We report a novel strategy, called end-product (EP) amplification, capable of enhancing the sensitivity of immunohistochemical procedures by about an order of magnitude or more. The strategy employs an antibody (anti-EP) to the product generated by the action of horseradish peroxidase on 3,3'-diaminobenzidine (DAB), and can be extended to the products of other enzymes as well, e.g., alkaline phosphatase. Amplification is the consequence of the ability of anti-EP to detect the multiplicity of product moelcules resulting from the turnover of substrate by a single enzyme molecule. The subsequent detection of anti-EP was by biotinylated goat anti-rabbit antibody, followed by avidin-peroxidase and DAB or by avidin-alkaline phosphatase and Vector Red. Further amplification can be accomplished by repeated cycles of the protocol. Anti-EP was produced by immunization with a bovine serum albumin (BSA) conjugate of a soluble polymer of DAB, prepared by a carefully controlled reaction of DAB with horseradish peroxidase and hydrogen peroxide. Coupling to BSA (and to RSA) was accomplished with glutaraldehyde. The titer of anti-EP was established by ELISA. Formalin-fixed, paraffin-embedded sections of five cases of Hodgkin's disease and five tonsils with follicular hyperplasia were immunolabeled for the following lymphoid markers: CD3, CD20, CD30, CD45RA, and CD68. EP amplification with anti-EP was also applied to cases of CMV pneumonia and cerebral toxoplasmosis to determine whether this procedure could improve detection of the infectious agents. Immunolabeling of the primary antibody was performed by the avidin-biotin-peroxidase technique with DAB as the reaction substrate. The specificity of EP amplification was tested by demonstrating binding of anti-EP with Vector Red with the generation of a fluorescence end-point. There was complete congruence in the distribution of the DAB signal and the red immunofluorescence representing EP amplification. The intensity of the DAB signal was increased as much as 16-fold by EP amplification, making possible a reduction in the amount of the primary antibody by as much as 85-90%. Sensitivity also increased with respect to weakly expressed antigens and low concentrations of infectious agents.
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PMID:A strategy for immunohistochemical signal enhancement by end-product amplification. 875 54

A 67-year-old female was admitted with fatigue. Peripheral blood examination showed severe pancytopenia. Bone marrow biopsy revealed hypoplastic marrow. She was diagnosed as having aplastic anemia. Steroid pulse therapy was not effective. After treatment with erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF), blasts which were positive for CD13, CD33, CD34 and HLA-DR and negative for myeloperoxidase appeared in the peripheral blood. At this time, bone marrow biopsy revealed myelofibrosis with increased blasts. Chromosome analysis showed 46XX, add (1) (p36), add (1) (q44), -2, -5, del (7) (q11), -12, +3mar. She died of pneumonia despite chemotherapy with etoposide. Administration of EPO and G-CSF may have led to the rapid development of leukemia and myelofibrosis.
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PMID:[Transformation of aplastic anemia to acute myeloid leukemia with myelofibrosis following treatment with granulocyte colony-stimulating factor and erythropoietin]. 877 84

We describe two cases (61-year-old female and 71-year-old male) with MPO-ANCA (myeloperoxidase-antineutrophil cytoplasmic antibody) positive who developed severe interstitial pneumonitis. They presented at our hospital with dyspnea and dry cough. The hypoxia and abnormal shadow on chest X-ray led to a diagnosis of interstitial pneumonitis. Serologic studies revealed the high titers of MPO-ANCA in two cases. They were treated with methylprednisolone, immunosuppressant agents and plasma exchange. The pneumonitis and the titers of MPO-ANCA improved on these therapies, The former was introduced continuous hemodialysis therapy and the later continued nephrotic syndrome. These renal damages did not recover, regardless of the reduction of the titers of MPO-ANCA. It is concluded that methylprednisolone pulse therapy, immunosuppressant agents and plasma exchange therapy are useful to interstitial pneumonitis in patient with positive of MPO-ANCA. The measurement of MPO-ANCA is useful to interstitial pneumonitis in patient with positive of MPO-ANCA. The measurement of MPO-ANCA is useful maker of interstitial pneumonitis for unknown causes.
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PMID:[MPO-ANCA positive two cases associated with interstitial pneumonitis]. 877 95

Lung tissues from calves naturally and experimentally infected with Mycoplasma bovis were subjected to histopathological and immunohistochemical examination. The latter was carried out with a monoclonal antibody raised against M. bovis, and an avidin-biotin-peroxidase complex (ABC) detection substrate system. Pulmonary lesions in naturally infected calves included exudative bronchopneumonia and extensive foci of coagulative necrosis surrounded by inflammatory cells. Experimentally infected lungs showed suppurative bronchiolitis and varying degrees of peribronchiolar mononuclear cell cuffing. M. bovis antigen in field cases was mainly detected at the periphery of the areas of coagulative necrosis, in necrotic exudates, and in close association with infiltrating macrophages and neutrophils. In lung tissue from calves with induced M. bovis pneumonia, antigen was located in epithelial cells, within inflammatory cells in airway lumina, and in alveolar walls. Other microbiological observations suggested that the ability of M. bovis to invade and cause lung parenchymal damage could be influenced by the participation of other pathogens.
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PMID:Pathological and immunohistochemical studies of natural and experimental Mycoplasma bovis pneumonia in calves. 891 Jul 43

An autopsy case of measles giant cell pneumonia with intranuclear inclusion bodies is reported. This case of giant cell pneumonia was studied by light microscopy and immunohistochemistry using monoclonal and polyclonal antibody to measles and by electron microscopy (EM). Light microscopic examination showed multinucleated epithelial giant cells with intranuclear and intracytoplasmic inclusions. The giant cells contained prominent, sharply marginated, eosinophilic intranuclear inclusions typical of classic measles pneumonia. Presence of measles antigen was confirmed using both monoclonal and polyclonal antibodies by peroxidase antiperoxidase method. Monoclonal antibody stained positively for intracytoplasmic and intranuclear inclusions. Electron microscopic examination of lung tissue showed intranuclear inclusions of filamentous or worm like nucleocapsid materials in multinucleated epithelial giant cells. The results suggest that this is a case of measles giant cell pneumonia and the intranuclear inclusion bodies are measles viral particles.
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PMID:Giant cell pneumonia: light microscopy, immunohistochemical, and ultrastructural study of an autopsy case. 894 Jul 66


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