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)

161 children followed up postoperatively following splenectomy, 29% had spherocytosis, 14% Hodgkin's disease, 12% traumatic rupture of the spleen, 11% portal hypertension and 7% idiopathic thrombocytopenia. Postoperatively a slight wound infection occurred in 5% of the children, while complications were seen in 2% which could be interpreted as directly caused by the operation; in 23 patients, however, (i.e. 15%), severely infections occurred such as pneumonia, meningitis and sepsis. The lethality rate of the infected children was 31.8%. Postoperatively we determined the leucocyte count, thrombocytes and erythrocyte count, the immunoglobulins IgG, IgA, IgM and IgE, the serum concentrations of the complement components C3, C4 and the serum proteins alpha 1-antitrypsin and transferrin. The data obtained were compared with the corresponding data reported in the literature.
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PMID:[Complications of splenectomy in childhood (author's transl)]. 704 92

Inhaled trimellitic anhydride (TMA) reacts with airway proteins to produce trimellityl (TM) proteins. THe TM-proteins result in both systemic and local immune responses, of which various proteins present in the airway can be used for markers. Thus TM-human serum albumin (HSA), TM-IgG, and TM-IgA can be used as hapten-protein complexes for immunologic studies in sera of humans exposed to TMA by inhalation. Various immunologic assays have been established to measure antibodies against TM-proteins and have various purposes. With TM-HSA as a model antigen, total serum antibody may be measured by the ammonium sulfate technique of coprecipitation of TM-125I HSA. By solid-phase radioimmunoassays, IgE, IgG, IgA, and IgM antibodies can be measured. Lymphocyte reactivity can be measured by 3H thymidine uptake of TM-protein-stimulated lymphocytes. Biological effects of IgE antibody can be measured by allergy skin tests and leukocyte histamine release with TM-proteins such as TM-HSA. The reaction of TMA with proteins results in alteration of those proteins that include changes in charge and physical conformation, the latter resulting in an apparent change in molecular size. These changes may relate to the observations that human antibody is not merely directed against the hapten in the hapten-human protein complex but also against new antigenic determinants formed by the TM-protein complex. Correlations have been made with certain human immunologic responses and lung disease after TMA inhalation, as follows: IgE antibody against TM-proteins correlates with TMA-induced rhinitis, conjunctivitis, and asthma; high levels of total antibody, IgG, and IgA antibody appear to correlate with the late respiratory systemic syndrome, probably a variant of hypersensitivity pneumonitis; workers exposed to TMA fumes (rather than TMA powder) have the highest levels of antibody, and this may correlate with occurrence of the hemorrhagic pneumonitis seen in this group of workers; patients with no symptoms or mild irritative symptoms have the lowest or no antibody levels. The immunopathogenetic relationships may be better understood with the further development of animal models to TMA lung disease now available.
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PMID:Immunology and immunopathology of trimellitic anhydride pulmonary reactions. 708

The pulmonary histopathology of four cases of allergic granulomatosis (Churg-Strauss syndrome) was reviewed. Renal tissue was also studied in one case. The patients were young and most presented with asthmatic symptomatology. They showed marked peripheral blood eosinophilia, and had fluffy nodular pulmonary infiltrates by chest x-ray. Serum IgE was elevated in the one patient in whom it was obtained. The lung tissue in all cases showed necrotizing giant-cell vasculitis, interstitial and perivascular granulomas, and eosinophilic pneumonia-like areas. These microscopic features distinguish allergic granulomatosis from other forms of pulmonary eosinophilia or vasculitis. Renal tissue showed necrotizing granulomatous vasculitis and interstitial eosinophilic nephritis, without evidence of glomerulonephritis. Electron-microscopic study of one lung biopsy and of the renal tissue demonstrated tissue eosinophilia and, in lung, a granuloma. There was no evidence of vascular or glomerular electron-dense deposits. These findings are discussed in the light of possible pathogenetic mechanisms of allergic granulomatosis.
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PMID:Allergic granulomatosis (Churg-Strauss syndrome): pulmonary and renal morphologic findings. 724 48

Eight cases of chronic eosinophilic pneumonia (CEP) diagnosed between January 1977 and December 1979 are described. Clinical manifestations included toxic syndrome, cough and fever, lasting from 1 to 15 months. Chest x-ray revealed peripheric bilateral infiltrates, with the exception of one case. In two patients there was no peripheral eosinophilia and five received antituberculous drugs at some point during the illness. In all cases tests for fungi and parasites were negative. In only two patients was an increase in IgE found. Hystological study confirmed CEP in 7 patients through either trans-bronchial biopsy or minimal thoracotomy. Treatment with corticosteroids was dramatically effective in all patients; both clinically and radiologically. In two cases which were asymptomatic, decreased carbon monoxide diffusing capacity persisted six months later. One hundred fifteen cases of CEP published since Carrington et al. first described CEP as a separate entity of the pulmonary infiltrates with eosinophilia syndrome are reviewed.
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PMID:[Chronic eosinophilic pneumonia: report of eight cases (author's transl)]. 725 63

We studied the appearance of IgE in the respiratory tract in 42 infants and young children with various forms of respiratory illness after infection by respiratory syncytial virus (RSV). IgE was bound to exfoliated nasopharyngeal epithelial cells in most patients with RSV infection during the acute phase of infection, regardless of the form of illness. However, the continued presence of cell-bound IgE was more common in patients with RSV-induced bronchiolitis or asthma than in patients with mild upper-respiratory-tract illness or pneumonia due to RSV. Persistence of IgE was also apparently related to the incidence of previous episodes of wheezing in patients or their families. The production of IgE and the subsequent release of chemical mediators of bronchospasm may contribute to the pathogenesis of acute illness due to RSV; persistence of IgE in the respiratory tract may explain the recurrent episodes of wheezing that occur in many patients after RSV-induced bronchiolitis.
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PMID:The appearance of cell-bound IgE in respiratory-tract epithelium after respiratory-syncytial-virus infection. 742 46

A 4-year old boy with chronic eczema since early infancy had been admitted thrice to the hospital because of recurrent staphylococcal infections including furunculosis, lymphadenitis, pneumonia and pyothorax. Exhaustive immunologic studies revealed normal humoral, cell-mediated and non-specific immunities except extremely high serum IgE level and dysfunctions of granulocytes including decreased Fc and complement receptors, lowered chemotactic response (around the lower range of normal), slightly impaired intracellular killing of staphylococci and possibly impaired reactions to candida and BCG. In spite of long-term antimicrobial prophylaxis, cold abscesses continued to appear and the eczematous skin lesions waxed and waned.
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PMID:[Job's syndrome--a case report (author's transl)]. 744 34

The respiratory mucosa is protected primarily by a secretory immune system that is under complex and only partly understood immunoregulatory control. Secretory immunoglobulins (SIgA and SIgM) protect the mucosal surface by immune exclusion of antigens. However, the fact that most IgA produced in the respiratory tract belongs to the IgA1 subclass renders SIgA in this region susceptible to IgA-specific proteases produced by Haemophilus influenzae, Streptococcus pneumonia, and Neisseria meningitidis. Immunoglobulin G can also perform immune exclusion at respiratory surfaces but, like IgE, it reaches the secretions merely by passive diffusion. The phlogistic properties of antibodies belonging to these classes explain their potential involvement in maintaining mucosal inflammation. In patients with selective IgA deficiency, SIgA is lacking and is not regularly compensated for satisfactorily by SIgM. In such patients unexplained immunoregulatory mechanisms, perhaps involving the local microbiota, give rise to a large number of IgD-producing cells in the upper respiratory tract. Immunoglobulin D cannot act as a secretory antibody and might block the protective properties of IgG; this could explain why these patients are particularly prone to recurrent infections. Our observations show that there are large individual variations in the mucosal immune system with regard to humoral immunity in the upper respiratory tract.
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PMID:The role of humoral mucosal immunity in the induction and maintenance of chronic airway infections. 776 61

An association of Chlamydia pneumoniae infection and reactive airway disease has been demonstrated in children. To determine if C. pneumoniae infection triggers production of C. pneumoniae-specific IgE, sera were examined from 45 children with and without C. pneumoniae infection. Anti-C. pneumoniae IgE was demonstrated by immunoblotting in 12 (85.7%) of 14 culture-positive asthmatic patients with wheezing compared with only 1 (9.1%) of 11 culture-positive patients with pneumonia, 2 (18.2%) of 11 culture-negative asthmatic children with wheezing, and 2 (22.2%) of 9 culture-negative asymptomatic patients. The most commonly recognized proteins were at 98 (82.4%), 78 (58.8%), 58-60 (70.6%), and 36 kDa (64.7%). The presence of anti-C. pneumoniae IgE by immunoblotting was not associated with the presence of anti-C. pneumoniae IgG and IgM by microimmunofluorescence. These results suggest that production of specific IgE may be an underlying mechanism leading to reactive airway disease in some patients with C. pneumoniae infection.
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PMID:Detection of anti-Chlamydia pneumoniae IgE in children with reactive airway disease. 779 28

Increasing evidence suggests an important role for cytokines in the regulation of eosinophilic inflammation. In the present study we investigated the distribution of leukocytes, lymphocyte subsets, their activation state, and the cytokine profile present in BAL fluid from patients with various lung diseases associated with eosinophilia. For this purpose, we analyzed the levels of IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-8, GM-CSF, TNF-alpha, and IFN-gamma, as well as soluble IL-2 and TNF receptors, in concentrated bronchoalveolar lavage (BAL) fluid obtained from clearly defined patients with allergic and nonallergic asthma, eosinophilic pneumonia, allergic bronchopulmonary aspergillosis (ABPA), hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis. BAL fluid from normal individuals and sarcoidosis patients was analyzed as noneosinophilic controls. BAL cytokine levels were compared with the cellular infiltrate and the activation state of CD4+ and CD8+ T cells as measured by the expression of IL-2 receptors (CD25), HLA-DR, and the very late activation antigen VLA-1. Beside the characteristic leukocyte infiltrate in the various lung diseases, all patients demonstrated significantly increased numbers of activated CD4 and CD8 T cells compared with normal individuals. The analysis of the cytokine profile present in BAL fluid revealed a T helper type 2 (Th2) cell cytokine pattern, with elevated IL-4 and IL-5 but normal levels of IL-2 or IFN-gamma in allergic asthma. ABPA patients demonstrated significantly increased levels of IL-4 and IL-5, with low but significantly elevated concentrations of IL-2 and IFN-gamma. In contrast, the analysis of the cytokine profile in sarcoidosis patients revealed a Th1 cell cytokine pattern characterized by increased concentrations of IL-2 and IFN-gamma but normal levels of IL-4 or IL-5. All other patient groups showed a cytokine pattern incompatible with a pure Th1 or Th2 cell response, because IL-5, IL-2, and IFN-gamma were found to be significantly increased. The BAL fluid analysis of the other, mainly non-T cell-derived cytokines and soluble receptors showed increased levels in all patients compared with normal individuals and may represent the ongoing inflammatory responses. In conclusion, whereas increased IL-4 levels were found only in diseases characterized by increased IgE production, IL-5 was elevated in all patients with increased numbers of eosinophils. The close correlation between IL-5 levels, number of eosinophils, and activated T cells further supports a role for IL-5 in causing tissue eosinophilia.
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PMID:Activated T cells and cytokines in bronchoalveolar lavages from patients with various lung diseases associated with eosinophilia. 792 34

We describe, to our knowledge, the first case of allergic bronchopulmonary mycosis (ABPM) caused by the basidiomycetous fungus Schizophyllum commune in an otherwise healthy woman. Bronchoscopic analysis repeatedly disclosed S. commune hyphae in the bronchi of the lingular lobe; these hyphae were originally misidentified as Aspergillus because the presence of clamp connections was overlooked. A lingular infiltrate with ectatic proximal bronchi, eosinophilia, an elevated serum level of IgE, and antibodies to S. commune supported the diagnosis. It is sometimes difficult to isolate and identify S. commune in clinical specimens, and hence only a limited number of cases of ABPM might have been correctly diagnosed in the past. We suspect, therefore, that some cases of ABPM caused by an allergic reaction to S. commune may be misdiagnosed as allergic bronchopulmonary aspergillosis or eosinophilic pneumonia of unknown origin. The significance of S. commune in allergic bronchopulmonary diseases is discussed.
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PMID:Allergic bronchopulmonary mycosis caused by the basidiomycetous fungus Schizophyllum commune. 801 8


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